A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions.
The largest of polypeptide chains comprising immunoglobulins. They contain 450 to 600 amino acid residues per chain, and have molecular weights of 51-72 kDa.
Genes encoding the different subunits of the IMMUNOGLOBULINS, for example the IMMUNOGLOBULIN LIGHT CHAIN GENES and the IMMUNOGLOBULIN HEAVY CHAIN GENES. The heavy and light immunoglobulin genes are present as gene segments in the germline cells. The completed genes are created when the segments are shuffled and assembled (B-LYMPHOCYTE GENE REARRANGEMENT) during B-LYMPHOCYTE maturation. The gene segments of the human light and heavy chain germline genes are symbolized V (variable), J (joining) and C (constant). The heavy chain germline genes have an additional segment D (diversity).
Immunoglobulin preparations used in intravenous infusion, containing primarily IMMUNOGLOBULIN G. They are used to treat a variety of diseases associated with decreased or abnormal immunoglobulin levels including pediatric AIDS; primary HYPERGAMMAGLOBULINEMIA; SCID; CYTOMEGALOVIRUS infections in transplant recipients, LYMPHOCYTIC LEUKEMIA, CHRONIC; Kawasaki syndrome, infection in neonates, and IDIOPATHIC THROMBOCYTOPENIC PURPURA.
Polypeptide chains, consisting of 211 to 217 amino acid residues and having a molecular weight of approximately 22 kDa. There are two major types of light chains, kappa and lambda. Two Ig light chains and two Ig heavy chains (IMMUNOGLOBULIN HEAVY CHAINS) make one immunoglobulin molecule.
Immunoglobulins produced in response to VIRAL ANTIGENS.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
One of the types of light chains of the immunoglobulins with a molecular weight of approximately 22 kDa.
The class of heavy chains found in IMMUNOGLOBULIN M. They have a molecular weight of approximately 72 kDa and they contain about 57 amino acid residues arranged in five domains and have more oligosaccharide branches and a higher carbohydrate content than the heavy chains of IMMUNOGLOBULIN G.
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
That region of the immunoglobulin molecule that varies in its amino acid sequence and composition, and comprises the binding site for a specific antigen. It is located at the N-terminus of the Fab fragment of the immunoglobulin. It includes hypervariable regions (COMPLEMENTARITY DETERMINING REGIONS) and framework regions.
An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
The principle immunoglobulin in exocrine secretions such as milk, respiratory and intestinal mucin, saliva and tears. The complete molecule (around 400 kD) is composed of two four-chain units of IMMUNOGLOBULIN A, one SECRETORY COMPONENT and one J chain (IMMUNOGLOBULIN J-CHAINS).
The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties.
A 15 kD "joining" peptide that forms one of the linkages between monomers of IMMUNOGLOBULIN A or IMMUNOGLOBULIN M in the formation of polymeric immunoglobulins. There is one J chain per one IgA dimer or one IgM pentamer. It is also involved in binding the polymeric immunoglobulins to POLYMERIC IMMUNOGLOBULIN RECEPTOR which is necessary for their transcytosis to the lumen. It is distinguished from the IMMUNOGLOBULIN JOINING REGION which is part of the IMMUNOGLOBULIN VARIABLE REGION of the immunoglobulin light and heavy chains.
An immunoglobulin which accounts for less than 1% of plasma immunoglobulin. It is found on the membrane of many circulating B LYMPHOCYTES.
A lymphoproliferative disorder characterized by pleomorphic B-LYMPHOCYTES including PLASMA CELLS, with increased levels of monoclonal serum IMMUNOGLOBULIN M. There is lymphoplasmacytic cells infiltration into bone marrow and often other tissues, also known as lymphoplasmacytic lymphoma. Clinical features include ANEMIA; HEMORRHAGES; and hyperviscosity.
Diagnostic procedures involving immunoglobulin reactions.
Crystallizable fragments composed of the carboxy-terminal halves of both IMMUNOGLOBULIN HEAVY CHAINS linked to each other by disulfide bonds. Fc fragments contain the carboxy-terminal parts of the heavy chain constant regions that are responsible for the effector functions of an immunoglobulin (COMPLEMENT fixation, binding to the cell membrane via FC RECEPTORS, and placental transport). This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
The type (and only) species of RUBIVIRUS causing acute infection in humans, primarily children and young adults. Humans are the only natural host. A live, attenuated vaccine is available for prophylaxis.
The domains of the immunoglobulin molecules that are invariable in their amino acid sequence within any class or subclass of immunoglobulin. They confer biological as well as structural functions to immunoglobulins. One each on both the light chains and the heavy chains comprises the C-terminus half of the IMMUNOGLOBULIN FAB FRAGMENT and two or three of them make up the rest of the heavy chains (all of the IMMUNOGLOBULIN FC FRAGMENT)
One of the types of light chain subunits of the immunoglobulins with a molecular weight of approximately 22 kDa.
Gene rearrangement of the B-lymphocyte which results in a substitution in the type of heavy-chain constant region that is expressed. This allows the effector response to change while the antigen binding specificity (variable region) remains the same. The majority of class switching occurs by a DNA recombination event but it also can take place at the level of RNA processing.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
Immunologic techniques based on the use of: (1) enzyme-antibody conjugates; (2) enzyme-antigen conjugates; (3) antienzyme antibody followed by its homologous enzyme; or (4) enzyme-antienzyme complexes. These are used histologically for visualizing or labeling tissue specimens.
The acquired form of infection by Toxoplasma gondii in animals and man.
Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualized by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (hemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1.
Antibodies produced by a single clone of cells.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
IMMUNOGLOBULINS on the surface of B-LYMPHOCYTES. Their MESSENGER RNA contains an EXON with a membrane spanning sequence, producing immunoglobulins in the form of type I transmembrane proteins as opposed to secreted immunoglobulins (ANTIBODIES) which do not contain the membrane spanning segment.
Partial immunoglobulin molecules resulting from selective cleavage by proteolytic enzymes or generated through PROTEIN ENGINEERING techniques.
Any discrete, presumably solitary, mass of neoplastic PLASMA CELLS either in BONE MARROW or various extramedullary sites.
Serological reactions in which an antiserum against one antigen reacts with a non-identical but closely related antigen.
Studies determining the effectiveness or value of processes, personnel, and equipment, or the material on conducting such studies. For drugs and devices, CLINICAL TRIALS AS TOPIC; DRUG EVALUATION; and DRUG EVALUATION, PRECLINICAL are available.
A genus of protozoa parasitic to birds and mammals. T. gondii is one of the most common infectious pathogenic animal parasites of man.
Heavy chains of IMMUNOGLOBULIN G having a molecular weight of approximately 51 kDa. They contain about 450 amino acid residues arranged in four domains and an oligosaccharide component covalently bound to the Fc fragment constant region. The gamma heavy chain subclasses (for example, gamma 1, gamma 2a, and gamma 2b) of the IMMUNOGLOBULIN G isotype subclasses (IgG1, IgG2A, and IgG2B) resemble each other more closely than the heavy chains of the other IMMUNOGLOBULIN ISOTYPES.
The period of recovery following an illness.
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)
Substances elaborated by bacteria that have antigenic activity.
An acute infectious disease caused by the RUBELLA VIRUS. The virus enters the respiratory tract via airborne droplet and spreads to the LYMPHATIC SYSTEM.
Allelic variants of the immunoglobulin light chains (IMMUNOGLOBULIN LIGHT CHAINS) or heavy chains (IMMUNOGLOBULIN HEAVY CHAINS) encoded by ALLELES of IMMUNOGLOBULIN GENES.
Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.
Serologic tests in which a known quantity of antigen is added to the serum prior to the addition of a red cell suspension. Reaction result is expressed as the smallest amount of antigen which causes complete inhibition of hemagglutination.
Specialized Fc receptors (RECEPTORS, FC) for polymeric immunoglobulins, which mediate transcytosis of polymeric IMMUNOGLOBULIN A and IMMUNOGLOBULIN M into external secretions. They are found on the surfaces of epithelial cells and hepatocytes. After binding to IMMUNOGLOBULIN A, the receptor-ligand complex undergoes endocytosis, transport by vesicle, and secretion into the lumen by exocytosis. Before release, the part of the receptor (SECRETORY COMPONENT) that is bound to IMMUNOGLOBULIN A is proteolytically cleaved from its transmembrane tail. (From Rosen et al., The Dictionary of Immunology, 1989)
Immunoglobulins produced in a response to PROTOZOAN ANTIGENS.
A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
Sensitive tests to measure certain antigens, antibodies, or viruses, using their ability to agglutinate certain erythrocytes. (From Stedman, 26th ed)
A segment of the immunoglobulin heavy chains, encoded by the IMMUNOGLOBULIN HEAVY CHAIN GENES in the J segment where, during the maturation of B-LYMPHOCYTES; the gene segment for the variable region upstream is joined to a constant region gene segment downstream. The exact position of joining of the two gene segments is variable and contributes to ANTIBODY DIVERSITY. It is distinguished from the IMMUNOGLOBULIN J CHAINS; a separate polypeptide that serves as a linkage piece in polymeric IGA or IGM.
A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.
Prenatal protozoal infection with TOXOPLASMA gondii which is associated with injury to the developing fetal nervous system. The severity of this condition is related to the stage of pregnancy during which the infection occurs; first trimester infections are associated with a greater degree of neurologic dysfunction. Clinical features include HYDROCEPHALUS; MICROCEPHALY; deafness; cerebral calcifications; SEIZURES; and psychomotor retardation. Signs of a systemic infection may also be present at birth, including fever, rash, and hepatosplenomegaly. (From Adams et al., Principles of Neurology, 6th ed, p735)
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
Transfer of immunity from immunized to non-immune host by administration of serum antibodies, or transplantation of lymphocytes (ADOPTIVE TRANSFER).
Immunoglobulins produced in a response to FUNGAL ANTIGENS.
Commercially prepared reagent sets, with accessory devices, containing all of the major components and literature necessary to perform one or more designated diagnostic tests or procedures. They may be for laboratory or personal use.
A protein present in the cell wall of most Staphylococcus aureus strains. The protein selectively binds to the Fc region of human normal and myeloma-derived IMMUNOGLOBULIN G. It elicits antibody activity and may cause hypersensitivity reactions due to histamine release; has also been used as cell surface antigen marker and in the clinical assessment of B lymphocyte function.
Syphilis acquired in utero and manifested by any of several characteristic tooth (Hutchinson's teeth) or bone malformations and by active mucocutaneous syphilis at birth or shortly thereafter. Ocular and neurologic changes may also occur.
Unique genetically-controlled determinants present on ANTIBODIES whose specificity is limited to a single group of proteins (e.g., another antibody molecule or an individual myeloma protein). The idiotype appears to represent the antigenicity of the antigen-binding site of the antibody and to be genetically codetermined with it. The idiotypic determinants have been precisely located to the IMMUNOGLOBULIN VARIABLE REGION of both immunoglobin polypeptide chains.
Polysaccharides found in bacteria and in capsules thereof.
Tests that are dependent on the clumping of cells, microorganisms, or particles when mixed with specific antiserum. (From Stedman, 26th ed)
Positive test results in subjects who do not possess the attribute for which the test is conducted. The labeling of healthy persons as diseased when screening in the detection of disease. (Last, A Dictionary of Epidemiology, 2d ed)
Substances elaborated by viruses that have antigenic activity.
INFLAMMATION of the LIVER in humans caused by a member of the HEPATOVIRUS genus, HUMAN HEPATITIS A VIRUS. It can be transmitted through fecal contamination of food or water.
Abnormal immunoglobulins characteristic of MULTIPLE MYELOMA.
Techniques for removal by adsorption and subsequent elution of a specific antibody or antigen using an immunosorbent containing the homologous antigen or antibody.
Contagious infection with human B19 Parvovirus most commonly seen in school age children and characterized by fever, headache, and rashes of the face, trunk, and extremities. It is often confused with rubella.
Sites on an antigen that interact with specific antibodies.
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
A phenomenon manifested by an agent or substance adhering to or being adsorbed on the surface of a red blood cell, as tuberculin can be adsorbed on red blood cells under certain conditions. (Stedman, 25th ed)
Substances, usually of biological origin, that cause cells or other organic particles to aggregate and stick to each other. They include those ANTIBODIES which cause aggregation or agglutination of particulate or insoluble ANTIGENS.
Genes and gene segments encoding the IMMUNOGLOBULIN HEAVY CHAINS. Gene segments of the heavy chain genes are symbolized V (variable), D (diversity), J (joining), and C (constant).
A programmed mutation process whereby changes are introduced to the nucleotide sequence of immunoglobulin gene DNA during development.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A viral encephalitis caused by the St. Louis encephalitis virus (ENCEPHALITIS VIRUS, ST. LOUIS), a FLAVIVIRUS. It is transmitted to humans and other vertebrates primarily by mosquitoes of the genus CULEX. The primary animal vectors are wild birds and the disorder is endemic to the midwestern and southeastern United States. Infections may be limited to an influenza-like illness or present as an ASEPTIC MENINGITIS or ENCEPHALITIS. Clinical manifestations of the encephalitic presentation may include SEIZURES, lethargy, MYOCLONUS, focal neurologic signs, COMA, and DEATH. (From Adams et al., Principles of Neurology, 6th ed, p750)
Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure MONOCLONAL ANTIBODIES or T-cell products, identical to those produced by the immunologically competent parent cell.
An encapsulated lymphatic organ through which venous blood filters.
Local surface sites on antibodies which react with antigen determinant sites on antigens (EPITOPES.) They are formed from parts of the variable regions of FAB FRAGMENTS.
An acute febrile disease transmitted by the bite of AEDES mosquitoes infected with DENGUE VIRUS. It is self-limiting and characterized by fever, myalgia, headache, and rash. SEVERE DENGUE is a more virulent form of dengue.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
An excess of GAMMA-GLOBULINS in the serum due to chronic infections or PARAPROTEINEMIAS.
Molecules found on the surface of some, but not all, B-lymphocytes, T-lymphocytes, and macrophages, which recognize and combine with the Fc (crystallizable) portion of immunoglobulin molecules.
The class of heavy chains found in IMMUNOGLOBULIN D. They have a molecular weight of approximately 64 kDa and they contain about 500 amino acid residues arranged in four domains and an oligosaccharide component covalently bound to the Fc fragment constant region.
A genus of PICORNAVIRIDAE causing infectious hepatitis naturally in humans and experimentally in other primates. It is transmitted through fecal contamination of food or water. HEPATITIS A VIRUS is the type species.
The processes triggered by interactions of ANTIBODIES with their ANTIGENS.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
A site located in the INTRONS at the 5' end of each constant region segment of a immunoglobulin heavy-chain gene where recombination (or rearrangement) occur during IMMUNOGLOBULIN CLASS SWITCHING. Ig switch regions are found on genes encoding all five classes (IMMUNOGLOBULIN ISOTYPES) of IMMUNOGLOBULIN HEAVY CHAINS.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
The class of heavy chains found in IMMUNOGLOBULIN A. They have a molecular weight of approximately 58 kDa and contain about 470 amino acid residues arranged in four domains and an oligosaccharide component bound covalently to their Fc fragment constant region.
A measure of the binding strength between antibody and a simple hapten or antigen determinant. It depends on the closeness of stereochemical fit between antibody combining sites and antigen determinants, on the size of the area of contact between them, and on the distribution of charged and hydrophobic groups. It includes the concept of "avidity," which refers to the strength of the antigen-antibody bond after formation of reversible complexes.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).
The type species of ERYTHROVIRUS and the etiological agent of ERYTHEMA INFECTIOSUM, a disease most commonly seen in school-age children.
A mosquito-borne encephalitis caused by the Japanese B encephalitis virus (ENCEPHALITIS VIRUS, JAPANESE) occurring throughout Eastern Asia and Australia. The majority of infections occur in children and are subclinical or have features limited to transient fever and gastrointestinal symptoms. Inflammation of the brain, spinal cord, and meninges may occur and lead to transient or permanent neurologic deficits (including a POLIOMYELITIS-like presentation); SEIZURES; COMA; and death. (From Adams et al., Principles of Neurology, 6th ed, p751; Lancet 1998 Apr 11;351(9109):1094-7)
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
A highly contagious infectious disease caused by MORBILLIVIRUS, common among children but also seen in the nonimmune of any age, in which the virus enters the respiratory tract via droplet nuclei and multiplies in the epithelial cells, spreading throughout the MONONUCLEAR PHAGOCYTE SYSTEM.
Serum globulins that migrate to the gamma region (most positively charged) upon ELECTROPHORESIS. At one time, gamma-globulins came to be used as a synonym for immunoglobulins since most immunoglobulins are gamma globulins and conversely most gamma globulins are immunoglobulins. But since some immunoglobulins exhibit an alpha or beta electrophoretic mobility, that usage is in decline.
Gram-negative helical bacteria, in the genus BORRELIA, that are the etiologic agents of LYME DISEASE. The group comprises many specific species including Borrelia afzelii, Borellia garinii, and BORRELIA BURGDORFERI proper. These spirochetes are generally transmitted by several species of ixodid ticks.
Specialized forms of antibody-producing B-LYMPHOCYTES. They synthesize and secrete immunoglobulin. They are found only in lymphoid organs and at sites of immune responses and normally do not circulate in the blood or lymph. (Rosen et al., Dictionary of Immunology, 1989, p169 & Abbas et al., Cellular and Molecular Immunology, 2d ed, p20)
The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.
Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.
A viral infection of the brain caused by serotypes of California encephalitis virus (ENCEPHALITIS VIRUS, CALIFORNIA) transmitted to humans by the mosquito AEDES triseriatus. The majority of cases are caused by the LA CROSSE VIRUS. This condition is endemic to the midwestern United States and primarily affects children between 5-10 years of age. Clinical manifestations include FEVER; VOMITING; HEADACHE; and abdominal pain followed by SEIZURES, altered mentation, and focal neurologic deficits. (From Joynt, Clinical Neurology, 1996, Ch26, p13)
The extracellular moiety of the POLYMERIC IMMUNOGLOBULIN RECEPTOR found alone or complexed with IGA or IGM, in a variety of external secretions (tears, bile, colostrum.) Secretory component is derived by proteolytic cleavage of the receptor during transcytosis. When immunoglobulins IgA and IgM are bound to the receptor, during their transcytosis secretory component becomes covalently attached to them generating SECRETORY IMMUNOGLOBULIN A or secretory IMMUNOGLOBULIN M.
A mosquito-borne viral illness caused by the WEST NILE VIRUS, a FLAVIVIRUS and endemic to regions of Africa, Asia, and Europe. Common clinical features include HEADACHE; FEVER; maculopapular rash; gastrointestinal symptoms; and lymphadenopathy. MENINGITIS; ENCEPHALITIS; and MYELITIS may also occur. The disease may occasionally be fatal or leave survivors with residual neurologic deficits. (From Joynt, Clinical Neurology, 1996, Ch26, p13; Lancet 1998 Sep 5;352(9130):767-71)
A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE). It can infect birds and mammals. In humans, it is seen most frequently in Africa, Asia, and Europe presenting as a silent infection or undifferentiated fever (WEST NILE FEVER). The virus appeared in North America for the first time in 1999. It is transmitted mainly by CULEX spp mosquitoes which feed primarily on birds, but it can also be carried by the Asian Tiger mosquito, AEDES albopictus, which feeds mainly on mammals.
An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
Established cell cultures that have the potential to propagate indefinitely.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE), which is the etiological agent of Japanese encephalitis found in Asia, southeast Asia, and the Indian subcontinent.
A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS.
Substances that are recognized by the immune system and induce an immune reaction.
Elements of limited time intervals, contributing to particular results or situations.
A species of the genus FLAVIVIRUS which causes an acute febrile and sometimes hemorrhagic disease in man. Dengue is mosquito-borne and four serotypes are known.
Infections with bacteria of the genus LEPTOSPIRA.
A group of related diseases characterized by an unbalanced or disproportionate proliferation of immunoglobulin-producing cells, usually from a single clone. These cells frequently secrete a structurally homogeneous immunoglobulin (M-component) and/or an abnormal immunoglobulin.
A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE), which is the etiologic agent of ST. LOUIS ENCEPHALITIS in the United States, the Caribbean, and Central and South America.
Suspensions of attenuated or killed bacteria administered for the prevention or treatment of infectious bacterial disease.
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
Allelic variants of the gamma-immunoglobulin heavy chain (IMMUNOGLOBULIN GAMMA-CHAINS) encoded by ALLELES of IMMUNOGLOBULIN HEAVY CHAIN GENES.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
The thin, yellow, serous fluid secreted by the mammary glands during pregnancy and immediately postpartum before lactation begins. It consists of immunologically active substances, white blood cells, water, protein, fat, and carbohydrates.
Infection with CYTOMEGALOVIRUS, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults.
An infectious disease caused by a spirochete, BORRELIA BURGDORFERI, which is transmitted chiefly by Ixodes dammini (see IXODES) and pacificus ticks in the United States and Ixodes ricinis (see IXODES) in Europe. It is a disease with early and late cutaneous manifestations plus involvement of the nervous system, heart, eye, and joints in variable combinations. The disease was formerly known as Lyme arthritis and first discovered at Old Lyme, Connecticut.
Conditions characterized by the presence of M protein (Monoclonal protein) in serum or urine without clinical manifestations of plasma cell dyscrasia.
A genus of aerobic, helical spirochetes, some species of which are pathogenic, others free-living or saprophytic.
Virus diseases caused by the TOGAVIRIDAE.
Cells of the lymphoid series that can react with antigen to produce specific cell products called antibodies. Various cell subpopulations, often B-lymphocytes, can be defined, based on the different classes of immunoglobulins that they synthesize.
Ordered rearrangement of B-lymphocyte variable gene regions of the IMMUNOGLOBULIN HEAVY CHAINS, thereby contributing to antibody diversity. It occurs during the first stage of differentiation of the IMMATURE B-LYMPHOCYTES.
Ordered rearrangement of B-lymphocyte variable gene regions coding for the IMMUNOGLOBULIN CHAINS, thereby contributing to antibody diversity. It occurs during the differentiation of the IMMATURE B-LYMPHOCYTES.
A specific immune response elicited by a specific dose of an immunologically active substance or cell in an organism, tissue, or cell.
Disease having a short and relatively severe course.
The natural bactericidal property of BLOOD due to normally occurring antibacterial substances such as beta lysin, leukin, etc. This activity needs to be distinguished from the bactericidal activity contained in a patient's serum as a result of antimicrobial therapy, which is measured by a SERUM BACTERICIDAL TEST.
Acute INFLAMMATION of the LIVER in humans; caused by HEPATITIS E VIRUS, a non-enveloped single-stranded RNA virus. Similar to HEPATITIS A, its incubation period is 15-60 days and is enterically transmitted, usually by fecal-oral transmission.
A common, acute infection usually caused by the Epstein-Barr virus (HERPESVIRUS 4, HUMAN). There is an increase in mononuclear white blood cells and other atypical lymphocytes, generalized lymphadenopathy, splenomegaly, and occasionally hepatomegaly with hepatitis.
A species of ALPHAVIRUS that is the etiologic agent of encephalomyelitis in humans and equines in the United States, southern Canada, and parts of South America.
Atypical gamma immunoglobulins characterized by their irreversible heat denaturation at 56-degrees C. Pyroprecipitation is inhibited at pH below 3 and above 9. The presence of pyroglobulins in the serum is the cause of pyroglobulinemia. They are frequently present in multiple myeloma and the pyroglobulin precipitate binds complement, reacts with rheumatoid factor, produces passive cutaneous anaphylaxis, generalized passive anaphylaxis and passive Arthus-type phenomena.
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
The sum of the weight of all the atoms in a molecule.
Infections of the brain caused by arthropod-borne viruses (i.e., arboviruses) primarily from the families TOGAVIRIDAE; FLAVIVIRIDAE; BUNYAVIRIDAE; REOVIRIDAE; and RHABDOVIRIDAE. Life cycles of these viruses are characterized by ZOONOSES, with birds and lower mammals serving as intermediate hosts. The virus is transmitted to humans by the bite of mosquitoes (CULICIDAE) or TICKS. Clinical manifestations include fever, headache, alterations of mentation, focal neurologic deficits, and COMA. (From Clin Microbiol Rev 1994 Jan;7(1):89-116; Walton, Brain's Diseases of the Nervous System, 10th ed, p321)
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.
A group of ALPHAVIRUS INFECTIONS which affect horses and man, transmitted via the bites of mosquitoes. Disorders in this category are endemic to regions of South America and North America. In humans, clinical manifestations vary with the type of infection, and range from a mild influenza-like syndrome to a fulminant encephalitis. (From Joynt, Clinical Neurology, 1996, Ch26, pp8-10)
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Techniques used to demonstrate or measure an immune response, and to identify or measure antigens using antibodies.
A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.
The clear, viscous fluid secreted by the SALIVARY GLANDS and mucous glands of the mouth. It contains MUCINS, water, organic salts, and ptylin.
The causative agent of venereal and non-venereal syphilis as well as yaws.
Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.
The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.
Proteins prepared by recombinant DNA technology.
Substances of fungal origin that have antigenic activity.
Virus infections caused by the PARVOVIRIDAE.
Immunoglobulins raised by any form of viral hepatitis; some of these antibodies are used to diagnose the specific kind of hepatitis.
Resistance to a disease-causing agent induced by the introduction of maternal immunity into the fetus by transplacental transfer or into the neonate through colostrum and milk.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
The type species of LYMPHOCRYPTOVIRUS, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans. It is thought to be the causative agent of INFECTIOUS MONONUCLEOSIS and is strongly associated with oral hairy leukoplakia (LEUKOPLAKIA, HAIRY;), BURKITT LYMPHOMA; and other malignancies.
Any part or derivative of any protozoan that elicits immunity; malaria (Plasmodium) and trypanosome antigens are presently the most frequently encountered.
An infant during the first month after birth.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
A positive-stranded RNA virus species in the genus HEPEVIRUS, causing enterically-transmitted non-A, non-B hepatitis (HEPATITIS E).
A species of ALPHAVIRUS causing encephalomyelitis in Equidae and humans. The virus ranges along the Atlantic seaboard of the United States and Canada and as far south as the Caribbean, Mexico, and parts of Central and South America. Infections in horses show a mortality of up to 90 percent and in humans as high as 80 percent in epidemics.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Any of numerous agile, hollow-horned RUMINANTS of the genus Capra, in the family Bovidae, closely related to the SHEEP.
A genus of FLAVIVIRIDAE containing several subgroups and many species. Most are arboviruses transmitted by mosquitoes or ticks. The type species is YELLOW FEVER VIRUS.
Genes and gene segments encoding the IMMUNOGLOBULIN LIGHT CHAINS. Gene segments of the light chain genes are designated as V (variable), J (joining), and C (constant).
The class of heavy chains found in IMMUNOGLOBULIN E. They have a molecular weight of approximately 72 kDa and they contain about 550 amino acid residues arranged in five domains and about three times more carbohydrate than the heavy chains of IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; and IMMUNOGLOBULIN G.
Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A gram-negative, rod-shaped to coccoid bacterium. It is the etiologic agent of SCRUB TYPHUS in humans and is transmitted by mites from rodent reservoirs.
A deep type of gyrate erythema that follows a bite by an ixodid tick; it is a stage-1 manifestation of LYME DISEASE. The site of the bite is characterized by a red papule that expands peripherally as a nonscaling, palpable band that clears centrally. This condition is often associated with systemic symptoms such as chills, fever, headache, malaise, nausea, vomiting, fatigue, backache, and stiff neck.
The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
A species in the genus HEPATOVIRUS containing one serotype and two strains: HUMAN HEPATITIS A VIRUS and Simian hepatitis A virus causing hepatitis in humans (HEPATITIS A) and primates, respectively.
The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development.
The hepatitis B antigen within the core of the Dane particle, the infectious hepatitis virion.
Antibodies to the HEPATITIS A ANTIGENS including antibodies to envelope, core, and non-structural proteins.
Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis.
The co-occurrence of pregnancy and an INFECTION. The infection may precede or follow FERTILIZATION.
A general term for various neoplastic diseases of the lymphoid tissue.
Ordered rearrangement of B-lymphocyte variable gene regions coding for the kappa or lambda IMMUNOGLOBULIN LIGHT CHAINS, thereby contributing to antibody diversity. It occurs during the second stage of differentiation of the IMMATURE B-LYMPHOCYTES.
An acute infectious disease caused by ORIENTIA TSUTSUGAMUSHI. It is limited to eastern and southeastern Asia, India, northern Australia, and the adjacent islands. Characteristics include the formation of a primary cutaneous lesion at the site of the bite of an infected mite, fever lasting about two weeks, and a maculopapular rash.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
Syndromes in which there is a deficiency or defect in the mechanisms of immunity, either cellular or humoral.
Incorrect diagnoses after clinical examination or technical diagnostic procedures.
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
Sudden increase in the incidence of a disease. The concept includes EPIDEMICS and PANDEMICS.
A dysgammaglobulinemia characterized by a deficiency of IMMUNOGLOBULIN A.
Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.

Features of the immune response to DNA in mice. I. Genetic control. (1/9010)

The genetic control of the immune response to DNA was studied in various strains of mice F1 hybrids and corresponding back-crosses immunized with single stranded DNA complexed to methylated bovine serum albumin. Anti-DNA antibody response was measured by radioimmuno-logical technique. High responder, low responder, and intermediate responder strains were found and the ability to respond to DNA was characterized as a dominant genetic trait which is not linked to the major locus of histocompatibility. Studies in back-crosses suggested that this immune response is under multigenic control. High responder mice produce both anti-double stranded DNA and anti-single stranded DNA 7S and 19S antibodies, while low responder mice produce mainly anti-single stranded DNA 19S antibodies.  (+info)

Skeletal muscle type ryanodine receptor is involved in calcium signaling in human B lymphocytes. (2/9010)

The regulation of intracellular free Ca2+ concentration ([Ca2+]i) in B cells remains poorly understood and is presently explained almost solely by inositol 1,4,5-triphosphate (IP3)-mediated Ca2+ release, followed by activation of a store-operated channel mechanism. In fact, there are reports indicating that IP3 production does not always correlate with the magnitude of Ca2+ release. We demonstrate here that human B cells express a ryanodine receptor (RYR) that functions as a Ca2+ release channel during the B cell antigen receptor (BCR)-stimulated Ca2+ signaling process. Immunoblotting studies showed that both human primary CD19(+) B and DAKIKI cells express a 565-kDa immunoreactive protein that is indistinguishable in molecular size and immunoreactivity from the RYR. Selective reverse transcription-polymerase chain reaction, restriction fragment length polymorphism, and sequencing of cloned cDNA indicated that the major isoform of the RYR expressed in primary CD19(+) B and DAKIKI cells is identical to the skeletal muscle type (RYR1). Saturation analysis of [3H]ryanodine binding yielded Bmax = 150 fmol/mg of protein and Kd = 110 nM in DAKIKI cells. In fluo-3-loaded CD19(+) B and DAKIKI cells, 4-chloro-m-cresol, a potent activator of Ca2+ release mediated by the ryanodine-sensitive Ca2+ release channel, induced Ca2+ release in a dose-dependent and ryanodine-sensitive fashion. Furthermore, BCR-mediated Ca2+ release in CD19(+) B cells was significantly altered by 4-chloro-m-cresol and ryanodine. These results indicate that RYR1 functions as a Ca2+ release channel during BCR-stimulated Ca2+ signaling and suggest that complex Ca2+ signals that control the cellular activities of B cells may be generated by cooperation of the IP3 receptor and RYR1.  (+info)

Human triclonal anti-IgG gammopathy. I. Iso-electric focusing characteristics of the IgG, IgA and IgM anti-IgG and their heavy and light chains. (3/9010)

Human IgG, IgA and IgM anti-IgG autoantibodies have been isolated from the serum of an individual with Felty's syndrome. These were initially noted as soluble circulating serum complexes by analytical ultracentrifugation. Isolation was accomplished by solid phase immunoadsorption and each of the three antibody populations obtained was shown to be of restricted heterogeneity by liquid and polyacrylamide gel electrofocussing methods. Type kappa light chains were obtained from each protein. Co-isoelectric focusing experiments of all possible pairs of these light chains showed them to have identical net charge characteristics. Heavy chains obtained from each protein were also monoclonal and of differing isoelectric point. The availability of this serum provides a human model with which to study the changes which may occur in autoantibodies during the autoimmune response.  (+info)

Pre-mRNA splicing of IgM exons M1 and M2 is directed by a juxtaposed splicing enhancer and inhibitor. (4/9010)

Splicing of certain pre-mRNA introns is dependent on an enhancer element, which is typically purine-rich. It is generally thought that enhancers increase the use of suboptimal splicing signals, and one specific proposal is that enhancers stabilize binding of U2AF65 to weak polypyrimidine (Py) tracts. Here, we test this model using an IgM pre-mRNA substrate, which contains a well-characterized enhancer. Although the enhancer was required for in vitro splicing, we found it had no effect on U2AF65 binding. Unexpectedly, replacement of the natural IgM Py tract, branchpoint, and 5' splice site with consensus splicing signals did not circumvent the enhancer requirement. These observations led us to identify a novel regulatory element within the IgM M2 exon that acts as a splicing inhibitor; removal of the inhibitor enabled splicing to occur in the absence of the enhancer. The IgM M2 splicing inhibitor is evolutionarily conserved, can inhibit the activity of an unrelated, constitutively spliced pre-mRNA, and acts by repressing splicing complex assembly. Interestingly, the inhibitor itself forms an ATP-dependent complex that contains U2 snRNP. We conclude that splicing of IgM exons M1 and M2 is directed by two juxtaposed regulatory elements-an enhancer and an inhibitor-and that a primary function of the enhancer is to counteract the inhibitor.  (+info)

Innate and acquired humoral immunities to influenza virus are mediated by distinct arms of the immune system. (5/9010)

"Natural" Igs, mainly IgM, comprise part of the innate immune system present in healthy individuals, including antigen-free mice. These Igs are thought to delay pathogenicity of infecting agents until antigen-induced high affinity Igs of all isotypes are produced. Previous studies suggested that the acquired humoral response arises directly from the innate response, i.e., that B cells expressing natural IgM, upon antigen encounter, differentiate to give rise both to cells that secrete high amounts of IgM and to cells that undergo affinity maturation and isotype switching. However, by using a murine model of influenza virus infection, we demonstrate here that the B cells that produce natural antiviral IgM neither increase their IgM production nor undergo isotype switching to IgG2a in response to the infection. These cells are distinct from the B cells that produce the antiviral response after encounter with the pathogen. Our data therefore demonstrate that the innate and the acquired humoral immunities to influenza virus are separate effector arms of the immune system and that antigen exposure per se is not sufficient to increase natural antibody production.  (+info)

Dietary effect of EPA-rich and DHA-rich fish oils on the immune function of Sprague-Dawley rats. (6/9010)

The dietary effect of fish oils (FOs) rich in eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) on the immune function of Sprague-Dawley rats was compared with that of safflower oil. After 3 weeks of feeding at the 10% level of a dietary fat, the IgG and IgM production by splenocytes and IgG production by mesenteric lymph node (MLN) lymphocytes were significantly higher in the FO-fed rats, while no significant difference was found in IgA or IgE productivity by both the spleen and MLN lymphocytes. In the FO-fed rats, peritoneal exudate cells released a lower amount of LTB4, reflecting their lower arachidonic acid level, and a higher amount of LTB5, reflecting their higher EPA level in phospholipids. On these EPA-rich FO exerted a stronger effect than DHA-rich FO immune functions.  (+info)

Immunodeficiency due to a unique protracted developmental delay in the B-cell lineage. (7/9010)

A unique immune deficiency in a 24-month-old male characterized by a transient but protracted developmental delay in the B-cell lineage is reported. Significant deficiencies in the number of B cells in the blood, the concentrations of immunoglobulins in the serum, and the titers of antibodies to T-dependent and T-independent antigens resolved spontaneously by the age of 39 months in a sequence that duplicated the normal development of the B-cell lineage: blood B cells followed by immunoglobulin M (IgM), IgG, IgA, and specific IgG antibodies to T-independent antigens (pneumococcal polysaccharides). Because of the sequence of recovery, the disorder could have been confused with other defects in humoral immunity, depending on when in the course of disease immunologic studies were conducted. Investigations of X-chromosome polymorphisms suggested that the disorder was not X linked in that the mother appeared to have identical X chromosomes. An autosomal recessive disorder involving a gene that controls B-cell development and maturation seems more likely. In summary, this case appears to be a novel protracted delay in the development of the B-cell lineage, possibly due to an autosomal recessive genetic defect.  (+info)

Predominant immunoglobulin A response to phase II antigen of Coxiella burnetii in acute Q fever. (8/9010)

Diagnosis of acute Q fever is usually confirmed by serology, on the basis of anti-phase II antigen immunoglobulin M (IgM) titers of >/=1:50 and IgG titers of >/=1:200. Phase I antibodies, especially IgG and IgA, are predominant in chronic forms of the disease. However, between January 1982 and June 1998, we observed anti-phase II antigen IgA titers of >/=1:200 as the sole or main antibody response in 10 of 1,034 (0.96%) patients with acute Q fever for whom information was available. In order to determine whether specific epidemiological or clinical factors were associated with these serological profiles, we conducted a retrospective case-control study that included completion of a standardized questionnaire, which was given to 40 matched controls who also suffered from acute Q fever. The mean age of patients with elevated phase II IgA titers was significantly higher than that usually observed for patients with acute Q fever (P = 0.026); the patients were also more likely than controls to live in rural areas (P = 0.026) and to have increased levels of transaminase in blood (P = 0.03). Elevated IgA titers are usually associated with chronic Q fever and are directed mainly at phase I antigens. Although the significance of our findings is unexplained, we herein emphasize the fact that IgA antibodies are not specific for chronic forms of Q fever and that they may occasionally be observed in patients with acute disease. Moreover, as such antibody profiles may not be determined by most laboratories, which test only for total antibody titers to phase I and II antigens, the three isotype-specific Ig titers should be determined as the first step in diagnosing Q fever.  (+info)

The disease is named after the Swedish physician Jan G. Waldenström, who first described it in 1944. It is also known as lymphoplasmacytic lymphoma or IgM multoculullarity.

The exact cause of Waldenström macroglobulinemia is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. The condition usually affects older adults and is more common in males than females.

Symptoms of Waldenström macroglobulinemia can include:

* Fatigue
* Weight loss
* Enlargement of the liver and spleen
* Swelling in the legs, ankles, and hands
* Pain in the bones or joints
* Increased risk of infections
* Numbness or tingling in the hands and feet

The diagnosis of Waldenström macroglobulinemia is based on a combination of physical examination, blood tests, and imaging studies. Treatment options include chemotherapy, immunomodulatory drugs, and stem cell transplantation. The prognosis for the disease varies depending on the severity of the symptoms and the response to treatment.

Overall, Waldenström macroglobulinemia is a rare and complex condition that requires careful management by a team of healthcare professionals. With appropriate treatment, many patients with this condition can experience long-term remission and improved quality of life.

The symptoms of toxoplasmosis can vary depending on the severity of the infection and the individual's overall health. In some cases, it may cause mild flu-like symptoms or no symptoms at all. However, in severe cases, it can lead to complications such as brain inflammation, eye infections, and pneumonia.

Toxoplasmosis is a significant public health concern due to its potential to affect anyone and its ability to cause serious complications, especially in certain populations such as pregnant women, people with weakened immune systems, and the elderly. It is important for individuals who may be at risk of contracting the disease to take preventive measures such as avoiding undercooked meat, washing hands frequently, and avoiding contact with cat feces.

Diagnosis of toxoplasmosis typically involves a combination of physical examination, laboratory tests, and imaging studies. Laboratory tests may include blood tests or polymerase chain reaction (PCR) to detect the parasite's DNA in the body. Imaging studies such as ultrasound or computerized tomography (CT) scans may be used to evaluate any complications of the disease.

Treatment for toxoplasmosis typically involves antibiotics to control the infection and manage symptoms. In severe cases, hospitalization may be necessary to monitor and treat any complications. Prevention is key to avoiding this disease, as there is no vaccine available to protect against it.

Plasmacytoma is a type of plasma cell dyscrasia, which is a group of diseases that affect the production and function of plasma cells. Plasma cells are a type of white blood cell that produces antibodies to fight infections. In plasmacytoma, the abnormal plasma cells grow and multiply out of control, leading to a tumor.

There are several subtypes of plasmacytoma, including:

* solitary plasmacytoma: A single tumor that occurs in one location.
* multiple myeloma: A type of cancer that affects the bones and is characterized by an overgrowth of malignant plasma cells in the bone marrow.
* extramedullary plasmacytoma: A tumor that occurs outside of the bone marrow, such as in soft tissue or organs.

Plasmacytoma is usually diagnosed through a combination of physical examination, imaging tests such as X-rays or CT scans, and biopsy. Treatment typically involves chemotherapy and/or radiation therapy to destroy the abnormal cells. In some cases, surgery may be necessary to remove the tumor.

Plasmacytoma is a relatively rare cancer, but it can be aggressive and potentially life-threatening if left untreated. It is important for patients with symptoms of plasmacytoma to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.

During convalescence, patients may be advised to follow specific dietary restrictions, engage in gentle exercise, and avoid strenuous activities that can exacerbate their condition or slow down the healing process. They may also receive medical treatment, such as physical therapy, medication, or other forms of supportive care, to aid in their recovery.

The duration of convalescence varies depending on the individual and the nature of their illness or injury. In general, convalescence can last anywhere from a few days to several weeks or even months, depending on the severity and complexity of the condition being treated.

Overall, the goal of convalescence is to allow the body to heal and recover fully, while also minimizing the risk of complications and promoting optimal functional outcomes.

Source: 'Rubella' in Duane Gubler (ed.), up-to-date online clinical reference, retrieved on March 14, 2023 from

Congenital toxoplasmosis is caused by the transmission of the Toxoplasma gondii parasite from the mother's bloodstream to the developing fetus during pregnancy. This can occur if the mother becomes infected with the parasite for the first time during pregnancy, or if she has a prior infection that reactivates during pregnancy.

The symptoms of congenital toxoplasmosis can vary depending on the severity of the infection and the organs affected. In some cases, the infection may be asymptomatic, while in others, it can cause a range of symptoms, including:

* Seizures
* Developmental delays
* Intellectual disability
* Vision loss or blindness
* Hearing loss or deafness
* Congenital anomalies such as heart defects or facial abnormalities

Congenital toxoplasmosis can be diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood tests or amniocentesis. Treatment for congenital toxoplasmosis typically involves antibiotics and supportive care, and the prognosis varies depending on the severity of the infection and the organs affected.

Prevention of congenital toxoplasmosis primarily involves avoiding exposure to the Toxoplasma gondii parasite during pregnancy. This can be achieved by avoiding contact with cat feces, not eating undercooked meat, and taking appropriate hygiene measures when handling raw meat or gardening. Pregnant women who are exposed to the parasite should seek medical attention immediately to reduce the risk of infection.

Symptoms of congenital syphilis may include:

* Deformities of the face, skull, or bones
* Developmental delays or intellectual disability
* Seizures, blindness, or hearing loss
* Swollen lymph nodes, liver, or spleen
* Rash, fever, or other signs of syphilis infection

Diagnosis of congenital syphilis is typically made through a combination of physical examination, laboratory tests, and medical imaging studies. Treatment involves antibiotics to clear the infection and manage symptoms. Early diagnosis and prompt treatment can help prevent long-term complications and improve outcomes for infected babies.

Preventive measures include screening pregnant women for syphilis and treating those who test positive promptly to prevent transmission of the infection to their developing fetuses. Safe sexual practices, such as using condoms, can also help reduce the risk of acquiring syphilis during pregnancy.

Hepatitis A is typically spread through contaminated food and water or through close contact with someone who has the infection. The virus can also be spread through sexual contact or sharing of needles.

Symptoms of hepatitis A usually appear two to six weeks after exposure and can last for several weeks or months. In some cases, the infection can lead to complications such as liver failure, which can be life-threatening.

There is a vaccine available for hepatitis A, which is recommended for individuals traveling to areas where the virus is common, people who engage in high-risk behaviors, and those with chronic liver disease. Treatment for hepatitis A typically focuses on relieving symptoms and supporting the liver as it recovers. In severe cases, hospitalization may be necessary.

Preventive measures to reduce the risk of hepatitis A infection include maintaining good hygiene practices, such as washing hands frequently, especially before eating or preparing food; avoiding consumption of raw or undercooked shellfish, particularly oysters; and avoiding close contact with people who have the infection.

The symptoms of Fifth Disease typically appear within 4 to 14 days after exposure and may include:

* Mild fever (usually less than 102°F)
* Headache
* Fatigue
* Muscle aches
* Runny nose
* Sore throat
* Swollen lymph nodes in the neck

The rash of Fifth Disease is characterized by flat, red areas on the skin that may be slightly raised and have a lace-like appearance. The rash typically appears on the cheeks, nose, arms, and legs and may be itchy or uncomfortable. In some cases, the rash may spread to other parts of the body, such as the torso or buttocks.

Fifth Disease is usually not serious and will resolve on its own within a week or two. However, in rare cases, it can lead to complications such as anemia, arthritis, or encephalitis (inflammation of the brain). Pregnant women who contract Fifth Disease are at risk for miscarriage or stillbirth, so they should seek medical attention if they suspect they have been infected.

There is no specific treatment for Fifth Disease, but symptoms can be managed with over-the-counter pain relievers, such as acetaminophen or ibuprofen, and plenty of rest. Antiviral medications may be prescribed in severe cases or for pregnant women who contract the virus.

Prevention measures for Fifth Disease include avoiding close contact with people who have the infection, washing hands frequently, and avoiding sharing personal items such as towels or utensils. Vaccination is not available for Fifth Disease, but it can be prevented by avoiding exposure to people who are infected.

In summary, Fifth Disease is a common viral infection that can cause mild symptoms such as fever, headache, and rash. While it is usually not serious, it can lead to complications in rare cases, particularly in pregnant women. There is no specific treatment for the disease, but symptoms can be managed with over-the-counter pain relievers and plenty of rest. Prevention measures include avoiding close contact with infected people, washing hands frequently, and avoiding sharing personal items.

Symptoms of SLE typically develop within 1-3 weeks after the mosquito bite and may include:

* Fever
* Headache
* Fatigue
* Confusion
* Seizures
* Weakness or paralysis
* Vision loss or double vision

The diagnosis of SLE is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include:

* Blood tests to detect the presence of antibodies against the virus
* Cerebrospinal fluid (CSF) analysis to detect inflammatory cells and viral antigens
* Imaging studies such as CT or MRI scans to evaluate brain injury

Treatment of SLE typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to control fever and pain. Antiviral medications may also be used in some cases. In severe cases, hospitalization is required to monitor and treat complications such as seizures, brain swelling, and respiratory failure.

Prevention of SLE involves controlling mosquito populations around homes and communities through measures such as:

* Eliminating standing water around homes and public areas
* Using mosquito repellents or insecticides
* Wearing protective clothing and applying insect repellent when outdoors during peak mosquito activity

Overall, SLE is a serious and potentially life-threatening condition that requires prompt medical attention if symptoms persist or worsen over time.

Symptoms of dengue fever typically begin within 2-7 days after the bite of an infected mosquito and can include:

* High fever
* Severe headache
* Pain behind the eyes
* Severe joint and muscle pain
* Rash
* Fatigue
* Nausea
* Vomiting

In some cases, dengue fever can develop into a more severe form of the disease, known as dengue hemorrhagic fever (DHF), which can be life-threatening. Symptoms of DHF include:

* Severe abdominal pain
* Vomiting
* Diarrhea
* Bleeding from the nose, gums, or under the skin
* Easy bruising
* Petechiae (small red spots on the skin)
* Black stools
* Decreased urine output

Dengue fever is diagnosed based on a combination of symptoms, physical examination findings, and laboratory tests. Treatment for dengue fever is primarily focused on relieving symptoms and managing fluid and electrolyte imbalances. There is no specific treatment for the virus itself, but early detection and proper medical care can significantly lower the risk of complications and death.

Prevention of dengue fever relies on measures to prevent mosquito bites, such as using insect repellents, wearing protective clothing, and eliminating standing water around homes and communities to reduce the breeding of mosquitoes. Vaccines against dengue fever are also being developed, but none are currently available for widespread use.

In summary, dengue is a viral disease that is transmitted to humans through the bite of infected mosquitoes and can cause a range of symptoms from mild to severe. Early detection and proper medical care are essential to prevent complications and death from dengue fever. Prevention of dengue relies on measures to prevent mosquito bites and eliminating standing water around homes and communities.

References:

1. World Health Organization. (2020). Dengue and severe dengue. Retrieved from
2. Centers for Disease Control and Prevention. (2020). Dengue fever: Background. Retrieved from
3. Mayo Clinic. (2020). Dengue fever. Retrieved from
4. MedlinePlus. (2020). Dengue fever. Retrieved from

There are several causes of hypergammaglobulinemia, including:

1. Chronic infections: Prolonged infections can cause an increase in the production of immunoglobulins to fight off the infection.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis can cause the immune system to produce excessive amounts of antibodies.
3. Cancer: Some types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause an increase in immunoglobulin production.
4. Genetic disorders: Certain genetic conditions, such as X-linked agammaglobulinemia, can lead to a deficiency or excess of immunoglobulins.
5. Medications: Certain medications, such as corticosteroids and chemotherapy drugs, can suppress the immune system and reduce the production of immunoglobulins.

Symptoms of hypergammaglobulinemia can include:

1. Infections: Recurring infections are a common symptom of hypergammaglobulinemia, as the excessive amount of antibodies can make it difficult for the body to fight off infections effectively.
2. Fatigue: Chronic infections and inflammation can cause fatigue and weakness.
3. Weight loss: Recurring infections and chronic inflammation can lead to weight loss and malnutrition.
4. Swollen lymph nodes: Enlarged lymph nodes are a common symptom of hypergammaglobulinemia, as the body tries to fight off infections.
5. Fever: Recurring fevers can be a symptom of hypergammaglobulinemia, as the body tries to fight off infections.
6. Night sweats: Excessive sweating at night can be a symptom of hypergammaglobulinemia.
7. Skin rashes: Certain types of skin rashes can be a symptom of hypergammaglobulinemia, such as a rash caused by allergic reactions to medications or infections.
8. Joint pain: Pain and stiffness in the joints can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the joints.
9. Headaches: Chronic headaches can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the brain or other parts of the body.
10. Swollen liver and spleen: Enlarged liver and spleen can be a symptom of hypergammaglobulinemia, as the body tries to filter out excess antibodies and fight off infections.

It is important to note that these symptoms can also be caused by other medical conditions, so it is essential to consult a healthcare professional for proper diagnosis and treatment. A healthcare professional may perform blood tests and other diagnostic procedures to determine the underlying cause of the symptoms and develop an appropriate treatment plan. Treatment for hypergammaglobulinemia typically involves addressing the underlying cause of the condition, such as infections, allergies, or autoimmune disorders, and may include medications to reduce inflammation and suppress the immune system.

Synonyms: JE

Definition:

A viral infection that affects the brain and is transmitted by the bite of an infected Culex species mosquito. The virus is found throughout Asia and the western Pacific region.

Symptoms:

* Fever
* Headache
* Vomiting
* Seizures
* Confusion
* Weakness in the limbs

Diagnosis:

* Blood tests to detect antibodies against the virus
* Imaging studies such as CT or MRI scans to look for signs of brain inflammation

Treatment:

* Supportive care, such as intravenous fluids and oxygen therapy, to manage symptoms and prevent complications
* Antiviral medications may be given in some cases

Prognosis:

* The prognosis for Japanese encephalitis is generally good if treatment is received promptly and the patient is otherwise healthy. However, in severe cases or those with underlying medical conditions, the virus can cause significant brain damage and lead to long-term complications or death.

Prevention:

* Vaccination against Japanese encephalitis is recommended for people who live in or travel to areas where the virus is common, particularly children and adults who plan to spend extended periods of time outdoors. The vaccine is effective in preventing severe illness and death from the virus.
* Mosquito control measures, such as using insect repellents and wearing protective clothing, can also help reduce the risk of infection.

Measles is caused by a virus that is transmitted through the air when an infected person coughs or sneezes. The virus can also be spread through direct contact with an infected person's saliva or mucus.

The symptoms of measles usually appear about 10-14 days after exposure to the virus, and may include:

* Fever
* Cough
* Runny nose
* Red, watery eyes
* Small white spots inside the mouth (Koplik spots)
* A rash that starts on the head and spreads to the rest of the body

Measles can be diagnosed through a physical examination, laboratory tests, or by observing the characteristic rash. There is no specific treatment for measles, but it can be treated with over-the-counter medications such as acetaminophen or ibuprofen to relieve fever and pain.

Complications of measles can include:

* Ear infections
* Pneumonia
* Encephalitis (inflammation of the brain)
* Seizures
* Death (rare)

Measles is highly contagious and can spread easily through schools, workplaces, and other communities. Vaccination is the best way to prevent measles, and the Measles, Mumps, and Rubella (MMR) vaccine is recommended for all children and adults who have not been previously infected with the virus or vaccinated.

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1. Centers for Disease Control and Prevention (CDC). (2022). Encephalitis. Retrieved from
2. Mayo Clinic. (2022). Encephalitis. Retrieved from
3. MedlinePlus. (2022). Encephalitis. Retrieved from
4. UC Davis Health System. (2022). Encephalitis. Retrieved from
5. California Department of Public Health. (2022). Encephalitis. Retrieved from

In the medical field, "Encephalitis, California" refers to a type of inflammatory disease that affects the brain and is caused by a viral or bacterial infection. The term specifically refers to cases of encephalitis that occur in the state of California.

Encephalitis is a serious condition that can cause a range of symptoms, including fever, headache, confusion, seizures, and loss of consciousness. In severe cases, it can lead to long-term complications, such as brain damage, or even be fatal.

The causes of encephalitis in California are typically viral or bacterial infections that are transmitted through mosquitoes, ticks, or other vectors. The most common viruses that cause encephalitis in the state include West Nile virus, Japanese encephalitis virus, and St. Louis encephalitis virus.

The diagnosis of encephalitis is typically made based on a combination of clinical symptoms, laboratory tests, and imaging studies such as CT or MRI scans. Treatment for encephalitis typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to manage fever and pain. In severe cases, antiviral or antibacterial medications may be administered to help reduce the severity of the infection.

Prevention of encephalitis in California is focused on reducing the risk of mosquito-borne and tick-borne infections. This includes using insect repellents, wearing protective clothing, and avoiding areas with high mosquito or tick activity. Vaccines are also available for some of the viruses that cause encephalitis, such as West Nile virus.

In summary, "Encephalitis, California" refers to a serious inflammatory disease that affects the brain and is caused by viral or bacterial infections in the state of California. The diagnosis and treatment of encephalitis are based on clinical symptoms and laboratory tests, and prevention strategies focus on reducing the risk of mosquito-borne and tick-borne infections.

The symptoms of West Nile Fever typically develop within 3-14 days after the bite of an infected mosquito and can range from mild to severe. Mild symptoms may include fever, headache, muscle weakness, and joint pain. Severe symptoms can include high fever, stiff neck, confusion, loss of consciousness, and in rare cases, death.

There is no specific treatment for West Nile Fever, but supportive care such as rest, hydration, and pain relief medications may be provided to help manage the symptoms. The prognosis for most people with West Nile Fever is generally good, but it can be more severe in older adults and those with underlying health conditions.

Prevention of West Nile Fever involves protecting oneself against mosquito bites by using insect repellents, wearing protective clothing, and staying indoors during peak mosquito activity. Eliminating standing water around homes and communities can also help reduce the risk of mosquito breeding and transmission of the virus.

In conclusion, West Nile Fever is a viral disease that is transmitted to humans through the bite of infected mosquitoes, and can cause mild to severe symptoms. Prevention involves protecting oneself against mosquito bites and eliminating standing water to reduce the risk of mosquito breeding and transmission of the virus.

People with agammaglobulinemia are more susceptible to infections, particularly those caused by encapsulated bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae type b. They may also experience recurrent sinopulmonary infections, ear infections, and gastrointestinal infections. The disorder can be managed with intravenous immunoglobulin (IVIG) therapy, which provides antibodies to help prevent infections. In severe cases, a bone marrow transplant may be necessary.

Agammaglobulinemia is an autosomal recessive disorder, meaning that a person must inherit two mutated copies of the BTK gene (one from each parent) to develop the condition. It is relatively rare, affecting approximately one in 1 million people worldwide. The disorder can be diagnosed through genetic testing and a complete blood count (CBC) that shows low levels of immunoglobulins.

Treatment for ag

The diagnosis of leptospirosis is based on a combination of clinical symptoms, laboratory tests, and the patient's exposure history. The most common diagnostic test is a blood test that detects antibodies against Leptospira. Treatment typically involves antibiotics and supportive care to manage symptoms.

Prevention of leptospirosis includes avoiding exposure to contaminated water, soil, or food, wearing protective clothing when working with animals or in areas where the bacteria may be present, and vaccinating animals that are at risk of infection. The disease is more common in tropical and subtropical regions, and it affects people who work outdoors or engage in activities that expose them to contaminated water, such as farmers, veterinarians, and sewer workers.

In medical terminology, leptospirosis is classified as a zoonotic disease, meaning it can be transmitted between animals and humans. The bacteria that cause the infection are gram-negative, aerobic, and helical shaped, and they belong to the family Leptospiraceae.

In summary, leptospirosis is a bacterial infection that can affect both humans and animals, and it is spread through contact with contaminated water, soil, or food. It can cause a wide range of symptoms, from mild to severe, and can lead to serious complications if left untreated. Prevention measures include avoiding exposure to contaminated sources, wearing protective clothing, and vaccinating animals at risk.

There are several types of paraproteinemias, including:

1. Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow, leading to an overproduction of immunoglobulins.
2. Monoclonal gammopathy of undetermined significance (MGUS): This is a condition in which there is an abnormal increase in the level of immunoglobulins in the blood, but the cause cannot be determined.
3. Waldenström macroglobulinemia: This is a rare type of cancer that affects the plasma cells in the bone marrow and leads to an overproduction of immunoglobulins.
4. Primary amyloidosis: This is a condition in which abnormal proteins called amyloids accumulate in the organs, leading to damage and dysfunction.
5. Secondary amyloidosis: This is a condition in which abnormal proteins called amyloids accumulate in the organs due to another underlying condition, such as rheumatoid arthritis or systemic lupus erythematosus.

The symptoms of paraproteinemias can vary depending on the type and severity of the disorder. Common symptoms include fatigue, weakness, weight loss, infections, kidney damage, and bone pain. Treatment options for paraproteinemias depend on the specific type of disorder and may include chemotherapy, radiation therapy, or medications to reduce protein production.

CMV infections are more common in people with weakened immune systems, such as those with HIV/AIDS, cancer, or taking immunosuppressive drugs after an organ transplant. In these individuals, CMV can cause severe and life-threatening complications, such as pneumonia, retinitis (inflammation of the retina), and gastrointestinal disease.

In healthy individuals, CMV infections are usually mild and may not cause any symptoms at all. However, in some cases, CMV can cause a mononucleosis-like illness with fever, fatigue, and swollen lymph nodes.

CMV infections are diagnosed through a combination of physical examination, blood tests, and imaging studies such as CT scans or MRI. Treatment is generally not necessary for mild cases, but may include antiviral medications for more severe infections. Prevention strategies include avoiding close contact with individuals who have CMV, practicing good hygiene, and considering immunoprophylaxis (prevention of infection through the use of immune globulin) for high-risk individuals.

Overall, while CMV infections can be serious and life-threatening, they are relatively rare in healthy individuals and can often be treated effectively with supportive care and antiviral medications.

Lyme disease is typically diagnosed based on a combination of physical symptoms, medical history, and laboratory tests. Treatment typically involves antibiotics, which can help to clear the infection and alleviate symptoms.

Prevention of Lyme disease involves protecting against tick bites by using insect repellents, wearing protective clothing when outdoors, and conducting regular tick checks. Early detection and treatment of Lyme disease can help to prevent long-term complications, such as joint inflammation and neurological problems.

In this definition, we have used technical terms such as 'bacterial infection', 'blacklegged tick', 'Borrelia burgdorferi', and 'antibiotics' to provide a more detailed understanding of the medical concept.

MGUS is relatively common, especially among older adults, and it often has no symptoms. However, some people with MGUS may experience fatigue, weakness, or bone pain. The condition is usually detected during a routine blood test that measures the level of M-protein in the blood.

There are several risk factors for developing MGUS, including age (it is more common among older adults), family history of multiple myeloma, and certain medical conditions such as hypertension or type 2 diabetes. The exact cause of MGUS is not known, but it is believed to be related to genetic mutations that occur in plasma cells.

Doctors use several criteria to diagnose MGUS, including the level of M-protein in the blood, the amount of other proteins in the blood, and the presence of certain abnormalities in the blood or bone marrow. Treatment for MGUS is typically observation and monitoring, as there is no specific therapy that can cure the condition. However, doctors may recommend treatment for any underlying medical conditions that are contributing to the development of MGUS.

The prognosis for MGUS varies depending on several factors, including the level of M-protein in the blood, the presence of certain abnormalities in the blood or bone marrow, and the patient's overall health status. In some cases, MGUS may progress to multiple myeloma over time, but this is not always the case.

The symptoms of Togaviridae infections can vary depending on the specific virus and the individual infected, but may include fever, headache, joint pain, muscle pain, and rash. In severe cases, these infections can lead to hemorrhagic fever, shock, and even death.

There is no specific treatment for Togaviridae infections, but early diagnosis and supportive care, such as fluid replacement and management of fever and pain, can help alleviate symptoms and improve outcomes. Prevention measures include avoiding mosquito bites by using insect repellents, wearing protective clothing, and staying in air-conditioned or screened areas. Vaccines are also available for some of the diseases caused by Togaviridae viruses, such as yellow fever.

Togaviridae infections are a significant public health concern in many parts of the world, particularly in tropical and subtropical regions where mosquitoes are more prevalent. Outbreaks of these diseases can have a significant impact on individuals, communities, and economies, highlighting the importance of continued research and development of effective prevention and control measures.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

Symptoms of hepatitis E can include fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, and yellowing of the skin and eyes (jaundice).

Hepatitis E is usually a self-limiting disease, meaning it will resolve on its own without treatment. However, in some cases, it can lead to fulminant hepatitis, which is a severe and potentially life-threatening form of liver disease.

There are several ways to diagnose hepatitis E, including blood tests to detect the presence of HEV antigens or antibodies, as well as imaging tests such as ultrasound or CT scans to evaluate liver function.

Treatment for hepatitis E is typically supportive, meaning it focuses on managing symptoms and maintaining hydration. In severe cases, hospitalization may be necessary to monitor and treat complications. Prevention of hepatitis E involves improving access to safe water and sanitation, as well as promoting good hygiene practices, such as washing hands regularly.

Vaccines are available for hepatitis E, but they are not widely available or recommended for most individuals. However, they may be recommended for certain high-risk groups, such as people living in areas with a high prevalence of HEV infection or those traveling to such areas.

The symptoms of infectious mononucleosis can vary in severity but typically include:

* Fatigue
* Fever
* Sore throat
* Swollen lymph nodes in the neck and armpits
* Enlarged spleen
* Headache
* Muscle weakness
* Rash
* Swollen liver or spleen

Infectious mononucleosis is usually diagnosed through a combination of physical examination, blood tests, and other laboratory tests. Treatment focuses on relieving symptoms and allowing the body to fight the infection on its own.

Prognosis for infectious mononucleosis is generally good, but it can take several weeks to recover fully. Complications are rare but can include inflammation of the spleen, liver disease, and a condition called splenomegaly (enlargement of the spleen).

Prevention includes avoiding close contact with people who have mononucleosis, washing hands frequently, and not sharing eating or drinking utensils. There is no vaccine available to protect against infectious mononucleosis.

Symptoms of arbovirus encephalitis can include fever, headache, confusion, seizures, and coma. In severe cases, the infection can be fatal.

Diagnosis of arbovirus encephalitis is typically made through a combination of physical examination, laboratory tests, and imaging studies such as CT or MRI scans. Laboratory tests may include blood tests to detect the presence of antibodies against the virus or PCR (polymerase chain reaction) to detect the virus itself in the blood or cerebrospinal fluid.

Treatment of arbovirus encephalitis typically involves supportive care, such as intravenous fluids, oxygen therapy, and pain management. Antiviral medications may be used in some cases to help reduce the severity of the infection. In severe cases, hospitalization may be necessary to provide more intensive care.

Prevention of arbovirus encephalitis primarily involves protecting against mosquito bites, such as using insect repellents, wearing protective clothing, and avoiding areas with high mosquito activity. Eliminating standing water around homes and communities can also help reduce the risk of mosquito breeding and transmission of the virus. Vaccines are not available for most arboviruses, but research is ongoing to develop effective vaccines against these viruses.

Symptoms of encephalomyelitis in horses can include fever, loss of appetite, depression, weakness, and difficulty walking or standing. In severe cases, the disease can cause seizures, paralysis, and even death.

Diagnosis of encephalomyelitis is typically made through a combination of physical examination, laboratory tests, and imaging studies such as CT or MRI scans. Treatment may include supportive care, antibiotics, and anti-inflammatory medications, depending on the underlying cause of the disease.

Prognosis for horses with encephalomyelitis is generally poor, as the disease can be difficult to treat and can result in long-term neurological damage or death. However, early diagnosis and treatment can improve the chances of a successful outcome.

The most common parvoviridae infection in animals is feline panleukopenia (FPV) or canine parvovirus (CPV), which affects dogs and cats. These infections are highly contagious and can cause a range of symptoms, including fever, vomiting, diarrhea, lethargy, and loss of appetite. In severe cases, they can lead to life-threatening complications such as anemia, bone marrow failure, and death.

There is no specific treatment for parvoviridae infections, but supportive care such as fluid therapy, antibiotics, and anti-inflammatory medication can help manage symptoms and prevent complications. Vaccination is the most effective way to prevent parvoviridae infections, and vaccines are available for dogs, cats, and other animals.

In humans, parvoviridae infections are rare but can occur through contact with infected animals or contaminated feces. The most common human parvoviridae infection is erythema infectiosum (Fifth disease), which causes a rash, fever, and mild symptoms. Pregnant women who contract parvoviridae infections may experience complications such as miscarriage or preterm labor. There is no specific treatment for human parvoviridae infections, but supportive care can help manage symptoms.

The term "erythema chronicum migrans" is derived from the Latin words "erythema," meaning redness, and "chronicum," meaning long-lasting. The term "migrans" refers to the fact that the rash typically spreads or migrates over time. ECM is considered a hallmark symptom of Lyme disease and is often used as a diagnostic criterion for the condition.

The exact cause of ECM is not fully understood, but it is thought to be due to an immune response to the bacterial infection. Treatment for ECM typically involves antibiotics to eradicate the infection, and symptoms may resolve within several weeks of treatment. However, some patients may experience persistent symptoms or develop long-term complications, such as arthritis or neurological problems.

1. Group B streptococcus (GBS): This type of bacterial infection is the leading cause of infections in newborns. GBS can cause a range of complications, including pneumonia, meningitis, and sepsis.
2. Urinary tract infections (UTIs): These are common during pregnancy and can be caused by bacteria such as Escherichia coli (E. coli) or Staphylococcus saprophyticus. UTIs can lead to complications such as preterm labor and low birth weight.
3. HIV: Pregnant women who are infected with HIV can pass the virus to their baby during pregnancy, childbirth, or breastfeeding.
4. Toxoplasmosis: This is an infection caused by a parasite that can be transmitted to the fetus through the placenta. Toxoplasmosis can cause a range of complications, including birth defects and stillbirth.
5. Listeriosis: This is a rare infection caused by eating contaminated food, such as soft cheeses or hot dogs. Listeriosis can cause complications such as miscarriage, stillbirth, and premature labor.
6. Influenza: Pregnant women who contract the flu can be at higher risk for complications such as pneumonia and hospitalization.
7. Herpes simplex virus (HSV): This virus can cause complications such as preterm labor, low birth weight, and neonatal herpes.
8. Human parvovirus (HPV): This virus can cause complications such as preterm labor, low birth weight, and stillbirth.
9. Syphilis: This is a sexually transmitted infection that can be passed to the fetus during pregnancy, leading to complications such as stillbirth, premature birth, and congenital syphilis.
10. Chickenpox: Pregnant women who contract chickenpox can be at higher risk for complications such as preterm labor and low birth weight.

It's important to note that the risks associated with these infections are relatively low, and many pregnant women who contract them will have healthy pregnancies and healthy babies. However, it's still important to be aware of the risks and take steps to protect yourself and your baby.

Here are some ways to reduce your risk of infection during pregnancy:

1. Practice good hygiene: Wash your hands frequently, especially before preparing or eating food.
2. Avoid certain foods: Avoid consuming raw or undercooked meat, eggs, and dairy products, as well as unpasteurized juices and soft cheeses.
3. Get vaccinated: Get vaccinated against infections such as the flu and HPV.
4. Practice safe sex: Use condoms or other forms of barrier protection to prevent the spread of STIs.
5. Avoid close contact with people who are sick: If someone in your household is sick, try to avoid close contact with them if possible.
6. Keep your environment clean: Regularly clean and disinfect surfaces and objects that may be contaminated with germs.
7. Manage stress: High levels of stress can weaken your immune system and make you more susceptible to infection.
8. Get enough rest: Adequate sleep is essential for maintaining a healthy immune system.
9. Stay hydrated: Drink plenty of water throughout the day to help flush out harmful bacteria and viruses.
10. Consider taking prenatal vitamins: Prenatal vitamins can help support your immune system and overall health during pregnancy.

Remember, it's always better to be safe than sorry, so if you suspect that you may have been exposed to an infection or are experiencing symptoms of an infection during pregnancy, contact your healthcare provider right away. They can help determine the appropriate course of action and ensure that you and your baby stay healthy.

There are several types of lymphoma, including:

1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.

The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching

Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.

Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.

The symptoms of scrub typhus can range from mild to severe and may include:

* Fever, headache, and body aches
* Rash, which may appear on the third to fifth day of infection
* Pneumonia, hepatitis, and meningitis
* In severe cases, scrub typhus can cause multiple organ failure and death

Diagnosis of scrub typhus is based on a combination of clinical presentation, laboratory tests, and serology. Treatment is typically with antibiotics, and early diagnosis and treatment can significantly improve outcomes. Prevention includes protective clothing, insect repellents, and avoiding contact with areas where the mite is found.

Scrub typhus is an important public health concern in many parts of the world, particularly in rural and semi-rural areas where exposure to infected mites is more common. It is essential to be aware of the risk of scrub typhus when traveling or living in areas where the disease is prevalent.

Examples of Immunologic Deficiency Syndromes include:

1. Primary Immunodeficiency Diseases (PIDDs): These are a group of genetic disorders that affect the immune system's ability to function properly. Examples include X-linked agammaglobulinemia, common variable immunodeficiency, and severe combined immunodeficiency.
2. Acquired Immunodeficiency Syndrome (AIDS): This is a condition that results from the human immunodeficiency virus (HIV) infection, which destroys CD4 cells, a type of immune cell that fights off infections.
3. Immune Thrombocytopenic Purpura (ITP): This is an autoimmune disorder that causes the immune system to attack and destroy platelets, which are blood cells that help the blood to clot.
4. Autoimmune Disorders: These are conditions in which the immune system mistakenly attacks and damages healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, and multiple sclerosis.
5. Immunosuppressive Therapy-induced Immunodeficiency: This is a condition that occurs as a side effect of medications used to prevent rejection in organ transplant patients. These medications can suppress the immune system, increasing the risk of infections.

Symptoms of Immunologic Deficiency Syndromes can vary depending on the specific disorder and the severity of the immune system dysfunction. Common symptoms include recurrent infections, fatigue, fever, and swollen lymph nodes. Treatment options for these syndromes range from medications to suppress the immune system to surgery or bone marrow transplantation.

In summary, Immunologic Deficiency Syndromes are a group of disorders that result from dysfunction of the immune system, leading to recurrent infections and other symptoms. There are many different types of these syndromes, each with its own set of symptoms and treatment options.

There are different types of immunoglobulins, also called antibodies, that the body produces to fight off infections. One type is called Immunoglobulin A (IgA), which is found in mucosal surfaces like the respiratory, gastrointestinal and genitourinary tracts. IgA plays a crucial role in protecting these areas from infection. It helps neutralize and remove pathogens from the body before they can cause harm.

IgA deficiency is when the body does not produce enough IgA, either due to a genetic defect or other underlying conditions. This deficiency may increase the risk of developing certain types of infections. People with IgA deficiency are more likely to get respiratory infections like bronchitis, pneumonia and sinusitis. They may also experience frequent ear infections, tonsillitis and other throat infections.

Some people are born with IgA deficiency due to genetic mutations that affect the production of this antibody. Others can develop it over time due to certain medical conditions or medications. For example, people with HIV/AIDS often have low levels of IgA. Certain drugs such as corticosteroids and chemotherapy can also reduce IgA production.

There are two main forms of the disease, depending on the species of parasite and the location where the infection is acquired:

* T. b. rhodesiense infection is found primarily in East and Southern Africa, and is characterized by a more severe form of the disease. Symptoms can include fever, headache, joint pain, and skin rashes, as well as swelling of the lymph nodes and spleen. If left untreated, the disease can progress to a more advanced stage, characterized by neurological symptoms such as confusion, seizures, and coma.
* T. b. gambiense infection is found primarily in West and Central Africa, and is characterized by a milder form of the disease. Symptoms can include fever, joint pain, and skin rashes, as well as swelling of the lymph nodes and spleen.

Both forms of the disease are treatable with antiparasitic drugs, but if left untreated, they can be fatal. Diagnosis is typically made through a combination of physical examination, laboratory tests, and imaging studies such as ultrasound or CT scans. Treatment is usually with melarsoprol or eflornithine, and in some cases, surgery may be necessary to remove affected tissue or organs.

Prevention of trypanosomiasis involves controlling the population of tsetse flies through the use of insecticides, traps, and other methods, as well as educating people about how to avoid being bitten by infected flies. There is also ongoing research into the development of a vaccine against trypanosomiasis.

There are two forms of trypanosomiasis, depending on the stage of the parasite:

1. Acute trypanosomiasis: This form of the disease occurs in the early stages of infection and is characterized by fever, headache, muscle pain, and joint swelling.
2. Chronic trypanosomiasis: This form of the disease occurs in the later stages of infection and is characterized by progressive neurological symptoms, including confusion, slurred speech, and difficulty walking.

If left untreated, trypanosomiasis can be fatal. Treatment typically involves the use of antiparasitic drugs, such as melarsoprol or eflornithine.

In addition to its medical significance, trypanosomiasis has also had significant social and economic impacts on affected communities, particularly in rural areas where the disease is more common. The stigma associated with the disease can lead to social isolation and marginalization of infected individuals and their families, while the financial burden of treatment can be a significant source of poverty.

Overall, trypanosomiasis is a serious and potentially deadly disease that requires prompt diagnosis and treatment to prevent complications and improve outcomes for affected individuals.

There are several types of dysgammaglobulinemia, including:

1. X-linked agammaglobulinemia (XLA): This is a rare genetic disorder caused by mutations in the Bruton's tyrosine kinase (BTK) gene. It results in a complete absence of immunoglobulins in the blood, leaving individuals with XLA susceptible to infections.
2. Common variable immunodeficiency (CVID): This is a relatively common autoimmune disorder that affects B cells and leads to low levels of immunoglobulins in the blood. It can be associated with other autoimmune disorders, such as hypothyroidism or rheumatoid arthritis.
3. Selective IgA deficiency: This is a relatively common condition characterized by low levels of IgA antibodies in the blood. It can increase the risk of infections, particularly in the respiratory and gastrointestinal tracts.
4. Other forms of dysgammaglobulinemia: There are several other less common forms of dysgammaglobulinemia that can be caused by a variety of genetic or acquired factors, such as mutations in the immunoglobulin genes, chronic infections, or certain medications.

The symptoms and signs of dysgammaglobulinemia depend on the specific type and severity of the disorder. Common symptoms include recurrent infections, particularly respiratory and gastrointestinal infections, as well as fatigue, fever, and night sweats. Diagnosis is typically made based on a combination of clinical findings, laboratory tests (such as measurements of immunoglobulin levels), and genetic testing. Treatment options include antibiotics for infections, immunoglobulin replacement therapy, and management of associated symptoms such as fatigue and fever.

The symptoms of coccidioidomycosis can vary depending on the severity of the infection and the individual's immune response. Some people may experience mild symptoms, such as fever, cough, and fatigue, while others may develop more severe symptoms, including pneumonia, meningitis, and bone or skin infections. Skin lesions and rashes are also common.

Diagnosis of coccidioidomycosis typically involves a combination of physical examination, laboratory tests, and imaging studies. Treatment may involve antifungal medications and supportive care to manage symptoms. In severe cases, hospitalization may be necessary.

Prevention is key in avoiding coccidioidomycosis, which includes avoiding areas with high concentrations of the fungus, using respiratory protection when working in areas where the fungus is present, and taking antifungal medications prophylactically for those who are at high risk.

Prognosis for coccidioidomycosis is generally good for those with mild infections, but can be poor for those with severe infections or underlying conditions such as HIV/AIDS or cancer. Long-term effects of the infection can include lung scarring and joint damage.

A viral infection that affects the brain and spinal cord, caused by a tick-borne virus. Also called TBEV (Tick-Borne Encephalitis Virus). The symptoms of this condition include fever, headache, muscle weakness, confusion, and difficulty speaking or understanding speech. In severe cases, it can lead to inflammation of the brain, seizures, and even death.

Tick-borne encephalitis is most commonly found in Asia, Europe, and parts of North America. It is transmitted to humans through the bite of infected ticks, typically found in forested areas and grasslands. There is no specific treatment for tick-borne encephalitis, but antiviral medications and supportive care may be given to help manage symptoms. Prevention involves avoiding tick habitats and using protective measures such as insect repellents and clothing coverage when outdoors.

Mumps is typically diagnosed based on a combination of symptoms and physical examination findings. Laboratory tests such as PCR or IgG antibody testing may also be performed to confirm the diagnosis. There is no specific treatment for mumps, but supportive care such as pain management and hydration may be provided to alleviate symptoms. Vaccines are available to prevent mumps, and they are most effective when given before exposure to the virus.

The medical field has a clear definition of mumps, which is essential for accurate diagnosis, treatment, and prevention of the disease. The World Health Organization (WHO) defines mumps as "a contagious viral infection that affects the salivary glands, particularly the parotid gland." The Centers for Disease Control and Prevention (CDC) also provides guidelines for diagnosis, treatment, and prevention of mumps.

In conclusion, mumps is a viral infection that affects the salivary glands and can cause pain, discomfort, and potentially serious complications. The medical field has a clear definition of mumps, which is essential for accurate diagnosis, treatment, and prevention of the disease. Vaccines are available to prevent mumps, and they are most effective when given before exposure to the virus.

Hantavirus infections can cause a range of diseases, including:

1. Hemorrhagic fever with renal syndrome (HFRS): This is the most common form of hantavirus infection and is characterized by fever, hemorrhaging, and failure of the kidneys.
2. Hypereosinophilic syndrome (HES): This is a rare form of hantavirus infection that is characterized by an abnormal increase in the number of eosinophils in the blood.
3. Pulmonary hantavirus infection: This is a rare form of hantavirus infection that affects the lungs and can cause respiratory failure.
4. Cardiac hantavirus infection: This is a rare form of hantavirus infection that affects the heart and can cause cardiac failure.

The symptoms of hantavirus infections can vary depending on the type of disease, but may include fever, headache, muscle pain, vomiting, diarrhea, and abdominal pain. In severe cases, hantavirus infections can lead to organ failure and death.

Hantaviruses are primarily transmitted through contact with the urine, saliva, or feces of infected rodents, such as mice and rats. The virus can also be spread through contact with contaminated materials, such as dust and soil, that have come into contact with infected rodents.

There is no specific treatment for hantavirus infections, but supportive care, such as fluid replacement and oxygen therapy, may be provided to manage symptoms. Prevention of hantavirus infections is primarily focused on avoiding contact with infected rodents and their bodily fluids, as well as taking precautions when cleaning up contaminated areas.

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

The symptoms of meningoencephalitis can vary depending on the cause, but common signs include fever, headache, stiff neck, confusion, seizures, and loss of consciousness. The disease can progress rapidly and can be fatal if not treated promptly.

Diagnosis is typically made through a combination of physical examination, laboratory tests (such as blood cultures and PCR), and imaging studies (such as CT or MRI scans). Treatment options depend on the underlying cause, but may include antibiotics, antiviral medications, and supportive care to manage symptoms and prevent complications.

Prognosis for meningoencephalitis depends on the severity of the disease and the promptness and effectiveness of treatment. In general, the prognosis is better for patients who receive prompt medical attention and have a mild form of the disease. However, the disease can be severe and potentially life-threatening, especially in young children, older adults, and those with weakened immune systems.

Multiple myeloma is the second most common type of hematologic cancer after non-Hodgkin's lymphoma, accounting for approximately 1% of all cancer deaths worldwide. It is more common in older adults, with most patients being diagnosed over the age of 65.

The exact cause of multiple myeloma is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. There are several risk factors that have been associated with an increased risk of developing multiple myeloma, including:

1. Family history: Having a family history of multiple myeloma or other plasma cell disorders increases the risk of developing the disease.
2. Age: The risk of developing multiple myeloma increases with age, with most patients being diagnosed over the age of 65.
3. Race: African Americans are at higher risk of developing multiple myeloma than other races.
4. Obesity: Being overweight or obese may increase the risk of developing multiple myeloma.
5. Exposure to certain chemicals: Exposure to certain chemicals such as pesticides, solvents, and heavy metals has been linked to an increased risk of developing multiple myeloma.

The symptoms of multiple myeloma can vary depending on the severity of the disease and the organs affected. Common symptoms include:

1. Bone pain: Pain in the bones, particularly in the spine, ribs, or long bones, is a common symptom of multiple myeloma.
2. Fatigue: Feeling tired or weak is another common symptom of the disease.
3. Infections: Patients with multiple myeloma may be more susceptible to infections due to the impaired functioning of their immune system.
4. Bone fractures: Weakened bones can lead to an increased risk of fractures, particularly in the spine, hips, or ribs.
5. Kidney problems: Multiple myeloma can cause damage to the kidneys, leading to problems such as kidney failure or proteinuria (excess protein in the urine).
6. Anemia: A low red blood cell count can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
7. Increased calcium levels: High levels of calcium in the blood can cause symptoms such as nausea, vomiting, constipation, and confusion.
8. Neurological problems: Multiple myeloma can cause neurological problems such as headaches, numbness or tingling in the arms and legs, and difficulty with coordination and balance.

The diagnosis of multiple myeloma typically involves a combination of physical examination, medical history, and laboratory tests. These may include:

1. Complete blood count (CBC): A CBC can help identify abnormalities in the numbers and characteristics of different types of blood cells, including red blood cells, white blood cells, and platelets.
2. Serum protein electrophoresis (SPEP): This test measures the levels of different proteins in the blood, including immunoglobulins (antibodies) and abnormal proteins produced by myeloma cells.
3. Urine protein electrophoresis (UPEP): This test measures the levels of different proteins in the urine.
4. Immunofixation: This test is used to identify the type of antibody produced by myeloma cells and to rule out other conditions that may cause similar symptoms.
5. Bone marrow biopsy: A bone marrow biopsy involves removing a sample of tissue from the bone marrow for examination under a microscope. This can help confirm the diagnosis of multiple myeloma and determine the extent of the disease.
6. Imaging tests: Imaging tests such as X-rays, CT scans, or MRI scans may be used to assess the extent of bone damage or other complications of multiple myeloma.
7. Genetic testing: Genetic testing may be used to identify specific genetic abnormalities that are associated with multiple myeloma and to monitor the response of the disease to treatment.

It's important to note that not all patients with MGUS or smoldering myeloma will develop multiple myeloma, and some patients with multiple myeloma may not have any symptoms at all. However, if you are experiencing any of the symptoms listed above or have a family history of multiple myeloma, it's important to talk to your doctor about your risk and any tests that may be appropriate for you.

Examples of pregnancy complications, parasitic include:

1. Toxoplasmosis: This is a condition caused by the Toxoplasma gondii parasite, which can infect the mother and/or the fetus during pregnancy. Symptoms include fever, headache, and fatigue. In severe cases, toxoplasmosis can cause birth defects, such as intellectual disability, blindness, and deafness.
2. Malaria: This is a condition caused by the Plasmodium spp. parasite, which can be transmitted to the mother and/or the fetus during pregnancy. Symptoms include fever, chills, and flu-like symptoms. In severe cases, malaria can cause anemia, organ failure, and death.
3. Schistosomiasis: This is a condition caused by the Schistosoma spp. parasite, which can infect the mother and/or the fetus during pregnancy. Symptoms include abdominal pain, diarrhea, and fatigue. In severe cases, schistosomiasis can cause organ damage and infertility.

Pregnancy complications, parasitic can be diagnosed through blood tests, imaging studies, and other medical procedures. Treatment depends on the type of parasite and the severity of the infection. In some cases, treatment may involve antibiotics, antimalarial drugs, or anti-parasitic medications.

Preventive measures for pregnancy complications, parasitic include:

1. Avoiding contact with cat feces, as Toxoplasma gondii can be transmitted through contaminated soil and food.
2. Avoiding travel to areas where malaria and other parasitic infections are common.
3. Taking antimalarial medications before and during pregnancy if living in an area where malaria is common.
4. Using insecticide-treated bed nets and wearing protective clothing to prevent mosquito bites.
5. Practicing good hygiene, such as washing hands regularly, especially after handling food or coming into contact with cats.
6. Avoiding drinking unpasteurized dairy products and undercooked meat, as these can increase the risk of infection.
7. Ensuring that any water used for cooking or drinking is safe and free from parasites.

Preventive measures for pregnancy complications, parasitic are important for women who are pregnant or planning to become pregnant, as well as for their partners and healthcare providers. By taking these preventive measures, the risk of infection and complications can be significantly reduced.

In conclusion, pregnancy complications, parasitic are a serious issue that can have severe consequences for both the mother and the fetus. However, by understanding the causes, risk factors, symptoms, diagnosis, treatment, and preventive measures, women can take steps to protect themselves and their unborn babies from these infections. It is important for healthcare providers to be aware of these issues and provide appropriate education and care to pregnant women to reduce the risk of complications.

FAQs
1. What are some common parasitic infections that can occur during pregnancy?
Ans: Some common parasitic infections that can occur during pregnancy include malaria, toxoplasmosis, and cytomegalovirus (CMV).
2. How do parasitic infections during pregnancy affect the baby?
Ans: Parasitic infections during pregnancy can have serious consequences for the developing fetus, including birth defects, growth restriction, and stillbirth.
3. Can parasitic infections during pregnancy be treated?
Ans: Yes, parasitic infections during pregnancy can be treated with antibiotics and other medications. Early detection and treatment are important to prevent complications.
4. How can I prevent parasitic infections during pregnancy?
Ans: Preventive measures include avoiding areas where parasites are common, using insect repellents, wearing protective clothing, and practicing good hygiene. Pregnant women should also avoid undercooked meat and unpasteurized dairy products.
5. Do all pregnant women need to be tested for parasitic infections?
Ans: No, not all pregnant women need to be tested for parasitic infections. However, certain groups of women, such as those who live in areas where parasites are common or have a history of previous parasitic infections, may need to be tested and monitored more closely.
6. Can I prevent my baby from getting a parasitic infection during pregnancy?
Ans: Yes, there are several steps you can take to reduce the risk of your baby getting a parasitic infection during pregnancy, such as avoiding certain foods and taking antibiotics if necessary. Your healthcare provider can provide guidance on how to prevent and treat parasitic infections during pregnancy.
7. How are parasitic infections diagnosed during pregnancy?
Ans: Parasitic infections can be diagnosed through blood tests, stool samples, or imaging tests such as ultrasound or MRI. Your healthcare provider may also perform a physical exam and take a medical history to determine the likelihood of a parasitic infection.
8. Can parasitic infections cause long-term health problems for my baby?
Ans: Yes, some parasitic infections can cause long-term health problems for your baby, such as developmental delays or learning disabilities. In rare cases, parasitic infections can also lead to more serious complications, such as organ damage or death.
9. How are parasitic infections treated during pregnancy?
Ans: Treatment for parasitic infections during pregnancy may involve antibiotics, antiparasitic medications, or other supportive care. Your healthcare provider will determine the best course of treatment based on the severity and type of infection, as well as your individual circumstances.
10. Can I take steps to prevent parasitic infections during pregnancy?
Ans: Yes, there are several steps you can take to prevent parasitic infections during pregnancy, such as avoiding undercooked meat and fish, washing fruits and vegetables thoroughly, and practicing good hygiene. Additionally, if you have a higher risk of parasitic infections due to travel or other factors, your healthcare provider may recommend preventative medications or screening tests.
11. I'm pregnant and have been exposed to a parasitic infection. What should I do?
Ans: If you suspect that you have been exposed to a parasitic infection during pregnancy, it is important to seek medical attention immediately. Your healthcare provider can perform tests to determine if you have an infection and provide appropriate treatment to prevent any potential complications for your baby.
12. Can I breastfeed while taking medication for a parasitic infection?
Ans: It may be safe to breastfeed while taking medication for a parasitic infection, but it is important to consult with your healthcare provider before doing so. Some medications may not be safe for your baby and could potentially be passed through your milk. Your healthcare provider can provide guidance on the safest treatment options for you and your baby.
13. What are some common complications of parasitic infections during pregnancy?
Ans: Complications of parasitic infections during pregnancy can include miscarriage, preterm labor, low birth weight, and congenital anomalies. In rare cases, parasitic infections can also be transmitted to the baby during pregnancy or childbirth, which can lead to serious health problems for the baby.
14. Can I get a parasitic infection from my pet?
Ans: Yes, it is possible to get a parasitic infection from your pet if you come into contact with their feces or other bodily fluids. For example, toxoplasmosis can be transmitted through contact with cat feces, while hookworm infections can be spread through contact with contaminated soil or feces. It is important to practice good hygiene and take precautions when handling pets or coming into contact with potentially contaminated areas.
15. How can I prevent parasitic infections?
Ans: Preventing parasitic infections involves taking steps to avoid exposure to parasites and their vectors, as well as practicing good hygiene and taking precautions when traveling or engaging in activities that may put you at risk. Some ways to prevent parasitic infections include:
* Avoiding undercooked meat, especially pork and wild game
* Avoiding raw or unpasteurized dairy products
* Avoiding contaminated water and food
* Washing your hands frequently, especially after using the bathroom or before handling food
* Avoiding contact with cat feces, as toxoplasmosis can be transmitted through contact with cat feces
* Using protective clothing and insect repellent when outdoors in areas where parasites are common
* Keeping your home clean and free of clutter to reduce the risk of parasite infestations
* Avoiding touching or eating wild animals or plants that may be contaminated with parasites
16. What are some common misconceptions about parasitic infections?
Ans: There are several common misconceptions about parasitic infections, including:
* All parasites are the same and have similar symptoms
* Parasitic infections are only a problem for people who live in developing countries or have poor hygiene
* Only certain groups of people, such as children or pregnant women, are at risk for parasitic infections
* Parasitic infections are rare in developed countries
* All parasites can be treated with antibiotics
* Parasitic infections are not serious and do not require medical attention
17. How can I diagnose a parasitic infection?
Ans: Diagnosing a parasitic infection typically involves a combination of physical examination, medical history, and laboratory tests. Some common methods for diagnosing parasitic infections include:
* Physical examination to look for signs such as skin lesions or abdominal pain
* Blood tests to check for the presence of parasites or their waste products
* Stool tests to detect the presence of parasite eggs or larvae
* Imaging tests, such as X-rays or CT scans, to look for signs of parasite infection in internal organs
* Endoscopy, which involves inserting a flexible tube with a camera into the body to visualize the inside of the digestive tract and other organs.
18. How are parasitic infections treated?
Ans: Treatment for parasitic infections depends on the type of parasite and the severity of the infection. Some common methods for treating parasitic infections include:
* Antiparasitic drugs, such as antibiotics or antimalarials, to kill the parasites
* Supportive care, such as fluids and electrolytes, to manage symptoms and prevent complications
* Surgery to remove parasites or repair damaged tissues
* Antibiotics to treat secondary bacterial infections that may have developed as a result of the parasitic infection.
It is important to seek medical attention if you suspect that you have a parasitic infection, as untreated infections can lead to serious complications and can be difficult to diagnose.
19. How can I prevent parasitic infections?
Ans: Preventing parasitic infections involves taking steps to avoid contact with parasites and their vectors, as well as maintaining good hygiene practices. Some ways to prevent parasitic infections include:
* Avoiding undercooked meat and unpasteurized dairy products, which can contain harmful parasites such as Trichinella spiralis and Toxoplasma gondii
* Washing your hands frequently, especially after using the bathroom or before eating
* Avoiding contact with contaminated water or soil, which can harbor parasites such as Giardia and Cryptosporidium
* Using insecticides and repellents to prevent mosquito bites, which can transmit diseases such as malaria and dengue fever
* Wearing protective clothing and applying insect repellent when outdoors in areas where ticks and other vectors are common
* Avoiding contact with animals that may carry parasites, such as dogs and cats that can transmit Toxoplasma gondii
* Using clean water and proper sanitation to prevent the spread of parasitic infections in communities and developing countries.
It is also important to be aware of the risks of parasitic infections when traveling to areas where they are common, and to take appropriate precautions such as avoiding undercooked meat and unpasteurized dairy products, and using insecticides and repellents to prevent mosquito bites.
20. What is the prognosis for parasitic infections?
Ans: The prognosis for parasitic infections varies depending on the specific type of infection and the severity of symptoms. Some parasitic infections can be easily treated with antiparasitic medications, while others may require more extensive treatment and management.
In general, the prognosis for parasitic infections is good if the infection is detected early and properly treated. However, some parasitic infections can cause long-term health problems or death if left untreated. It is important to seek medical attention if symptoms persist or worsen over time.
It is also important to note that some parasitic infections can be prevented through public health measures such as using clean water and proper sanitation, and controlling the spread of insect vectors. Prevention is key to avoiding the negative outcomes associated with these types of infections.
21. What are some common complications of parasitic infections?
Ans: Some common complications of parasitic infections include:
* Anemia and other blood disorders, such as thrombocytopenia and leukopenia
* Allergic reactions to parasite antigens
* Inflammation and damage to organs and tissues, such as the liver, kidneys, and brain
* Increased risk of infections with other microorganisms, such as bacteria and viruses
* Malnutrition and deficiencies in essential nutrients
* Organ failure and death.
22. Can parasitic infections be prevented? If so, how?
Ans: Yes, some parasitic infections can be prevented through public health measures such as:
* Using clean water and proper sanitation to reduce the risk of ingesting infected parasites.
* Avoiding contact with insect vectors, such as mosquitoes and ticks, by using repellents, wearing protective clothing, and staying indoors during peak biting hours.
* Properly cooking and storing food to kill parasites that may be present.
* Avoiding consuming undercooked or raw meat, especially pork and wild game.
* Practicing safe sex to prevent the transmission of parasitic infections through sexual contact.
* Keeping children away from areas where they may come into contact with contaminated soil or water.
* Using antiparasitic drugs and other treatments as recommended by healthcare providers.
* Implementing control measures for insect vectors, such as spraying insecticides and removing breeding sites.
30. Can parasitic infections be treated with antibiotics? If so, which ones and why?
Ans: No, antibiotics are not effective against parasitic infections caused by protozoa, such as giardiasis and amoebiasis, because these organisms are not bacteria. However, antibiotics may be used to treat secondary bacterial infections that can develop as a complication of parasitic infections.
32. What is the difference between a parasite and a pathogen?
Ans: A parasite is an organism that lives on or in another organism, called the host, and feeds on the host's tissues or fluids without providing any benefits. A pathogen, on the other hand, is an organism that causes disease. While all parasites are pathogens, not all pathogens are parasites. For example, bacteria and viruses can cause diseases but are not considered parasites because they do not live within the host's body.

a type of epidemic pleurisy that occurs in clusters or outbreaks and is characterized by inflammation of the pleura, chest pain, cough, fever, and difficulty breathing. also called "welsh" or "brown's" disease. it is caused by a virus, most commonly a member of the paramyxovirus family.

pleurodynia: [ plyoo-roh-dy-nee-ah ]
inflammation of the pleura.

The symptoms of Lassa fever can vary from mild to severe and include fever, headache, muscle pain, vomiting, diarrhea, and bleeding. In severe cases, the virus can cause multi-organ failure and death.

There is no specific treatment for Lassa fever, but supportive care, such as intravenous fluids and oxygen therapy, can help manage symptoms. Ribavirin, an antiviral drug, has been shown to be effective in treating the virus in some cases.

Prevention of Lassa fever involves reducing exposure to infected rodents, such as by storing food in rat-proof containers and avoiding contact with rodents that may be carrying the virus. Vaccines are also being developed to protect against the virus.

Overall, Lassa fever is a serious and potentially deadly disease that requires prompt medical attention if symptoms persist or worsen over time. Early diagnosis and treatment can improve outcomes for patients infected with the virus.

Colorado tick fever (CTF) is a viral disease that affects humans and is transmitted by the bite of an infected tick. The disease is most commonly found in the western United States, particularly in Colorado, where it was first identified in 1948.

Symptoms:

The symptoms of CTF typically develop within 7-10 days after being bitten by an infected tick and can include:

* Fever
* Headache
* Muscle aches
* Joint pain
* Nausea and vomiting
* Diarrhea
* Rash (in some cases)

Diagnosis:

CTF is diagnosed based on a combination of symptoms, medical history, and laboratory tests. Laboratory tests may include blood tests to detect the presence of antibodies against the virus or PCR (polymerase chain reaction) tests to detect the genetic material of the virus in the blood.

Treatment:

There is no specific treatment for CTF, but symptoms can be managed with rest, hydration, and over-the-counter pain relievers such as acetaminophen or ibuprofen. Antiviral medications may be prescribed in severe cases.

Prevention:

Prevention of CTF involves protecting against tick bites. This can include:

* Avoiding areas with high grass and leaf litter, where ticks are more common
* Wearing protective clothing such as long-sleeved shirts and pants when outdoors
* Applying insect repellents that contain DEET or permethrin to exposed skin and clothing
* Checking for ticks on the body after spending time outdoors, and removing any found ticks promptly

Prognosis:

Most people with CTF experience mild symptoms and recover fully within a few days to a week without complications. However, in rare cases, the disease can progress to more severe forms, such as meningitis or encephalitis, which can be life-threatening.

Complications:

While rare, CTF can lead to complications such as:

* Meningitis: Inflammation of the membranes that cover the brain and spinal cord
* Encephalitis: Inflammation of the brain itself
* Arthritis: Painful joint inflammation
* Myocarditis: Inflammation of the heart muscle

It is important to seek medical attention if symptoms worsen or new symptoms develop, as early treatment can improve outcomes.

Bunyaviridae infections can be severe and potentially life-threatening, especially in certain populations such as young children, older adults, and people with weakened immune systems. Symptoms of Bunyaviridae infections can include fever, headache, muscle pain, vomiting, diarrhea, and in severe cases, hemorrhagic symptoms such as bleeding from the eyes, ears, or gastrointestinal tract.

There is no specific treatment for Bunyaviridae infections, but supportive care and management of symptoms can help alleviate the severity of the illness. Prevention of Bunyaviridae infections includes avoiding insect bites by using protective clothing and insect repellents, as well as controlling the populations of potential vector insects in affected areas.

Examples of diseases caused by Bunyaviridae viruses include Rift Valley fever, which is common in Africa and the Middle East, and Crimean-Congo hemorrhagic fever, which is found in parts of Europe, Asia, and Africa. Other examples of Bunyaviridae infections include La Crosse encephalitis, which is found in North America, and Japanese encephalitis, which is prevalent in parts of Asia.

It's important to note that Bunyaviridae infections can be challenging to diagnose, as the symptoms can be similar to other viral or bacterial infections. Laboratory testing, such as PCR or ELISA assays, is often necessary to confirm the presence of a Bunyaviridae virus.

Prevention and control measures for Bunyaviridae infections include avoiding insect bites, controlling vector populations, and implementing public health measures such as surveillance, education, and vaccination programs. Research into the development of vaccines and antiviral drugs against Bunyaviridae viruses is ongoing, but there are currently no licensed treatments available for these infections.

There are three stages of syphilis:

1. Primary stage: A small, painless sore or ulcer (called a chancre) appears at the site of infection, usually on the genitals, rectum, or mouth. This sore heals on its own within 2-6 weeks, but the infection remains in the body.
2. Secondary stage: A rash and other symptoms can appear weeks to months after the primary stage. The rash can be accompanied by fever, fatigue, and swollen lymph nodes.
3. Latent stage: After the secondary stage, the infection can enter a latent (hidden) phase, during which there are no visible symptoms but the infection remains in the body. If left untreated, syphilis can progress to the tertiary stage, which can cause serious complications such as damage to the heart, brain, and other organs.

Syphilis is diagnosed through a physical examination, blood tests, and/or a lumbar puncture (spinal tap). Treatment typically involves antibiotics, and early treatment can cure the infection and prevent long-term complications.

Prevention measures include safe sex practices such as using condoms and dental dams, avoiding sexual contact with someone who has syphilis, and getting regularly tested for STIs. It is important to seek medical attention if symptoms of syphilis are present, as early treatment can prevent long-term complications.

Flavivirus infections can cause a range of symptoms, including fever, headache, muscle and joint pain, and skin rashes. In severe cases, these infections can lead to hemorrhagic fever, which can be fatal.

The transmission of flaviviruses is typically through the bite of an infected mosquito or other insect vectors, although some viruses can also be transmitted through blood transfusions or organ transplantation.

There is no specific treatment for flavivirus infections, but supportive care such as hydration, pain relief, and antipyretic medications may be provided to manage symptoms. Prevention includes avoiding mosquito bites by using insect repellents, wearing protective clothing, and eliminating standing water around homes and communities to reduce the number of mosquito breeding sites.

In addition, vaccines are available for some flaviviruses, such as yellow fever and dengue fever, which can provide protection against infection.

Overall, flavivirus infections are a significant public health concern, particularly in tropical and subtropical regions where these viruses are most commonly found.

The disease is primarily transmitted through inhalation of infected particles, such as dust or aerosols, which contain the bacterium. People working in close contact with animals, such as veterinarians and farmers, are at higher risk of contracting Q fever.

Symptoms of Q fever typically develop within 2-3 weeks after exposure and may include fever, headache, fatigue, muscle pain, and respiratory symptoms such as cough and shortness of breath. In severe cases, the infection can spread to the heart, liver, and other organs, leading to life-threatening complications.

Diagnosis of Q fever is based on a combination of clinical findings, laboratory tests, and epidemiological investigations. Laboratory confirmation of the disease requires the isolation of Coxiella burnetii from blood or other bodily fluids.

Treatment of Q fever typically involves antibiotics, which can effectively cure the infection if administered early. However, treatment is not always necessary for mild cases, and some people may recover without any treatment.

Prevention of Q fever primarily involves avoiding exposure to infected animals or their tissues, as well as practicing good hygiene practices such as wearing personal protective equipment (PPE) when handling animals or their tissues. Vaccination is also available for high-risk groups, such as veterinarians and farmers.

Overall, Q fever is an important zoonotic disease that can cause significant illness in humans and a range of animal species. Prompt diagnosis and appropriate treatment are critical to preventing complications and ensuring effective management of the disease.

Types of experimental neoplasms include:

* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.

The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.

1. Respiratory distress syndrome (RDS): This is a breathing disorder that occurs when the baby's lungs are not fully developed, causing difficulty in breathing. RDS can be treated with oxygen therapy and other medical interventions.
2. Jaundice: Jaundice is a yellowish tint to the skin and eyes caused by high levels of bilirubin in the blood. It is a common condition in newborns, but if left untreated, it can lead to brain damage. Treatment may involve phototherapy or blood exchange transfusions.
3. Neonatal jaundice: This is a milder form of jaundice that occurs in the first few days of life. It usually resolves on its own within a week, but if it persists, treatment may be necessary.
4. Premature birth: Premature babies are at risk for various health issues, including respiratory distress syndrome, intraventricular hemorrhage (bleeding in the brain), and retinopathy (eye problems).
5. Congenital heart disease: This is a heart defect that occurs during fetal development. It can range from mild to severe and may require surgical intervention.
6. Infections: Newborns are susceptible to bacterial and viral infections, such as group B strep, pneumonia, and urinary tract infections. These can be treated with antibiotics if caught early.
7. Hypoglycemia (low blood sugar): This is a condition that occurs when the baby's blood sugar levels drop too low. It can cause seizures, lethargy, and other symptoms. Treatment involves feeding or providing glucose supplements.
8. Hyperbilirubinemia (high bilirubin levels): Bilirubin is a yellow pigment produced during the breakdown of red blood cells. High levels can cause jaundice, which can lead to kernicterus, a condition that can cause brain damage and hearing loss.
9. Intracranial hemorrhage (bleeding in the brain): This is a serious condition that occurs when there is bleeding in the baby's brain. It can be caused by various conditions, including premature birth, abruption, and vasculitis.
10. Meconium aspiration: This occurs when the baby inhales a mixture of meconium (a substance produced by the intestines) and amniotic fluid during delivery. It can cause respiratory problems and other complications.

It's important to note that while these conditions can be serious, many babies born at 37 weeks gestation do not experience any complications. Proper prenatal care and a healthy pregnancy can help reduce the risk of these conditions.

Symptoms:

* Fever
* Cough
* Chest pain or tightness
* Shortness of breath
* Headache
* Muscle aches
* Fatigue

Diagnosis:

* Physical examination
* Complete blood count (CBC)
* Blood cultures
* Chest X-ray
* Polymerase chain reaction (PCR)

Treatment:

* Antibiotics (macrolides, fluoroquinolones, and aminoglycosides)
* Supportive care (fluids, oxygen therapy, pain management)

Prevention:

* Vaccination (not available in the US)
* Good hand hygiene
* Avoiding close contact with people who are sick

Prognosis:

* Most cases of Mycoplasma pneumoniae pneumonia are mild and resolve quickly with antibiotic treatment.
* In severe cases, the infection can spread to other parts of the body and cause serious complications such as respiratory failure, sepsis, and meningitis.

Epidemiology:

* Mycoplasma pneumoniae is a common cause of community-acquired pneumonia (CAP) worldwide.
* It is more common in children than adults.
* The incidence of Mycoplasma pneumoniae infection varies by age, with the highest incidence in children under 5 years old.

The two main types of lymphoid leukemia are:

1. Acute Lymphoblastic Leukemia (ALL): This type of leukemia is most commonly seen in children, but it can also occur in adults. It is characterized by a rapid increase in the number of immature white blood cells in the blood and bone marrow.
2. Chronic Lymphocytic Leukemia (CLL): This type of leukemia usually affects older adults and is characterized by the gradual buildup of abnormal white blood cells in the blood, bone marrow, and lymph nodes.

Symptoms of lymphoid leukemia include fatigue, fever, night sweats, weight loss, and swollen lymph nodes. Treatment options for lymphoid leukemia can vary depending on the type of cancer and the severity of symptoms, but may include chemotherapy, radiation therapy, or bone marrow transplantation.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

1. Common cold: A viral infection that affects the upper respiratory tract and causes symptoms such as sneezing, running nose, coughing, and mild fever.
2. Influenza (flu): A viral infection that can cause severe respiratory illness, including pneumonia, bronchitis, and sinus and ear infections.
3. Measles: A highly contagious viral infection that causes fever, rashes, coughing, and redness of the eyes.
4. Rubella (German measles): A mild viral infection that can cause fever, rashes, headache, and swollen lymph nodes.
5. Chickenpox: A highly contagious viral infection that causes fever, itching, and a characteristic rash of small blisters on the skin.
6. Herpes simplex virus (HSV): A viral infection that can cause genital herpes, cold sores, or other skin lesions.
7. Human immunodeficiency virus (HIV): A viral infection that attacks the immune system and can lead to acquired immunodeficiency syndrome (AIDS).
8. Hepatitis B: A viral infection that affects the liver, causing inflammation and damage to liver cells.
9. Hepatitis C: Another viral infection that affects the liver, often leading to chronic liver disease and liver cancer.
10. Ebola: A deadly viral infection that causes fever, vomiting, diarrhea, and internal bleeding.
11. SARS (severe acute respiratory syndrome): A viral infection that can cause severe respiratory illness, including pneumonia and respiratory failure.
12. West Nile virus: A viral infection that can cause fever, headache, and muscle pain, as well as more severe symptoms such as meningitis or encephalitis.

Viral infections can be spread through contact with an infected person or contaminated surfaces, objects, or insects such as mosquitoes. Prevention strategies include:

1. Practicing good hygiene, such as washing hands frequently and thoroughly.
2. Avoiding close contact with people who are sick.
3. Covering the mouth and nose when coughing or sneezing.
4. Avoiding sharing personal items such as towels or utensils.
5. Using condoms or other barrier methods during sexual activity.
6. Getting vaccinated against certain viral infections, such as HPV and hepatitis B.
7. Using insect repellents to prevent mosquito bites.
8. Screening blood products and organs for certain viruses before transfusion or transplantation.

Treatment for viral infections depends on the specific virus and the severity of the illness. Antiviral medications may be used to reduce the replication of the virus and alleviate symptoms. In severe cases, hospitalization may be necessary to provide supportive care such as intravenous fluids, oxygen therapy, or mechanical ventilation.

Prevention is key in avoiding viral infections, so taking the necessary precautions and practicing good hygiene can go a long way in protecting oneself and others from these common and potentially debilitating illnesses.

There are several causes of IgG deficiency, including:

1. Genetic defects: Some people may be born with a genetic predisposition to have low levels of IgG.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis or lupus can cause the immune system to attack and destroy IgG antibodies.
3. Infections: Certain infections, such as HIV or hepatitis B, can cause a decrease in IgG levels.
4. Malnutrition: A diet that is deficient in certain nutrients, such as protein or vitamin D, can lead to low IgG levels.
5. Medications: Certain medications, such as corticosteroids or chemotherapy drugs, can suppress the immune system and reduce IgG production.
6. Pregnancy: Pregnant women may have lower levels of IgG due to changes in their immune system.
7. Age: IgG levels tend to decline with age, especially after the age of 60.

Symptoms of IgG deficiency may include:

1. Frequent or recurring infections, such as sinus infections, ear infections, or pneumonia
2. Slowed growth and development in children
3. Fatigue or weakness
4. Swollen lymph nodes
5. Skin rashes or lesions
6. Easy bruising or bleeding
7. Difficulty healing from injuries or surgery

Treatment of IgG deficiency depends on the underlying cause and may include:

1. Antibiotics to treat infections
2. Immune globulin injections to boost IgG levels
3. Changes to diet and lifestyle to address malnutrition or other underlying causes
4. Medications to manage related conditions, such as autoimmune disorders or inflammatory diseases.

It's important to note that some cases of IgG deficiency may be mild and not require treatment, while others may be more severe and require ongoing management. If you suspect you or your child may have an IgG deficiency, it's important to consult with a healthcare professional for proper diagnosis and treatment.

Melioidosis is typically acquired through contact with contaminated soil or water in tropical and subtropical regions of Asia and Africa. The bacteria can enter the body through open wounds, cuts, or through the eyes, nose, or mouth. Once inside the body, the bacteria can multiply and cause a wide range of symptoms including fever, chills, headache, muscle and joint pain, and skin lesions.

If left untreated, melioidosis can lead to serious complications such as sepsis, meningitis, and pneumonia, which can be fatal. The disease is diagnosed through a combination of physical examination, laboratory tests, and imaging studies. Treatment typically involves antibiotics, and early treatment is essential for effective management of the disease.

In addition to being an important medical condition, melioidosis is also of interest to researchers studying the bacteria that cause the disease. Burkholderia pseudomallei has been found to have a unique ability to survive in a variety of environments, including soil and water, and has been studied for its potential as a bioterrorism agent.

In summary, melioidosis is a serious bacterial infection caused by Burkholderia pseudomallei that can affect multiple organ systems and cause severe illness if left untreated. It is typically acquired through contact with contaminated soil or water in tropical and subtropical regions of Asia and Africa and is diagnosed through a combination of physical examination, laboratory tests, and imaging studies. Early treatment is essential for effective management of the disease.

The symptoms of CVID can vary from person to person and may include:

1. Frequent or recurring infections, such as sinus infections, ear infections, and pneumonia.
2. Poor response to vaccines.
3. Delayed growth and development in children.
4. Autoimmune disorders, such as thyroiditis or arthritis.
5. Increased risk of developing certain types of cancer, such as lymphoma.

CVID is caused by mutations in several genes that are involved in the immune system. These genes play a role in the development and function of immune cells, such as T cells and B cells. The exact cause of CVID is often not known, but it can be inherited or acquired through genetic mutations.

There is no cure for CVID, but treatment can help manage the symptoms and prevent complications. Treatment typically involves antibiotics to fight off infections, immunoglobulin replacement therapy to boost the immune system, and medication to manage autoimmune disorders. In some cases, a bone marrow transplant may be recommended.

The prognosis for CVID varies depending on the severity of the disorder and the presence of any complications. With proper treatment, many people with CVID can lead normal lives and have a good quality of life. However, some individuals may experience ongoing health problems and a higher risk of developing certain types of cancer.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

There are several forms of HFRS, including:

1. Severe Hemorrhagic Fever (SHF): This form of the disease is characterized by rapid onset of severe symptoms, including fever, hemorrhaging, and renal failure.
2. Epidemic Hemorrhagic Fever (EHF): This form of the disease is similar to SHF but has a milder course.
3. African Hemorrhagic Fever (AHF): This form of the disease is found primarily in sub-Saharan Africa and is characterized by a severe course with high mortality rates.
4. Crimean-Congo Hemorrhagic Fever (CCHF): This form of the disease is found in parts of Europe, Asia, and Africa and is transmitted through tick bites or contact with infected animals.

The symptoms of HFRS can include fever, headache, muscle pain, joint pain, nausea, vomiting, diarrhea, abdominal pain, and hemorrhaging. In severe cases, the disease can lead to kidney failure, shock, and death.

Diagnosis of HFRS is based on a combination of clinical symptoms, laboratory tests (such as PCR and ELISA), and serology. Treatment is primarily supportive, with management of symptoms and fluid replacement. Antiviral medications may be used in some cases.

Prevention of HFRS includes tick control measures, protective clothing, and avoiding contact with potentially infected animals or ticks. Vaccines are available for some forms of the disease, particularly CCHF.

There are several subtypes of lymphoma, B-cell, including:

1. Diffuse large B-cell lymphoma (DLBCL): This is the most common type of B-cell lymphoma and typically affects older adults.
2. Follicular lymphoma: This type of lymphoma grows slowly and often does not require treatment for several years.
3. Marginal zone lymphoma: This type of lymphoma develops in the marginal zone of the spleen or other lymphoid tissues.
4. Hodgkin lymphoma: This is a type of B-cell lymphoma that is characterized by the presence of Reed-Sternberg cells, which are abnormal cells that can be identified under a microscope.

The symptoms of lymphoma, B-cell can vary depending on the subtype and the location of the tumor. Common symptoms include swollen lymph nodes, fatigue, fever, night sweats, and weight loss.

Treatment for lymphoma, B-cell usually involves chemotherapy, which is a type of cancer treatment that uses drugs to kill cancer cells. Radiation therapy may also be used in some cases. In some cases, bone marrow or stem cell transplantation may be recommended.

Prognosis for lymphoma, B-cell depends on the subtype and the stage of the disease at the time of diagnosis. In general, the prognosis is good for patients with early-stage disease, but the cancer can be more difficult to treat if it has spread to other parts of the body.

Prevention of lymphoma, B-cell is not possible, as the exact cause of the disease is not known. However, avoiding exposure to certain risk factors, such as viral infections and pesticides, may help reduce the risk of developing the disease. Early detection and treatment can also improve outcomes for patients with lymphoma, B-cell.

Lymphoma, B-cell is a type of cancer that affects the immune system and can be treated with chemotherapy and other therapies. The prognosis varies depending on the subtype and stage of the disease at diagnosis. Prevention is not possible, but early detection and treatment can improve outcomes for patients with this condition.

The symptoms of cryptococcosis vary depending on the location and severity of the infection. In lung infections, patients may experience fever, cough, chest pain, and difficulty breathing. In CNS infections, patients may experience headaches, confusion, seizures, and loss of coordination. Skin infections can cause skin lesions, and eye infections can cause vision problems.

Cryptococcosis is diagnosed by culturing the fungus from body fluids or tissue samples. Treatment typically involves antifungal medications, such as amphotericin B or fluconazole, which may be given intravenously or orally, depending on the severity and location of the infection. In severe cases, surgery may be required to remove infected tissue or repair damaged organs.

Preventive measures for cryptococcosis include avoiding exposure to fungal spores, practicing good hygiene, and maintaining a healthy immune system. For individuals with HIV/AIDS, antiretroviral therapy can help reduce the risk of developing cryptococcosis.

Overall, while rare, cryptococcosis is a serious opportunistic infection that can affect individuals with compromised immune systems. Early diagnosis and prompt treatment are essential to prevent complications and improve outcomes.

Aseptic meningitis can cause a range of symptoms, including headache, fever, stiff neck, nausea and vomiting, sensitivity to light, and confusion. In severe cases, it can lead to brain damage, seizures, and even death.

Aseptic meningitis is diagnosed through a combination of physical examination, medical history, laboratory tests (such as blood cultures and cerebrospinal fluid analysis), and imaging studies (such as CT or MRI scans). Treatment typically involves supportive care, such as intravenous fluids and pain management, as well as addressing any underlying causes. In some cases, antibiotics may be prescribed if a bacterial infection is suspected.

Aseptic meningitis can affect anyone, but it is more common in certain groups, such as children under the age of 5 and people with weakened immune systems. It is important to seek medical attention immediately if symptoms persist or worsen over time.

The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.

There are several subtypes of LES, including:

1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.

There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.

It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.

There are several types of brucellosis, including:

1. Brucella abortus: This type is primarily found in cattle and is the most common form of the disease in humans.
2. Brucella suis: This type is found in pigs and is less common in humans.
3. Brucella melitensis: This type is found in sheep, goats, and other animals, and is more virulent than B. abortus.
4. Brucella canis: This type is found in dogs and is rare in humans.

The symptoms of brucellosis can vary depending on the severity of the infection and the individual's overall health. Common symptoms include:

1. Fever
2. Headache
3. Joint pain
4. Muscle pain
5. Swelling of the lymph nodes and spleen
6. Fatigue
7. Loss of appetite
8. Weight loss

In severe cases, brucellosis can cause complications such as:

1. Endocarditis (infection of the heart valves)
2. Meningitis (inflammation of the lining around the brain and spinal cord)
3. Osteomyelitis (infection of the bone)
4. Testicular inflammation in men
5. Epididymitis (inflammation of the epididymis, a tube that carries sperm from the testicle to the penis)
6. Inflammation of the heart muscle and valves
7. Pneumonia
8. Inflammation of the liver and spleen

Brucellosis is diagnosed through a combination of physical examination, laboratory tests, and imaging studies. Treatment typically involves antibiotics, and early treatment can help prevent complications. Prevention measures include avoiding contact with infected animals and ensuring proper hygiene practices when handling livestock or wild game.

GN IGA is one of the most common forms of idiopathic membranous nephropathy, which means it has no known cause. It can occur at any age but is more common in adults between the ages of 20 and 40. The disease often progresses slowly over several years, and some people may experience no symptoms at all.

The diagnosis of GN IGA is based on a combination of clinical findings, laboratory tests, and kidney biopsy. Laboratory tests may show abnormal levels of proteins in the urine, such as albumin, and a high level of IgA in the blood. A kidney biopsy is often necessary to confirm the diagnosis and to rule out other kidney diseases.

There is no cure for GN IGA, but treatment can help slow the progression of the disease. Treatment options may include medications to control high blood pressure, reduce proteinuria (excess protein in the urine), and suppress the immune system. In severe cases, dialysis or a kidney transplant may be necessary.

Preventive measures for GN IGA are not well established, but maintaining a healthy lifestyle, including a balanced diet, regular exercise, and avoiding exposure to toxins, may help reduce the risk of developing the disease. It is also important to manage any underlying medical conditions, such as high blood pressure or diabetes, which can increase the risk of kidney damage.

Alphaviruses are a group of viruses that cause a range of diseases, including arthritis, encephalitis, and fever. These viruses are typically found in tropical and subtropical regions of the world and are transmitted to humans through the bite of infected mosquitoes or other insects.

There are several different types of alphaviruses, including:

* Chikungunya virus (CHIKV)
* Sindbis virus (SINV)
* Ross River virus (RRV)
* Barmah Forest virus (BFV)

The symptoms of alphavirus infections can vary depending on the specific type of virus and the severity of the infection. Common symptoms include:

* Fever
* Headache
* Muscle and joint pain
* Swelling and inflammation
* Rash
* Fatigue
* Weakness

In some cases, alphavirus infections can lead to more serious complications, such as meningitis or encephalitis (inflammation of the brain). These complications are more likely to occur in older adults or people with weakened immune systems.

There is no specific treatment for alphavirus infections, but symptoms can be managed with over-the-counter pain relievers, fever reducers, and anti-inflammatory medications. Rest, hydration, and supportive care may also be recommended. Prevention is key to avoiding alphavirus infections, and this includes protecting against mosquito bites by using insect repellents, wearing protective clothing, and staying in air-conditioned or screened areas. Vaccines are also being developed to protect against some of the most common types of alphaviruses.

Some common types of Chlamydophila infections include:

1. Pneumonia: Chlamydophila pneumoniae can cause pneumonia, which is an inflammation of the lungs that can lead to fever, cough, chest pain, and difficulty breathing.
2. Trachoma: Chlamydia trachomatis can cause trachoma, a highly contagious eye infection that can lead to blindness if left untreated.
3. Pelvic inflammatory disease (PID): Chlamydia trachomatis and Chlamydia psittaci can cause PID, an infection of the female reproductive organs that can lead to chronic pelvic pain, infertility, and ectopic pregnancy.
4. Urinary tract infections (UTIs): Chlamydia trachomatis and Chlamydia caviae can cause UTIs, which are infections of the urinary tract that can lead to symptoms such as burning during urination and frequent urination.
5. Rectal infections: Chlamydia trachomatis and Chlamydia psittaci can cause rectal infections, which can lead to symptoms such as rectal pain, bleeding, and discharge.

Chlamydophila infections are typically treated with antibiotics, and early treatment can help prevent long-term complications and reduce the risk of transmission to others. It is important to practice safe sex and good hygiene to prevent the spread of these infections.

The most common symptoms of enterovirus infections include:

* Diarrhea
* Vomiting
* Fever
* Abdominal pain
* Headache
* Fatigue

In some cases, enterovirus infections can lead to more severe complications, such as:

* Hand, foot, and mouth disease (HFMD)
* Aseptic meningitis
* Encephalitis
* Myocarditis

Enteroviruses are highly contagious and can be spread through:

* Close contact with an infected person
* Contaminated food and water
* Insect vectors

There is no specific treatment for enterovirus infections, but symptoms can be managed with supportive care, such as hydration, rest, and pain relief. Antiviral medications may be used in severe cases.

Prevention measures include:

* Good hygiene practices, such as frequent handwashing
* Avoiding close contact with people who are sick
* Properly preparing and storing food and water
* Avoiding sharing items that come into contact with the mouth, such as utensils and drinking glasses.

The symptoms of hepatitis B can range from mild to severe and may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, joint pain, and jaundice (yellowing of the skin and eyes). In some cases, hepatitis B can be asymptomatic, meaning that individuals may not experience any symptoms at all.

Hepatitis B is diagnosed through blood tests that detect the presence of HBV antigens or antibodies in the body. Treatment for acute hepatitis B typically involves rest, hydration, and medication to manage symptoms, while chronic hepatitis B may require ongoing therapy with antiviral drugs to suppress the virus and prevent liver damage.

Preventive measures for hepatitis B include vaccination, which is recommended for individuals at high risk of infection, such as healthcare workers, sexually active individuals, and those traveling to areas where HBV is common. In addition, safe sex practices, avoiding sharing of needles or other bodily fluids, and proper sterilization of medical equipment can help reduce the risk of transmission.

Overall, hepatitis B is a serious infection that can have long-term consequences for liver health, and it is important to take preventive measures and seek medical attention if symptoms persist or worsen over time.

Exanthema is often used interchangeably with the term "rash," but it specifically refers to a type of rash that is accompanied by other symptoms such as fever, headache, or joint pain. Exanthematous rashes can be contagious and may require treatment with antiviral or antibacterial medications, depending on the underlying cause.

Some common types of exanthema include:

* Measles: a highly contagious viral infection that causes a characteristic rash and other symptoms such as fever and cough.
* Roseola: a viral infection that causes a high fever followed by a rash.
* Fifth disease: a mild viral infection that causes a rash on the face and body.
* Hand, foot and mouth disease: a viral infection that causes a rash on the hands, feet, and mouth.

It's important to note that exanthema can be a symptom of various conditions, so it's important to seek medical attention if you or your child experiences a rash with other symptoms, especially if it's accompanied by fever, headache, or joint pain. A healthcare professional can diagnose the underlying cause and recommend appropriate treatment.

Symptoms of EBV infection can vary widely, ranging from asymptomatic to severe, and may include:

* Fatigue
* Fever
* Sore throat
* Swollen lymph nodes in the neck and armpits
* Swollen liver or spleen
* Rash
* Headaches
* Muscle weakness

In some cases, EBV can lead to more serious complications such as infectious mononucleosis (IM), also known as glandular fever, which can cause:

* Enlarged liver and spleen
* Splenomegaly (enlargement of the spleen)
* Hepatomegaly (enlargement of the liver)
* Thrombocytopenia (low platelet count)
* Anemia (low red blood cell count)
* Leukopenia (low white blood cell count)

EBV is also associated with an increased risk of developing certain types of cancer, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma.

There is no specific treatment for EBV infections, and most cases resolve on their own within a few weeks. Antiviral medications may be prescribed in severe cases or to prevent complications. Rest, hydration, and over-the-counter pain relief medication can help alleviate symptoms.

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Naïve mature B cells produce both IgM and IgD, which are the first two heavy chain segments in the immunoglobulin locus. After ... Immunoglobulin+class+switching at the US National Library of Medicine Medical Subject Headings (MeSH) (Articles with short ... Immunoglobulin class switching, also known as isotype switching, isotypic commutation or class-switch recombination (CSR), is a ... Laffleur B, Bardet SM, Garot A, Brousse M, Baylet A, Cogné M (2014). "Immunoglobulin genes undergo legitimate repair in human B ...
The immunoglobulin is categorized as immunoglobulin G (IgG). Since the tetanus toxin permanently binds to human tissues, only ... Anti-tetanus immunoglobulin, also known as tetanus immune globulin (TIG) and tetanus antitoxin, is a medication made up of ... unbounded molecules can be neutralized by the immunoglobulin. Use of the horse version became common in the 1910s, while the ...
The immunoglobulin light chain is the small polypeptide subunit of an antibody (immunoglobulin). A typical antibody is composed ... The immunoglobulin light chain genes in tetrapods can be classified into three distinct groups: kappa (κ), lambda (λ), and ... Immunoglobulin+Light+Chains at the US National Library of Medicine Medical Subject Headings (MeSH) Educational Resource for ... There are two types of light chain in humans: kappa (κ) chain, encoded by the immunoglobulin kappa locus (IGK@) on chromosome 2 ...
pIgR has a strong specificity to polymeric immunoglobulins and is not responsive to monomeric immunoglobulin. The ligand's J- ... "Entrez Gene: PIGR polymeric immunoglobulin receptor". Kaetzel CS (August 2005). "The polymeric immunoglobulin receptor: ... Polymeric immunoglobulin receptor (pIgR) is a transmembrane protein that in humans is encoded by the PIGR gene. It is an Fc ... Polymeric+Immunoglobulin+Receptor at the US National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology This ...
The immunoglobulin heavy chain (IgH) is the large polypeptide subunit of an antibody (immunoglobulin). In human genome, the IgH ... There are five types of mammalian immunoglobulin heavy chain: γ, δ, α, μ and ε. They define classes of immunoglobulins: IgG, ... Each heavy chain has two regions: a constant region (which is the same for all immunoglobulins of the same class but differs ... a variable region that differs between different B cells, but is the same for all immunoglobulins produced by the same B cell ...
... , or sometimes Immunoglobulin binding protein is a generic name for any protein that binds ... Immunoglobulin-binding protein 1 (IGBP1), a protein that binds B-cells in the blood. Protein A, a 42 kDa protein originally ... It, therefore, can mean: Binding immunoglobulin protein (BiP, or heat shock 70 kDa protein 5, with an official symbol HSPA5), a ...
V-set domains are found in diverse protein families, including immunoglobulin light and heavy chains; in several T-cell ... "Phosphocholine binding immunoglobulin Fab McPC603. An X-ray diffraction study at 2.7 A". J. Mol. Biol. 190 (4): 593-604. doi: ... Immunoglobulin V-set, subgroup InterPro: IPR003596 T-cell surface antigen CD2 InterPro: IPR013285 ACAM; ACAN; ADAMTSL1; AGC1; ...
The underlying cause of MIDD is the production of monoclonal immunoglobulins. Monoclonal immunoglobulins are produced in ... The immunoglobulin heavy chain in HCDD is frequently a truncated heavy chain. HCDD is the rarest subtype of MIDD. Serum protein ... Monoclonal immunoglobulins are produced by monoclonal plasma cells, which are found in a variety of plasma cell dyscrasias. The ... Monoclonal Immunoglobulin Deposition Disorder, or MIDD, is a disease characterised by the deposition of monoclonal ...
MAdCAM-1 belongs to a subclass of the immunoglobulin superfamily (IgSF), the members of which are ligands for integrins. The ... In molecular biology, the adhesin molecule (immunoglobulin-like) is a protein domain. This domain is found in mucosal vascular ... "The structure of immunoglobulin superfamily domains 1 and 2 of MAdCAM-1 reveals novel features important for integrin ... crystal structure of this domain has been reported; it adopts an immunoglobulin-like beta-sandwich structure, with seven ...
Selective immunoglobulin A (IgA) deficiency (SIgAD) is a genetic immunodeficiency, a type of hypogammaglobulinemia. People with ... They rarely present with severe reactions, including anaphylaxis, to blood transfusions or intravenous immunoglobulin due to ... There is an inherited inability to produce immunoglobulin A (IgA), a part of the body's defenses against infection at the ... There is a historical popularity in using intravenous immunoglobulin (IVIG) to treat SIgAD, but the consensus is that there is ...
I-set domains are found in several cell adhesion molecules, including vascular (VCAM), intercellular (ICAM), neural (NCAM) and mucosal addressin (MADCAM) cell adhesion molecules, as well as junction adhesion molecules (JAM). I-set domains are also present in several other diverse protein families, including several tyrosine-protein kinase receptors, the hemolymph protein hemolin, the muscle proteins titin, telokin, and twitchin, the neuronal adhesion molecule axonin-1, and the signalling molecule semaphorin 4D that is involved in axonal guidance, immune function and angiogenesis. ADAMTSL1, ADAMTSL3, ALPK3, AXL, BOC, C9orf94, CADM2, CADM4, CCDC141, CDON, CEACAM7, CHL1, CILP2, CNTN1, CNTN2, CNTN3, CNTN4, CNTN5, CNTN6, CXADR, DCC, DSCAM, DSCAML1, ESAM, FGFR1, FGFR3, FGFR4, FGFRL1, FLT1, FLT4, FSTL4, FSTL5, HMCN1, HNT, HSPG2, ICAM5, IGFBP7, IGFBPL1, IGSF10, IGSF22, IGSF9, ISLR, KALRN, KAZALD1, KDR, KIAA0626, KIRREL, KIRREL2, KIRREL3, L1CAM, LINGO1, LINGO2, LRFN2, LRFN3, LRFN4, LRFN5, LRIG1, LRIG2, ...
The leukocyte immunoglobulin-like receptors (LILR) are a family of receptors possessing extracellular immunoglobulin domains. ... LAIR1 Killer-cell immunoglobulin-like receptor David E. Sloane; Nicodemus Tedla; Muyiwa Awoniyi; Donald W. MacGlashan Jr.; Luis ... v t e v t e v t e (Protein pages needing a picture, Immunoglobulin superfamily, All stub articles, Biochemistry stubs, Receptor ... Borges; K. Frank Austen; Jonathan P. Arm (November 2004). "Leukocyte immunoglobulin-like receptors: novel innate receptors for ...
... is a protein that in humans is encoded by the IGSF3 gene. The protein encoded by this gene ... "Entrez Gene: Immunoglobulin superfamily member 3". Retrieved 2018-10-06. v t e This article incorporates text from the United ... is an immunoglobulin-like membrane protein containing several V-type Ig-like domains. A mutation in this gene has been ...
C1-set domains are found almost exclusively in molecules involved in the immune system, such as in immunoglobulin light and ...
CD2 CD4 VCAM1 Smith DK, Xue H (1997). "Sequence profiles of immunoglobulin and immunoglobulin-like domains". J. Mol. Biol. 274 ... Immunoglobulin-like domains that are related in both sequence and structure can be found in several diverse protein families. ... CD4 is the primary receptor for HIV-1. CD4 has four immunoglobulin-like domains in its extracellular region that share the same ... The basic structure of immunoglobulin (Ig) molecules is a tetramer of two light chains and two heavy chains linked by ...
... (TIM) proteins are a family of cell surface immunomodulatory proteins. TIM1 Kane ...
Members of the IgSF family include the human killer cell immunoglobulin-like receptor (KIR) and the Immunoglobulin-like ... includes immunoglobulin-like transcripts (ILT, also known as leukocyte immunoglobulin-like receptors (LIRs)), leukocyte- ... Human killer cell immunoglobulin-like receptors recognize the α1 and α2 domains of class I human leukocyte antigens (HLA-A, -B ... Killer-cell immunoglobulin-like receptors (KIRs), are a family of type I transmembrane glycoproteins expressed on the plasma ...
... is a immunoglobulin gene with symbol IGHA1. It encodes a constant (C) segment of ... Immunoglobulin A is an antibody that plays a critical role in immune function in the mucous membranes. IgA shows the same ... "Entrez Gene: IGHA1 immunoglobulin heavy constant alpha 1". Kratzin, H.; Altevogt, P.; Ruban, E.; Kortt, A.; Staroscik, K.; ... "IGHA1 immunoglobulin heavy constant alpha 1 [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2016-10-16 ...
Immunoglobulins. Class Summary. Human Ig prevents or modifies measles in susceptible individuals if administered within 6 days ...
Immunoglobulin A level (IGA), Immunoglobulin M level (IGM), Alternative complement pathway activity (AH50), Total complement ... IGA, (Immunoglobulin A, Total). Related Tests. Primary Immunodeficiency Screen, Pneumococcal polysaccharide IgG antibody [12 ...
FIGURE 1. Number of specimens (N = 568) testing positive for West Nile virus immunoglobulin M antibodies, using one lot from a ... FIGURE 2. Number of persons (N = 518) testing positive for West Nile virus immunoglobulin M antibodies using one lot from a ... Alternative Text: The figure above shows the 568 specimens testing positive for West Nile virus immunoglobulin M antibodies, ... False-Positive Results with a Commercially Available West Nile Virus Immunoglobulin M Assay --- United States, 2008. In ...
The specificity of immunoglobulin G and immunoglobulin M in the fluorescent antibody test for malaria parasites in mice / by F ... Evaluation of commercially available anti-dengue virus immunoglobulin M tests  Pediatric Dengue Vaccine Initiative; UNICEF/ ... Reversed enzyme-linked immunosorbent assay for detection of specific anti-Plasmodium falciparum immunoglobulin M antibodies / M ...
IgG stands for immunoglobulin G. It is a type of antibody. Antibodies are proteins that your immune system makes to fight germs ... URL of this page: https://medlineplus.gov/lab-tests/csf-immunoglobulin-g-igg-index/ CSF Immunoglobulin G (IgG) Index. ... Other names: cerebrospinal fluid IgG level, cerebrospinal fluid IgG measurement, CSF IgG level, IgG (Immunoglobulin G) spinal ... Immunoglobulin G Index; [cited 2022 May 24]; [about 4 screens]. Available from: https://www.labcorp.com/tests/002238/ ...
ICD-10 code T50.Z13 for Poisoning by immunoglobulin, assault is a medical classification as listed by WHO under the range - ... ICD-10-CM Code for Poisoning by immunoglobulin, assault T50.Z13 ICD-10 code T50.Z13 for Poisoning by immunoglobulin, assault is ...
Immunoglobulin G in Ebola Outbreak Survivors, Gabon. Emerging Infectious Diseases. 2009;15(7):1136-1137. doi:10.3201/ ... Wauquier, N., Becquart, P., Gasquet, C., & Leroy, E. M. (2009). Immunoglobulin G in Ebola Outbreak Survivors, Gabon. Emerging ... Immunoglobulin G in Ebola Outbreak Survivors, Gabon. Volume 15, Number 7-July 2009 ... and immunoglobulin (Ig) G ELISA at Centre International de Recherches Médicales de Franceville (CIRMF) in Gabon. ...
View mouse Lrig3 Chr10:125802088-125851228 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
Immunoglobulin light chain kappa constant domain, CL-kappa ... Protein Immunoglobulin light chain kappa constant domain, CL- ... Fold b.1: Immunoglobulin-like beta-sandwich [48725] (28 superfamilies). sandwich; 7 strands in 2 sheets; greek-key. some ... Superfamily b.1.1: Immunoglobulin [48726] (5 families) *. Family b.1.1.2: C1 set domains (antibody constant domain-like) [48942 ... Lineage for Protein: Immunoglobulin light chain kappa constant domain, CL-kappa. *Root: SCOPe 2.03 *. Class b: All beta ...
Southern blot analysis of the bone marrow cells showed rearrangement of the immunoglobulin heavy chain gene, a genetic hallmark ... Acute Leukemia Showing t(8;22)(p11;q11), Myelodysplasia, CD13/CD33/CD19 Expression and Immunoglobulin Heavy Chain Gene ... CD13/CD33/CD19 Expression and Immunoglobulin Heavy Chain Gene Rearrangement. Acta Haematol 1 May 2013; 129 (4): 238-242. https ...
... website isotypes bio meaning isotypes of antibodies isotypes of antibodies and their function isotypes of immunoglobulin ...
The aim of this study was to create universal chimeric conjugates able to react with both avian and mammalian immunoglobulins ... Immunoglobulins; ELISA; Immunoglobulin-binding bacterial proteins; Protein conjugates. Introduction. Immunoglobulin-binding ... in the detection of immunoglobulins. All NSC bound to mammalian immunoglobulins, but failed to bind avian immunoglobulin Y (IgY ... 2013) Immunoglobulin-binding Bacterial Proteins (IBP) Conjugates and their Reactivity with Immunoglobulin in Enzyme-Linked ...
Intravenous immunoglobulin for the management of Netherton syndrome ... Response to low-dose intravenous immunoglobulin in a case of recalcitrant Darier disease.. JAAD Case Rep. 2020;6:189-91. [ ... How to cite this article: Neema S, Vasudevan B, Rathod A, Mukherjee S, Vendhan S, Gera V. Intravenous immunoglobulin for the ... Intravenous immunoglobulin has achieved success in most cases, and appears to be safe and effective for managing Netherton ...
Recurrence of Hepatitis B Infection in Liver Transplant Patients Receiving Long-Term Hepatitis B Immunoglobulin Prophylaxis. ... Recurrence of Hepatitis B Infection in Liver Transplant Patients Receiving Long-Term Hepatitis B Immunoglobulin Prophylaxis. ... infection after liver transplantation using hepatitis B immunoglobulin (HBIg) and nucleos(t)ide analogue (NUC) prophylaxis. ...
Mouse Immunoglobulin G (IgG) (Fc) Antibody Mouse Immunoglobulin G (IgG) (Fc) Antibody (Biotin Conjugate) Mouse Immunoglobulin G ... Bovine Immunoglobulin G (IgG) Antibody Bovine Immunoglobulin G (IgG) Antibody (Biotin Conjugate) Bovine Immunoglobulin G (IgG) ... Sheep Immunoglobulin G (IgG) Antibody Sheep Immunoglobulin G (IgG) Antibody (Biotin Conjugate) Sheep Immunoglobulin G (IgG) ... Rabbit Immunoglobulin G (IgG) Antibody Rabbit Immunoglobulin G (IgG) Antibody (Biotin Conjugate) Rabbit Immunoglobulin G (IgG) ...
Keywords: Immunoglobulin A (IgA) nephropathy, Oxford classification, crescent lesions, meta-analysis. Received: September 26, ... Evaluation of crescent formation as a predictive marker in immunoglobulin A nephropathy: a systematic review and meta-analysis ... The 2009 Oxford Classification of immunoglobulin A (IgA) nephropathy (IgAN) identifies four histological features as predictors ...
Mucosal surfaces in teleost fish harbor B cells that produce IgT, a secretory mucosal immunoglobulin. To investigate how IgT ...
Intravenous immunoglobulin. Intravenous immunoglobulin (IVIG) may be effective by interfering with ANCAs and thus inhibiting ... Goodpasture syndrome: Linear deposition of immunoglobulin G and C3 are observed on a renal biopsy specimen from a patient with ... Abatacept is a soluble, cytotoxic T-lymphocyte Ag-4 immunoglobulin that binds CD28, in that way inhibiting T-cell activation. ... Intravenous immunoglobulins for relapses of systemic vasculitides associated with antineutrophil cytoplasmic autoantibodies: ...
Intravenous Immunoglobulin. In IVIG, antibodies from healthy people are injected into a vein, usually in your forearm. It can ...
Recurrent Stent Thrombosis Secondary to Immunoglobulin G4-Related Disease. *. Chieh Yang Koo, MBBS Chieh Yang Koo ... Immunoglobulin G4-related disease (IgG4-RD) is an insidiously progressive multiorgan disease. However, lack of familiarity with ... Coronary artery disease concomitant with immunoglobulin G4-related disease: a case report and literature review. ...
Dai Y. Dai Y Dai, Yuchen. Comparing plasmapheresis and immunoglobulin-first therapy for patients with Stevens-Johnson syndrome ... immunoglobulin (IVIG) therapy for patients with SJS or TEN, who had previous ineffective systemic corticosteroid therapy. ... Dai Y. Dai Y Dai, Yuchen. (2023). Comparing plasmapheresis and immunoglobulin-first therapy for patients with stevens-johnson ... Dai Y. Dai Y Dai, Yuchen. "Comparing plasmapheresis and immunoglobulin-first therapy for patients with Stevens-Johnson syndrome ...
Evaluate humoral immunity; monitor therapy in IgG myeloma; quantitate IgG; evaluate patients, especially children and those with lymphoma, with propensity to infections. In congenital hypogammaglobulinemia, the IgG is less than 200 mg/dL by 6 months of age. Acquired hypogammaglobulinemia may occur at any age and has IgG concentrations less than 500 mg/dL. IgG concentrations may also be decreased in combined cell-mediated and antibody immunodeficiencies.. ...
We understand that having to change immunoglobulin products is an anxious and disturbing time for people who are dependant on ... immunoglobulin treatment as a life-long therapy. This article aims to help guide and reassure you through this process, and ... Are all immunoglobulin products the same?. Immunoglobulin products are not all the same. Whether a particular IG product is ... Switching immunoglobulin products. We understand that having to change immunoglobulin products is an anxious and disturbing ...
"Immunoglobulin Class Switching" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ... This graph shows the total number of publications written about "Immunoglobulin Class Switching" by people in UAMS Profiles by ... Below are the most recent publications written about "Immunoglobulin Class Switching" by people in Profiles over the past ten ... Below are MeSH descriptors whose meaning is more general than "Immunoglobulin Class Switching". ...
Autopsy case with concurrent transthyretin and immunoglobulin amyloidosis. Autopsy case with concurrent transthyretin and ... Immunohistochemical (IHC) analysis revealed immunoglobulin (Ig) λ light chain (-λ) in systemic blood vessels and transthyretin ... immunoglobulin amyloidosis. Shintani-Domoto, Yukako; Ishino, Kousuke; Naiki, Hironobu; Sakatani, Takashi; Ohashi, Ryuji. ...
Address : P.O. Box 15770 Flat No. 1, Bldg. No. 50, Road No. 2901, 329 Salmaniya - Bahrain ...
sacredazn on Unrearranged immunoglobulin gene. seagull on Decreased binding of RNA polymerase. seagull on Anticholinergic. ...
... immunoglobulin a qn serum, immunoglobulin e ige, immunoglobulin e total, immunoglobulin g1, immunoglobulin igg, immunoglobulin ... infusion, immunoglobulin m low, immunoglobulin structure, immunoglobulin test, immunoglobulin therapy, immunoglobulin types, ... immunoglobulin therapy GENTAUR SPARCL Rabbit IgG SPARCL Assay. April 8, 2022. by Gentaur ... immunoglobulina, immunoglobuline, immunoglobuliner, immunoglobulins blood test, immunoglobulins definition, western blot ...
  • IgA vasculitis, formerly called Henoch-Schönlein purpura or HSP, is a disease that causes the antibody immunoglobulin A to collect in small blood vessels, which then become inflamed and leak blood. (nih.gov)
  • IgG stands for immunoglobulin G . It is a type of antibody. (nih.gov)
  • Many different syndromes are known to lead to high levels of an antibody called immunoglobulin E, or IgE. (nih.gov)
  • A British study performed in 2022 evaluated serum anti-SARS-CoV-2-spike antibody titers before and after IVIG infusion in 35 patients with primary immunodeficiencies who were receiving regular immunoglobulin replacement therapy. (nih.gov)
  • Immunoglobulins are also called antibodies. (medlineplus.gov)
  • IgM antibodies are the first immunoglobulins your body makes after you're exposed to germs. (medlineplus.gov)
  • antibodies or immunoglobulins , particularly immunoglobulin M (IgM) or immunoglobulin G (IgG). (nih.gov)
  • Antibodies are proteins (immunoglobulins, (IgM), (IgG) etc) that are critical and key components of the immune system. (diabeteshealthmatters.com)
  • When patients have immunodeficiency conditions that require immunoglobulin therapy (IVIG), clinicians must consider carefully which IVIG product will have the fewest adverse effects and the highest level of efficacy. (pharmacytimes.com)
  • The COVID-19 Treatment Guidelines Panel (the Panel) recommends against the use of intravenous immunoglobulin (IVIG) for the treatment of acute COVID-19 in adults and children, except in a clinical trial ( AIII ) . (nih.gov)
  • 1. No significant difference in mortality rates between inpatients with Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) who received either plasmapheresis or immunoglobulin (IVIG) therapy first after ineffective systemic corticosteroid therapy. (mhmedical.com)
  • Therefore, this Japan-based retrospective cohort study aimed to investigate the efficacy of plasmapheresis vs. immunoglobulin (IVIG) therapy for patients with SJS or TEN, who had previous ineffective systemic corticosteroid therapy. (mhmedical.com)
  • The immunoglobulin is given by different mode of delivery like intravenous, subcutaneous. (axiommrc.com)
  • In September 2008, CDC, the Food and Drug Administration (FDA), and state health departments began a nationwide investigation into an increase in false-positive test results obtained with a commercially available West Nile virus (WNV) immunoglobulin M (IgM) capture enzyme-linked immunosorbent assay (ELISA). (cdc.gov)
  • Of the fatal and nonfatal cases 31 and 24, respectively, were confirmed by real-time reverse transcription-PCR, antigen detection, and immunoglobulin (Ig) G ELISA at Centre International de Recherches Médicales de Franceville (CIRMF) in Gabon. (cdc.gov)
  • You may also need this test if your provider thinks you may have high levels of immunoglobulins from an autoimmune disease or a cancer that affects your blood, bone marrow, and/or immune system. (medlineplus.gov)
  • Specifically, this altered glycoprotein is an immunoglobulin G (IgG) molecule reactive to the heterophilic alpha-Gal epitope [Galalpha-1-3Galbeta1-(3)4GlcNAc-R]. While similar changes in glycosylation have been observed in several autoimmune diseases, the specific immunoglobulins and their antigen recognition profiles were not determined. (nih.gov)
  • Besides the immunoglobulin products is used replacement therapy for immunodeficiency patient or as immunomodulatory therapy for autoimmune and alloimmune disorders. (axiommrc.com)
  • The periodate method was used in the conjugation process of linking horseradish peroxidase to immunoglobulin-binding bacterial proteins. (omicsonline.org)
  • Immunoglobulin-binding bacterial proteins (IBBP) are molecules that are widely found in the cell walls of several bacteria and they have the capacity to bind to the F c or F ab regions of immunoglobulins from different mammalian species. (omicsonline.org)
  • None of the commercially-available conjugates react universally to both avian and mammalian immunoglobulins . (omicsonline.org)
  • Finally, at the age of 10, Spero was diagnosed with Hyper-Immunoglobulin E Syndrome (HIES), also known as Job's syndrome. (nih.gov)
  • BACKGROUND Long-term real-world data are relatively sparse regarding recurrence of chronic hepatitis B virus (HBV) infection after liver transplantation using hepatitis B immunoglobulin (HBIg) and nucleos(t)ide analogue (NUC) prophylaxis. (eur.nl)
  • Increased levels of galactose-deficient anti-Gal immunoglobulin G in the sera of hepatitis C virus-infected individuals with fibrosis and cirrhosis. (nih.gov)
  • The human hepatitis C immunoglobulin (HCIG) Civacir is an investigational drug that is currently being developed in an ongoing phase 3 clinical trial assessing its safety and efficacy at preventing HCV recurrence after liver transplantation (LT) in the United States. (nottingham.ac.uk)
  • If you have too few immunoglobulins, you have an immunodeficiency. (medlineplus.gov)
  • You may need an immunoglobulins test if immunodeficiency runs in your family, or your health care provider thinks you may have a problem making normal levels of immunoglobulins. (medlineplus.gov)
  • The key factor contributing in the global immunoglobulin market are rising in prevalence of immunodeficiency diseases. (axiommrc.com)
  • North America is projected to lead in the global Immunoglobulin market owing to increasing demand from hospital and clinics for the treatment of primary immunodeficiency disease in patient. (axiommrc.com)
  • An immunoglobulins blood test measures the amounts of IgM, IgG, and IgA in your blood to help diagnose different types of health conditions that may affect your immune system. (medlineplus.gov)
  • With these disorders your immune system attacks your own healthy cells by mistake, including cells that make immunoglobulins. (medlineplus.gov)
  • For instance, Grifols has announced the launch of latest immunoglobulin innovation, XEMBIFY which is immune globulin subcutaneous human- klhw. (axiommrc.com)
  • The 2009 Oxford Classification of immunoglobulin A (IgA) nephropathy (IgAN) identifies four histological features as predictors of renal prognosis: mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental glomerulosclerosis (S), and tubular atrophy/interstitial fibrosis (T). However, the clinical and prognostic significance of crescent formation still remains controversial. (oncotarget.com)
  • Balancing somatic hypermutation and DNA repair in immunoglobulin genes / Patricia Gearhart. (nih.gov)
  • The variable domain of an immunoglobulin (IG) sequence is encoded by multiple genes, including the variable (V) gene, the diversity (D) gene and the joining (J) gene. (nih.gov)
  • ELISAs were used to prove the efficacy of the conjugates, namely newly synthesize conjugates (NSC) in the detection of immunoglobulins . (omicsonline.org)
  • Igg Serum Laboratories manufactures the immunoglobulin a/e/g/m serum reagents distributed by Genprice. (cd1234567890.com)
  • The Immunoglobulin A/E/G/M Serum reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (cd1234567890.com)
  • Immunoglobulin is a protein which is produce by plasma cells and lymphocytes. (axiommrc.com)
  • Thus, we provide the first report identifying the specific antigenic recognition profile of an immunoglobulin molecule containing altered glycosylation as a function of liver disease. (nih.gov)
  • All NSC bound to mammalian immunoglobulins, but failed to bind avian immunoglobulin Y (IgY), with the exception of the SpLAG-anti-IgY-HRP that was the most versatile binding to the all panel of purified immunoglobulin and sera. (omicsonline.org)
  • Medications used in the treatment or prevention of measles include vitamin A, antivirals (eg, ribavirin), measles virus vaccine, and human immunoglobulin (Ig). (medscape.com)
  • Immunohistochemical (IHC) analysis revealed immunoglobulin (Ig) λ light chain (-λ) in systemic blood vessels and transthyretin (TTR) in the heart and lungs . (bvsalud.org)
  • You may need this test if you have symptoms that could mean your immunoglobulin levels are too low. (medlineplus.gov)
  • So, even though your levels are high, you may have frequent infections and other symptoms of low immunoglobulin levels. (medlineplus.gov)
  • Your results can mean different things, depending on which immunoglobulins are high or low, your symptoms, and any conditions you may have. (medlineplus.gov)
  • What are the symptoms for immunoglobulin deficiency? (diabeteshealthmatters.com)
  • IgG is widely used product in the immunoglobulin market owing to its potential to eliminate the infectious agent further the product can be ideally used for patient once a week or every two weeks. (axiommrc.com)
  • PRODUCTION OF BOTULINUM ANTI-TOXIN IMMUNOGLOBULIN Release Date: June 13, 2002 NOTICE: NOT-AI-02-030 National Institute of Allergy and Infectious Diseases (NIAID) ( http://www.niaid.nih.gov ) Receipt Date for Letter of Interest: July 12, 2002 The National Institute of Allergy and Infectious Diseases (NIAID) is interested in supporting the development and licensure of botulinum anti-toxin immunoglobulin as a part of our Biodefense program. (nih.gov)
  • levels of immunoglobulin and neutrophils with poor patient survival. (nih.gov)
  • this case, patients have abnormally low levels of immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin E (IgE). (nih.gov)
  • They are considered rather than specific, universal conjugates (bind too many diverse immunoglobulins), including SpA-HRP, SpG-HRP, SpL-HRP, recombinant chimeric SpL-SpA-HRP (SpLA-HRP) [ 5 , 6 ], and some others, such as recombinant chimeric SpA-SpG-HRP (SpAG-HRP) and SpL-SpG-HRP (SpLG-HRP). (omicsonline.org)
  • There are no known risk factors for immunoglobulin deficiency, but research may suggest a low percentage of inheritance. (diabeteshealthmatters.com)
  • Filled with passionate debate, this exciting meeting had been arranged by Potter (above, third from the left) and Martin Weigert from the Institute for Cancer Research, Philadelphia, to discuss the newest results and ideas in immunoglobulin research. (nih.gov)
  • The exclusive COVID 19 impact analysis report by Axiom MRC provides a 3600 analysis of micro and macro-economic factors on the immunoglobulin market. (axiommrc.com)
  • Coronary artery disease concomitant with immunoglobulin G4-related disease: a case report and literature review. (onlinecjc.ca)
  • Southern blot analysis of the bone marrow cells showed rearrangement of the immunoglobulin heavy chain gene, a genetic hallmark of B-cell differentiation. (karger.com)
  • Hypogammaglobulinemia is anticipated to gain market in the global immunoglobulin market. (axiommrc.com)
  • Autopsy case with concurrent transthyretin and immunoglobulin amyloidosis. (bvsalud.org)
  • Mucosal surfaces in teleost fish harbor B cells that produce IgT, a secretory mucosal immunoglobulin. (socmucimm.org)
  • The immunoglobulin market is segmented based on product, mode of delivery, application and geography. (axiommrc.com)
  • This key factor of product is expected to drive the growth of product segment thereby fueling the growth of the immunoglobulin market. (axiommrc.com)
  • The aim of this study was to create universal chimeric conjugates able to react with both avian and mammalian immunoglobulins to be used as a reagent in Enzyme-linked Immunosorbent Assays (ELISAs). (omicsonline.org)
  • Since immunoglobulin deficiency is an issue that passes down to an individual through their family, it cannot be prevented. (diabeteshealthmatters.com)