A bacteriostatic antibacterial agent that interferes with folic acid synthesis in susceptible bacteria. Its broad spectrum of activity has been limited by the development of resistance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p208)
A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.
This drug combination has proved to be an effective therapeutic agent with broad-spectrum antibacterial activity against both gram-positive and gram-negative organisms. It is effective in the treatment of many infections, including PNEUMOCYSTIS PNEUMONIA in AIDS.
A sulfone active against a wide range of bacteria but mainly employed for its actions against MYCOBACTERIUM LEPRAE. Its mechanism of action is probably similar to that of the SULFONAMIDES which involves inhibition of folic acid synthesis in susceptible organisms. It is also used with PYRIMETHAMINE in the treatment of malaria. (From Martindale, The Extra Pharmacopoeia, 30th ed, p157-8)
Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection.
Substances that reduce the growth or reproduction of BACTERIA.
Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.
A pulmonary disease in humans occurring in immunodeficient or malnourished patients or infants, characterized by DYSPNEA, tachypnea, and HYPOXEMIA. Pneumocystis pneumonia is a frequently seen opportunistic infection in AIDS. It is caused by the fungus PNEUMOCYSTIS JIROVECII. The disease is also found in other MAMMALS where it is caused by related species of Pneumocystis.
Nonsusceptibility of bacteria to the action of TRIMETHOPRIM.
A short-acting sulfonamide antibacterial with activity against a wide range of gram- negative and gram-positive organisms.
The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The ability of bacteria to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
DNA elements that include the component genes and insertion site for a site-specific recombination system that enables them to capture mobile gene cassettes.
Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.
A species of PNEUMOCYSTIS infecting humans and causing PNEUMOCYSTIS PNEUMONIA. It also occasionally causes extrapulmonary disease in immunocompromised patients. Its former name was Pneumocystis carinii f. sp. hominis.
Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of PNEUMOCYSTIS pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects.
A genus of gram-positive bacteria in the family Cellulomonadaceae.
Inflammatory responses of the epithelium of the URINARY TRACT to microbial invasions. They are often bacterial infections with associated BACTERIURIA and PYURIA.
A species of STENOTROPHOMONAS, formerly called Xanthomonas maltophilia, which reduces nitrate. It is a cause of hospital-acquired ocular and lung infections, especially in those patients with cystic fibrosis and those who are immunosuppressed.
One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.
A sulfanilamide antibacterial agent.
An enzyme that catalyzes the formation of dihydropteroate from p-aminobenzoic acid and dihydropteridine-hydroxymethyl-pyrophosphate. EC 2.5.1.15.
An aminobenzoic acid isomer that combines with pteridine and GLUTAMIC ACID to form FOLIC ACID. The fact that 4-aminobenzoic acid absorbs light throughout the UVB range has also resulted in its use as an ingredient in SUNSCREENS.
Infections with bacteria of the genus NOCARDIA.
The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
A chronic systemic infection by a gram-positive bacterium, Tropheryma whippelii, mainly affecting the SMALL INTESTINE but also the JOINTS; CARDIOVASCULAR SYSTEM; and the CENTRAL NERVOUS SYSTEM. The disease is characterized by fat deposits in the INTESTINAL MUCOSA and LYMPH NODES, malabsorption, DIARRHEA with fatty stools, MALNUTRITION, and ARTHRITIS.
Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response.
The action of a drug in promoting or enhancing the effectiveness of another drug.
Infections with bacteria of the species ESCHERICHIA COLI.
A lactose-fermenting bacterium causing dysentery.
A genus of gram-positive, aerobic bacteria whose species are widely distributed and are abundant in soil. Some strains are pathogenic opportunists for humans and animals.
Substances capable of killing agents causing urinary tract infections or of preventing them from spreading.
Red blood cell precursors, corresponding to ERYTHROBLASTS, that are larger than normal, usually resulting from a FOLIC ACID DEFICIENCY or VITAMIN B 12 DEFICIENCY.
Inhibitors of the enzyme, dihydrofolate reductase (TETRAHYDROFOLATE DEHYDROGENASE), which converts dihydrofolate (FH2) to tetrahydrofolate (FH4). They are frequently used in cancer chemotherapy. (From AMA, Drug Evaluations Annual, 1994, p2033)
Adverse cutaneous reactions caused by ingestion, parenteral use, or local application of a drug. These may assume various morphologic patterns and produce various types of lesions.
A genus of ascomycetous FUNGI, family Pneumocystidaceae, order Pneumocystidales. It includes various host-specific species causing PNEUMOCYSTIS PNEUMONIA in humans and other MAMMALS.
Strains of VIBRIO CHOLERAE containing O ANTIGENS group 1. All are CHOLERA-causing strains (serotypes). There are two biovars (biotypes): cholerae and eltor (El Tor).
A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that ferments sugar without gas production. Its organisms are intestinal pathogens of man and other primates and cause bacillary dysentery (DYSENTERY, BACILLARY).
A broad-spectrum antimicrobial carboxyfluoroquinoline.
Organic compounds that contain the (-NH2OH) radical.
A subgenus of Salmonella containing several medically important serotypes. The habitat for the majority of strains is warm-blooded animals.
A family of gram-negative, facultatively anaerobic, rod-shaped bacteria that do not form endospores. Its organisms are distributed worldwide with some being saprophytes and others being plant and animal parasites. Many species are of considerable economic importance due to their pathogenic effects on agriculture and livestock.
A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that utilizes citrate as a sole carbon source. It is pathogenic for humans, causing enteric fevers, gastroenteritis, and bacteremia. Food poisoning is the most common clinical manifestation. Organisms within this genus are separated on the basis of antigenic characteristics, sugar fermentation patterns, and bacteriophage susceptibility.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)
Gel electrophoresis in which the direction of the electric field is changed periodically. This technique is similar to other electrophoretic methods normally used to separate double-stranded DNA molecules ranging in size up to tens of thousands of base-pairs. However, by alternating the electric field direction one is able to separate DNA molecules up to several million base-pairs in length.
A synthetic 1,8-naphthyridine antimicrobial agent with a limited bacteriocidal spectrum. It is an inhibitor of the A subunit of bacterial DNA GYRASE.
Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)
An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is VIBRIO CHOLERAE. This condition can lead to severe dehydration in a matter of hours unless quickly treated.
A group of compounds that contain the structure SO2NH2.
Infections caused by bacteria that show up as pink (negative) when treated by the gram-staining method.
An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863)

Methemoglobin formation by hydroxylamine metabolites of sulfamethoxazole and dapsone: implications for differences in adverse drug reactions. (1/488)

Differences in the incidence of adverse drug reactions to trimethoprim-sulfamethoxazole and dapsone may result from differences in the formation, disposition, toxicity, and/or detoxification of their hydroxylamine metabolites. In this study, we examine whether differences in the biochemical processing of sulfamethoxazole hydroxylamine (SMX-NOH) and dapsone hydroxylamine (DDS-NOH) by erythrocytes [red blood cells (RBCs)] contribute to this differential incidence. The methemoglobin (MetHgb)-forming capacity of both metabolites was compared after a 60-min incubation with washed RBCs from four healthy human volunteers. DDS-NOH was significantly more potent (P =.004) but equally efficacious with SMX-NOH in its ability to form MetHgb. The elimination of potential differences in disposition by lysing RBCs did not change the MetHgb-forming potency of either hydroxylamine. At pharmacologically relevant concentrations, greater reduction to the parent amine occurred with DDS-NOH. Maintenance of MetHgb-forming potency was dependent on recycling with glutathione, but no difference in cycling efficiency was observed between DDS-NOH and SMX-NOH. In contrast, the pharmacodynamics of hydroxylamine-induced MetHgb formation were not changed by pretreatment with the glucose 6-phosphate dehydrogenase inhibitor epiandrosterone or by compounds that alter normal antioxidant enzyme activity. Methylene blue, which stimulates NADPH-dependent MetHgb reductase activity, decreased MetHgb levels but did not alter the differential potency of these hydroxylamines. DDS-NOH was also significantly more potent when incubated with purified human hemoglobin A0. Collectively, these data suggest that the inherently greater reactivity of DDS-NOH with hemoglobin, the greater conversion of DDS-NOH to its parent amine, and potential differences in disposition of hydroxylamine metabolites may contribute to the preferential development of dapsone-induced hemotoxicity and sulfamethoxazole-induced hypersensitivity reactions.  (+info)

Renal stones and urinary infection: a study of antibiotic treatment. (2/488)

Twenty-two patients in whom renal calculi and urinary infection were closely associated were studied over two to five years. Four patients had previously had stones surgically removed, and five underwent pyelolithotomy during the course of the study. Urinary infection was treated with an appropriate antibacterial agent, and treatment was followed by long-term prophylaxis, usually with cotrimoxazole. A sterile urine was maintained for long periods in all these patients. In four patients, however, apparent stone growth occurred while the urine was sterile. On entering the study 21 of the 22 patients complained of symptoms. After treatment 19 of the 20 patients who were still attending were symptom-free. Six of the 22 patients entered the study with raised levels of serum creatinine; levels fell in four and remained raised in two. This antibacterial regimen, either alone or after surgery, will usually relieve symptoms and may prevent deterioration of renal function.  (+info)

Cellular disposition of sulphamethoxazole and its metabolites: implications for hypersensitivity. (3/488)

1. Bioactivation of sulphamethoxazole (SMX) to chemically-reactive metabolites and subsequent protein conjugation is thought to be involved in SMX hypersensitivity. We have therefore examined the cellular metabolism, disposition and conjugation of SMX and its metabolites in vitro. 2. Flow cytometry revealed binding of N-hydroxy (SMX-NHOH) and nitroso (SMX-NO) metabolites of SMX, but not of SMX itself, to the surface of viable white blood cells. Cellular haptenation by SMX-NO was reduced by exogenous glutathione (GSH). 3. SMX-NHOH and SMX-NO were rapidly reduced back to the parent compound by cysteine (CYS), GSH, human peripheral blood cells and plasma, suggesting that this is an important and ubiquitous bioinactivation mechanism. 4. Fluorescence HPLC showed that SMX-NHOH and SMX-NO depleted CYS and GSH in buffer, and to a lesser extent, in cells and plasma. 5. Neutrophil apoptosis and inhibition of neutrophil function were induced at lower concentrations of SMX-NHOH and SMX-NO than those inducing loss of membrane viability, with SMX having no effect. Lymphocytes were significantly (P<0.05) more sensitive to the direct cytotoxic effects of SMX-NO than neutrophils. 6. Partitioning of SMX-NHOH into red blood cells was significantly (P<0.05) lower than with the hydroxylamine of dapsone. 7. Our results suggest that the balance between oxidation of SMX to its toxic metabolites and their reduction is an important protective cellular mechanism. If an imbalance exists, haptenation of the toxic metabolites to bodily proteins including the surface of viable cells can occur, and may result in drug hypersensitivity.  (+info)

Multisite reproducibility of results obtained by the broth microdilution method for susceptibility testing of Mycobacterium abscessus, Mycobacterium chelonae, and Mycobacterium fortuitum. (4/488)

A multicenter study was conducted to assess the interlaboratory reproducibility of broth microdilution testing of the more common rapidly growing pathogenic mycobacteria. Ten isolates (four Mycobacterium fortuitum group, three Mycobacterium abscessus, and three Mycobacterium chelonae isolates) were tested against amikacin, cefoxitin, ciprofloxacin, clarithromycin, doxycycline, imipenem, sulfamethoxazole, and tobramycin (M. chelonae only) in four laboratories. At each site, isolates were tested three times on each of three separate days (nine testing events per isolate) with a common lot of microdilution trays. Agreement among MICs (i.e., mode +/- 1 twofold dilution) varied considerably for the different drug-isolate combinations and overall was best for cefoxitin (91.7 and 97.2% for one isolate each and 100% for all others), followed by doxycycline, amikacin, and ciprofloxacin. Agreement based on the interpretive category, using currently suggested breakpoints, also varied and overall was best for doxycycline (97.2% for one isolate and 100% for the rest), followed by ciprofloxacin and clarithromycin. Reproducibility among MICs and agreement by interpretive category was most variable for imipenem. Based on results reported from the individual sites, it appears that inexperience contributed significantly to the wide range of MICs of several drugs, especially clarithromycin, ciprofloxacin, and sulfamethoxazole. New interpretive guidelines are presented for the testing of M. fortuitum against clarithromycin; M. abscessus and M. chelonae against the aminoglycosides; and all three species against cefoxitin, doxycycline, and imipenem.  (+info)

Pharmacokinetics and efficacy of trimethoprim-sulfamethoxazole in the treatment of gastroenteritis in children. (5/488)

In vitro studies indicates that the constitutents of the drug combination co-trimoxazole are synergistic against Salmonella and effective against shigella isolated from children ill with gastroenteritis. The drug is well absorbed in children with gastroenteritis due to a variety of causes and is distributed, excreted and metabolized in a manner similar to that seen in normal adult volunteers. The drug is tolerated well by children with gastroenteritis even in very high dosages. Despite its in vitro and pharmacokinetic advantages, co-trimoxazole was not any more efficient than any other durg or no therapy in the treatment of salmonella gastroenteritis; it seems to have a role, however, in the treatment of typhoid fever and may be life-saving in patients infected with ampicillin- and chloramphenical-resistant strains. It is also effective in the treatment of shigella gastroenteritis and is recommended where ampicillin-resistant strains are encountered. Its potential usefulenss for the treatment of other bacterial causes of gastroenteritis in children must be evaluated by further controlled therapeutic trials.  (+info)

Cytotoxicity of sulfonamide reactive metabolites: apoptosis and selective toxicity of CD8(+) cells by the hydroxylamine of sulfamethoxazole. (6/488)

Treatment with sulfonamide antibiotics in HIV-infected patients is associated with a high incidence (> 40%) of adverse drug events, including severe hypersensitivity reactions. Sulfonamide reactive metabolites have been implicated in the pathogenesis of these adverse reactions. Sulfamethoxazole hydroxylamine (SMX-HA) induces lymphocyte toxicity and suppression of proliferation in vitro; the mechanism(s) of these immunomodulatory effects remain unknown. We investigated the cytotoxicity of SMX-HA via apoptosis on human peripheral blood mononuclear cells and purified cell subpopulations in vitro. CD19(+), CD4(+), and CD8(+) cells were isolated from human peripheral blood by positive selection of cell surface molecules by magnetic bead separation. SMX-HA induced significant CD8(+) cell death (67 +/- 7%) at 100 microM SMX-HA, with only minimal CD4(+) cell death (8 +/- 4%). No significant subpopulation toxicity was shown when incubated with parent drug (SMX). Flow cytometry measuring phosphatidylserine externalization 24 h after treatment with 100 microM and 400 microM SMX-HA revealed 14.1 +/- 0.7% and 25. 6 +/- 4.2% annexin-positive cells, respectively, compared to 3.7 +/- 1.2% in control PBMCs treated with 400 microM SMX. Internucleosomal DNA fragmentation was observed in quiescent and stimulated PBMCs 48 h after incubation with SMX-HA. Our data show that CD8(+) cells are highly susceptible to the toxic effects of SMX-HA through enhanced cell death by apoptosis.  (+info)

Is hydroxylamine-induced cytotoxicity a valid marker for hypersensitivity reactions to sulfamethoxazole in human immunodeficiency virus-infected individuals? (7/488)

Hypersensitivity (HS) reactions to sulfonamides and sulfones continue to limit their use in human immunodeficiency virus (HIV)-infected individuals. In vitro cytotoxicity of hydroxylamine metabolites toward peripheral blood mononuclear cells (PBMCs) has been proposed as a marker for these HS reactions. To test the validity of this in vitro system, we determined the selective susceptibility of PBMCs from HIV-infected patients to the cytotoxic effects of hydroxylamine metabolites of sulfamethoxazole (SMX) and dapsone (DDS). Concentration-cytotoxic response data were collected using PBMCs from 12 sulfa-HS (10 SMX-HS and 2 SMX/DDS-HS) and 10 sulfa-tolerant HIV-infected individuals. Although sulfamethoxazole hydroxylamine (SMX-NOH) and dapsone hydroxylamine (DDS-NOH) both caused concentration-dependent increases in cell death, DDS-NOH was significantly more potent in each subject (P <.0001). A comparison of a variety of mean data for sulfa-HS and -tolerant patient populations failed to demonstrate the increased susceptibility of PBMCs from HS patients, noted by others, to either SMX-NOH or DDS-NOH. Moreover, any trend toward an increased susceptibility of PBMCs from HS patients was eliminated when adjusted for control cell death. PBMCs from sulfa-HS patients showed significantly greater susceptibility to the stress of short term in vitro incubation (P <. 02). Mean (S.D.) vehicle control cell death values were 24.1% (7.6%) for HS patients and 17.1% (4.4%) for tolerant patients. No significant correlation was observed between hydroxylamine-induced or control cell death and any of the recorded clinical parameters. Although several potential reasons are proposed to explain the disparity with past investigations, the data suggest that in vitro cytotoxicity is not a valid marker for HS reactions in HIV-infected individuals using currently accepted experimental procedures.  (+info)

Cerebral toxoplasmosis - a late complication of allogeneic haematopoietic stem cell transplantation. (8/488)

Toxoplasma gondii infection reactivation predominantly occurs among patients after allogeneic haematopoietic stem cell transplantation. Mostly, reactivation occurs during first 3 months after transplant, especially when risk factors are present. We report a case of late cerebral toxoplasmosis reactivation, which was probably triggered by a brief course of corticosteroids, administered for chronic graft-versus-host disease (cGVHD). In the presence of risk factors, such as cGVHD, prophylactic treatment for toxoplasmosis should be reinstituted; Trimethoprim-sulfamethoxasole most probably prevented earlier reactivation of toxoplasmosis in our patient.  (+info)

There are several different types of drug hypersensitivity reactions, including:

1. Maculopapular exanthema (MPE): This is a type of allergic reaction that causes a red, itchy rash to appear on the skin. It can be caused by a variety of medications, including antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).
2. Exfoliative dermatitis: This is a more severe form of MPE that can cause widespread scaling and peeling of the skin. It is often associated with reactions to antibiotics and other medications.
3. Stevens-Johnson syndrome (SJS): This is a rare but potentially life-threatening condition that can be caused by certain medications, including antibiotics and NSAIDs. SJS can cause blisters to form on the skin and mucous membranes, as well as fever and fatigue.
4. Toxic epidermal necrolysis (TEN): This is a severe and potentially life-threatening condition that can be caused by certain medications, including antibiotics and NSAIDs. TEN can cause widespread peeling of the skin, as well as fever and fatigue.
5. Anaphylaxis: This is a severe allergic reaction that can be caused by a variety of medications, including antibiotics and NSAIDs. It can cause symptoms such as hives, itching, swelling, and difficulty breathing.

Drug hypersensitivity reactions can be diagnosed through a combination of physical examination, medical history, and laboratory tests. Treatment typically involves discontinuing the medication that is causing the reaction, as well as providing supportive care to manage symptoms such as fever, itching, and pain. In severe cases, hospitalization may be necessary to monitor and treat the reaction.

Prevention of drug hypersensitivity reactions can be challenging, but there are several strategies that can help reduce the risk. These include:

1. Gradual dose escalation: When starting a new medication, it is important to gradually increase the dose over time to allow the body to adjust.
2. Monitoring for signs of a reaction: Patients should be monitored closely for signs of a reaction, such as hives, itching, or difficulty breathing.
3. Avoiding certain medications: In some cases, it may be necessary to avoid certain medications that are known to cause hypersensitivity reactions.
4. Skin testing: Skin testing can be used to determine whether a patient is allergic to a particular medication before starting treatment.
5. Desensitization: In some cases, desensitization therapy may be used to gradually expose the patient to the medication that is causing the reaction, with the goal of reducing the risk of an adverse event.

This type of pneumonia can cause severe respiratory symptoms, including cough, fever, chest pain, and difficulty breathing. It can also lead to respiratory failure and other complications if left untreated.

Pneumocystis pneumonia is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or CT scans, and blood tests. Treatment typically involves antifungal medications, and hospitalization may be necessary for severe cases.

Prevention measures include avoiding exposure to people with weakened immune systems, avoiding smoking, and maintaining good hygiene practices. Vaccines are also available for some populations at high risk of developing Pneumocystis pneumonia.

Symptoms of a UTI can include:

* Painful urination
* Frequent urination
* Cloudy or strong-smelling urine
* Blood in the urine
* Pelvic pain in women
* Rectal pain in men

If you suspect that you have a UTI, it is important to seek medical attention as soon as possible. UTIs can lead to more serious complications if left untreated, such as kidney damage or sepsis.

Treatment for a UTI typically involves antibiotics to clear the infection. It is important to complete the full course of treatment to ensure that the infection is completely cleared. Drinking plenty of water and taking over-the-counter pain relievers may also help alleviate symptoms.

Preventive measures for UTIs include:

* Practicing good hygiene, such as wiping from front to back and washing hands after using the bathroom
* Urinating when you feel the need, rather than holding it in
* Avoiding certain foods that may irritate the bladder, such as spicy or acidic foods
* Drinking plenty of water to help flush bacteria out of the urinary tract.

Symptoms of nocardiosis can vary depending on the site of infection and severity of disease. Respiratory symptoms may include cough, fever, chest pain, and shortness of breath. Skin infections may cause swelling, redness, and warmth at the site of infection. Bone and joint infections can lead to pain, swelling, and limited mobility.

Diagnosis is based on a combination of clinical findings, laboratory tests, and radiographic imaging. Laboratory tests may include blood cultures, polymerase chain reaction (PCR), and other techniques to detect the presence of Nocardia in body fluids or tissues. Imaging studies such as chest X-rays, computed tomography (CT) scans, or magnetic resonance imaging (MRI) may be used to evaluate the extent of disease.

Treatment of nocardiosis typically involves a combination of antibiotics and surgical debridement of infected tissues. The choice of antibiotics depends on the severity and location of infection, as well as the patient's age, health status, and other medical conditions. Surgical intervention may be necessary to drain abscesses, repair damaged tissues, or remove infected bone or joint segments.

Preventive measures for nocardiosis include avoiding exposure to risk factors such as soil or contaminated water, practicing good hygiene and infection control practices, and following proper sterilization techniques when handling instruments or equipment. Vaccination against Nocardia is not available, and there is currently no effective prophylactic therapy for nocardiosis.

Nocardiosis can be a challenging disease to diagnose and treat, particularly in cases of disseminated infection or those with underlying medical conditions. Prompt recognition and aggressive management are critical to improving patient outcomes.

The disease is named after George Hoyt Whipple, an American physician who first described it in 1907. Whipple disease is rare, with an estimated incidence of 1 to 5 cases per million people per year. It can affect individuals of all ages but is more common in middle-aged adults.

The cause of Whipple disease is a bacterium called Tropheryma whipplei, which is found in soil and the feces of infected animals. The bacteria enter the body through contaminated food or water or through direct exposure to soil or animal waste. Once inside the body, the bacteria multiply and produce toxins that damage the lining of the small intestine and other parts of the gastrointestinal tract.

Symptoms of Whipple disease can vary in severity and may include diarrhea, abdominal pain, weight loss, fatigue, and malabsorption. If left untreated, the disease can lead to complications such as intestinal obstruction, bowel perforation, and malnutrition.

Diagnosis of Whipple disease typically involves a combination of clinical evaluation, laboratory tests, and imaging studies. Treatment usually involves antibiotics and supportive care to manage symptoms and prevent complications. In severe cases, surgery may be necessary to remove affected tissue or repair damaged areas.

Overall, Whipple disease is a rare and potentially life-threatening condition that requires prompt diagnosis and treatment. With appropriate management, many individuals with Whipple disease can recover and lead normal lives.

Here are some common types of E. coli infections:

1. Urinary tract infections (UTIs): E. coli is a leading cause of UTIs, which occur when bacteria enter the urinary tract and cause inflammation. Symptoms include frequent urination, burning during urination, and cloudy or strong-smelling urine.
2. Diarrheal infections: E. coli can cause diarrhea, abdominal cramps, and fever if consumed through contaminated food or water. In severe cases, this type of infection can lead to dehydration and even death, particularly in young children and the elderly.
3. Septicemia (bloodstream infections): If E. coli bacteria enter the bloodstream, they can cause septicemia, a life-threatening condition that requires immediate medical attention. Symptoms include fever, chills, rapid heart rate, and low blood pressure.
4. Meningitis: In rare cases, E. coli infections can spread to the meninges, the protective membranes covering the brain and spinal cord, causing meningitis. This is a serious condition that requires prompt treatment with antibiotics and supportive care.
5. Hemolytic-uremic syndrome (HUS): E. coli infections can sometimes cause HUS, a condition where the bacteria destroy red blood cells, leading to anemia, kidney failure, and other complications. HUS is most common in young children and can be fatal if not treated promptly.

Preventing E. coli infections primarily involves practicing good hygiene, such as washing hands regularly, especially after using the bathroom or before handling food. It's also essential to cook meat thoroughly, especially ground beef, to avoid cross-contamination with other foods. Avoiding unpasteurized dairy products and drinking contaminated water can also help prevent E. coli infections.

If you suspect an E. coli infection, seek medical attention immediately. Your healthcare provider may perform a urine test or a stool culture to confirm the diagnosis and determine the appropriate treatment. In mild cases, symptoms may resolve on their own within a few days, but antibiotics may be necessary for more severe infections. It's essential to stay hydrated and follow your healthcare provider's recommendations to ensure a full recovery.

Types of Drug Eruptions:

1. Maculopapular exanthema (MPE): This is a common type of drug eruption characterized by flat, red patches on the skin that may be accompanied by small bumps or hives. MPE typically occurs within 1-2 weeks of starting a new medication and resolves once the medication is discontinued.
2. Stevens-Johnson syndrome (SJS): This is a more severe type of drug eruption that can cause blisters, skin sloughing, and mucosal lesions. SJS typically occurs within 2-4 weeks of starting a new medication and can be life-threatening in some cases.
3. Toxic epidermal necrolysis (TEN): This is a severe, life-threatening type of drug eruption that can cause widespread skin death and mucosal lesions. TEN typically occurs within 2-4 weeks of starting a new medication and requires immediate hospitalization and treatment.

Causes of Drug Eruptions:

1. Allergic reactions to medications: This is the most common cause of drug eruptions. The body's immune system overreacts to certain medications, leading to skin symptoms.
2. Adverse effects of medications: Certain medications can cause skin symptoms as a side effect, even if the person is not allergic to them.
3. Infections: Bacterial, fungal, or viral infections can cause drug eruptions, particularly if the medication is used to treat the infection.
4. Autoimmune disorders: Certain autoimmune disorders, such as lupus or rheumatoid arthritis, can increase the risk of developing drug eruptions.

Diagnosis and Treatment of Drug Eruptions:

1. Medical history and physical examination: A thorough medical history and physical examination are essential to diagnose a drug eruption. The healthcare provider will look for patterns of skin symptoms that may be related to a specific medication.
2. Skin biopsy: In some cases, a skin biopsy may be necessary to confirm the diagnosis of a drug eruption and to rule out other conditions.
3. Medication history: The healthcare provider will ask about all medications taken by the patient, including over-the-counter medications and supplements.
4. Treatment: Depending on the severity of the drug eruption, treatment may include stopping the offending medication, administering corticosteroids or other immunosuppressive medications, and providing supportive care to manage symptoms such as itching, pain, and infection. In severe cases, hospitalization may be necessary.
5. Monitoring: Patients with a history of drug eruptions should be closely monitored by their healthcare provider when starting new medications, and any changes in their skin should be reported promptly.

Prevention of Drug Eruptions:

1. Allergy testing: Before starting a new medication, the healthcare provider may perform allergy testing to determine the patient's sensitivity to specific medications.
2. Medication history: The healthcare provider should take a thorough medication history to identify potential allergens and avoid prescribing similar medications that may cause an adverse reaction.
3. Gradual introduction of new medications: When starting a new medication, it is recommended to introduce the medication gradually in small doses to monitor for any signs of an adverse reaction.
4. Monitoring: Patients should be closely monitored when starting new medications, and any changes in their skin or symptoms should be reported promptly to their healthcare provider.
5. Avoiding certain medications: In some cases, it may be necessary to avoid certain medications that are more likely to cause a drug eruption based on the patient's medical history and other factors.

Conclusion:

Drug eruptions can present with various symptoms and can be challenging to diagnose. A thorough medical history and physical examination are essential to diagnose a drug eruption. Treatment depends on the severity of the reaction and may include stopping the offending medication, administering corticosteroids, and providing supportive care. Prevention is key, and healthcare providers should be aware of potential allergens and take steps to minimize the risk of adverse reactions. By being vigilant and proactive, healthcare providers can help prevent drug eruptions and ensure the best possible outcomes for their patients.

The symptoms of cholera include:

1. Diarrhea: Cholera causes profuse, watery diarrhea that can last for several days.
2. Dehydration: The loss of fluids and electrolytes due to diarrhea can lead to severe dehydration, which can be life-threatening if not treated promptly.
3. Nausea and vomiting: Cholera patients may experience nausea and vomiting, especially in the early stages of the disease.
4. Abdominal cramps: The abdomen may become tender and painful due to the inflammation caused by the bacteria.
5. Low-grade fever: Some patients with cholera may experience a mild fever, typically less than 102°F (39°C).

Cholera is spread through the fecal-oral route, which means that it is transmitted when someone ingests food or water contaminated with the bacteria. The disease can also be spread by direct contact with infected fecal matter, such as through poor hygiene practices or inadequate waste disposal.

There are several ways to diagnose cholera, including:

1. Stool test: A stool sample can be tested for the presence of Vibrio cholerae using a microscope or a rapid diagnostic test (RDT).
2. Blood test: A blood test can detect the presence of antibodies against Vibrio cholerae, which can indicate that the patient has been infected with the bacteria.
3. Physical examination: A healthcare provider may perform a physical examination to look for signs of dehydration and other symptoms of cholera.

Treatment of cholera typically involves replacing lost fluids and electrolytes through oral rehydration therapy (ORT) or intravenous fluids. Antibiotics may also be given to shorten the duration of diarrhea and reduce the risk of complications. In severe cases, hospitalization may be necessary to provide more intensive treatment.

Prevention of cholera involves maintaining good hygiene practices, such as washing hands with soap and water, and avoiding consumption of contaminated food and water. Vaccines are also available to protect against cholera, particularly for people living in areas where the disease is common.

In conclusion, cholera is a highly infectious disease that can cause severe dehydration and even death if left untreated. Early diagnosis and treatment are critical to preventing complications and reducing the risk of transmission. Prevention measures such as vaccination and good hygiene practices can also help control the spread of the disease.

Gram-negative bacterial infections can be difficult to treat because these bacteria are resistant to many antibiotics. In addition, some gram-negative bacteria produce enzymes called beta-lactamases, which break down the penicillin ring of many antibiotics, making them ineffective against the infection.

Some common types of gram-negative bacterial infections include:

* Pneumonia
* Urinary tract infections (UTIs)
* Bloodstream infections (sepsis)
* Meningitis
* Skin and soft tissue infections
* Respiratory infections, such as bronchitis and sinusitis

Examples of gram-negative bacteria that can cause infection include:

* Escherichia coli (E. coli)
* Klebsiella pneumoniae
* Pseudomonas aeruginosa
* Acinetobacter baumannii
* Proteus mirabilis

Gram-negative bacterial infections can be diagnosed through a variety of tests, including blood cultures, urine cultures, and tissue samples. Treatment typically involves the use of broad-spectrum antibiotics, such as carbapenems or cephalosporins, which are effective against many types of gram-negative bacteria. In some cases, the infection may require hospitalization and intensive care to manage complications such as sepsis or organ failure.

Prevention of gram-negative bacterial infections includes good hand hygiene, proper use of personal protective equipment (PPE), and appropriate use of antibiotics. In healthcare settings, infection control measures such as sterilization and disinfection of equipment, and isolation precautions for patients with known gram-negative bacterial infections can help prevent the spread of these infections.

Overall, gram-negative bacterial infections are a significant public health concern, and proper diagnosis and treatment are essential to prevent complications and reduce the risk of transmission.

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  • 2 When administered together as sulfamethoxazole and trimethoprim, neither sulfamethoxazole nor trimethoprim affects the urinary excretion pattern of the other. (nih.gov)
  • We report a woman, 78 years of age, who was treated with trimethoprim/sulfamethoxazole after a tick bite, in whom myocarditis was subsequently diagnosed. (cdc.gov)
  • To reduce the development of drug-resistant bacteria and maintain the effectiveness of sulfamethoxazole and trimethoprim oral suspension and other antibacterial drugs, sulfamethoxazole and trimethoprim oral suspension should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria. (nih.gov)
  • Sulfamethoxazole and trimethoprim oral suspension is a synthetic antibacterial combination product available in a suspension for oral administration, with each teaspoonful (5 mL) containing 200 mg sulfamethoxazole and 40 mg trimethoprim. (nih.gov)
  • Sulfamethoxazole and trimethoprim oral suspension is rapidly absorbed following oral administration. (nih.gov)
  • Sulfamethoxazole and Trimethoprim Oral Suspension is a synthetic antibacterial combination product. (nih.gov)
  • Bactrim DS (Trimethoprim/Sulfamethoxazole) is used to treat a wide variety of bacterial based infections, however its primary use is to fight UTI (urinary tract infections). (unitedpharmacies.com)
  • Bactrim DS (Trimethoprim/Sulfamethoxazole) should only ever be used as prescribed by your physician. (unitedpharmacies.com)
  • While taking Bactrim DS (Trimethoprim/Sulfamethoxazole), report all side effects to your physician promptly. (unitedpharmacies.com)
  • 2018. https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_HIV_Guide/545258/0/Trimethoprim_+_Sulfamethoxazole. (hopkinsguides.com)
  • 2023. https://nursing.unboundmedicine.com/nursingcentral/view/Davis-Drug-Guide/109135/2/sulfamethoxazole. (unboundmedicine.com)
  • Sulfamethoxazole is metabolized in humans to at least 5 metabolites: the N 4 -acetyl-, N 4 -hydroxy-, 5-methylhydroxy-, N 4 -acetyl-5methylhydroxy- sulfamethoxazole metabolites, and an N-glucuronide conjugate. (nih.gov)
  • The native compounds and the metabolites of trimethoprim and sulfamethoxazole are excreted primarily in the urine. (nih.gov)
  • In addition, the synergistic Cu 2 O/TiO 2 -NF photocatalyst showed significant oxidative-degradation of sulfamethoxazole (7 × 10 -2 mmol g −1 min -1 ) and was highly stable during five cycles. (elsevier.com)
  • Efficacy and safety of ciprofloxacin oral suspension versus trimethoprim-sulfamethoxazole oral suspension for treatment of older women with acute urinary tract infection. (druglib.com)
  • Comparison of atovaquone and azithromycin with trimethoprim-sulfamethoxazole for the prevention of serious bacterial infections in children with HIV infection. (druglib.com)
  • Sulfamethoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with para -aminobenzoic acid (PABA). (nih.gov)
  • In vitro studies have shown that bacterial resistance develops more slowly with this combination than with either sulfamethoxazole or trimethoprim alone. (nih.gov)
  • Short- and long-term cure rates of short-duration trimethoprim-sulfamethoxazole treatment in female dogs with uncomplicated bacterial cystitis. (druglib.com)
  • Trimethoprim-sulfamethoxazole versus norfloxacin in the prophylaxis of spontaneous bacterial peritonitis in cirrhosis. (druglib.com)
  • Efficacy of trimethoprim-sulfamethoxazole for the prevention of bacterial infections in a randomized prophylaxis trial of patients with advanced HIV infection. (druglib.com)
  • An overview of Genetic Toxicology Bacterial Mutagenicity study conclusions related to Sulfamethoxazole (723-46-6). (nih.gov)
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  • Sulfamethoxazole, an ingredient in Bactrim, is one of a group of drugs called sulfonamides, which prevent the growth of bacteria in the body. (1meds.com)
  • If you are sensitive to or have ever had an allergic reaction to trimethoprim, sulfamethoxazole, or other sulfa drugs, you should not take this medication. (1meds.com)
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  • Cenizal MJ, Skiest D, Luber S, Bedimo R, Davis P, Fox P, Delaney K, Hardy RD. Prospective randomized trial of empiric therapy with trimethoprim-sulfamethoxazole or doxycycline for outpatient skin and soft tissue infections in an area of high prevalence of methicillin-resistant Staphylococcus aureus. (umassmed.edu)
  • The current recommendation is a four-drug regimen (trimethoprim [TMP], sulfamethoxazole [SMX], doxycycline, and chloramphenicol) and a total treatment time of 12 to 20 weeks. (tropmedres.ac)
  • The average percentage of the dose recovered in urine from 0 to 72 hours after a single oral dose of sulfamethoxazole and trimethoprim is 84.5% for total sulfonamide and 66.8% for free trimethoprim. (nih.gov)
  • A Four-Center Retrospective Study of the Efficacy and Toxicity of Low-Dose Trimethoprim-Sulfamethoxazole for the Treatment of Pneumocystis Pneumonia in Patients without HIV Infection. (nih.gov)
  • Trimethoprim-sulfamethoxazole (TMP-SMZ) dose escalation versus direct rechallenge for Pneumocystis Carinii pneumonia prophylaxis in human immunodeficiency virus-infected patients with previous adverse reaction to TMP-SMZ. (druglib.com)
  • The amount of a single dose of sulfamethoxazole and trimethoprim that is either associated with symptoms of overdosage or is likely to be life-threatening has not been reported. (medlibrary.org)
  • Thirty percent of the total sulfonamide is excreted as free sulfamethoxazole, with the remaining as N 4 -acetylated metabolite.2 When administered together, neither sulfamethoxazole nor trimethoprim affects the urinary excretion pattern of the other. (nih.gov)
  • Comparison of trimethoprim-sulfamethoxazole, cephadroxil and cefprozil as prophylaxis for recurrent urinary tract infections in children. (druglib.com)
  • Gastrointestinal bleeding secondary to trimethoprim-sulfamethoxazole-induced vitamin K deficiency. (bvsalud.org)
  • In vitro studies suggest that trimethoprim is a substrate of P-glycoprotein, OCT1 and OCT2, and that sulfamethoxazole is not a substrate of P-glycoprotein. (nih.gov)
  • The antimicrobial combination of trimethoprim and sulfamethoxazole is active in vitro against a variety of gram-positive and gram-negative bacteria. (nih.gov)
  • Standard versus newer antibacterial agents in the treatment of severe acute exacerbation of chronic obstructive pulmonary disease: a randomized trial of trimethoprim-sulfamethoxazole versus ciprofloxacin. (druglib.com)
  • Two randomized controlled trials of ceftazidime alone versus ceftazidime in combination with trimethoprim-sulfamethoxazole for the treatment of severe melioidosis. (druglib.com)
  • Efficacy of trimethoprim-sulfamethoxazole compared with sulfadoxine-pyrimethamine plus erythromycin for the treatment of uncomplicated malaria in children with integrated management of childhood illness dual classifications of malaria and pneumonia. (druglib.com)
  • Effectiveness of trimethoprim/sulfamethoxazole for children with chronic active otitis media: a randomized, placebo-controlled trial. (druglib.com)
  • Trimethoprim-sulfamethoxazole in children with chronic otitis media: a randomized comparison of costs and effects. (druglib.com)
  • Trimethoprim-sulfamethoxazole by itself or in combination with other antimicrobial agents is effective for most Nocardia asteroides infections. (nih.gov)
  • Oral rifampin and trimethoprim/sulfamethoxazole therapy in asymptomatic carriers of methicillin-resistant Staphylococcus aureus infections. (umassmed.edu)
  • Clindamycin versus trimethoprim-sulfamethoxazole for uncomplicated skin infections. (druglib.com)
  • Trimethoprim-sulfamethoxazole as a viable treatment option for infections caused by methicillin-resistant Staphylococcus aureus. (druglib.com)
  • Bactrim (Sulfamethoxazole and Trimethoprim) is used for treating infections caused by certain bacteria. (rxsat.com)
  • trimethoprim does not influence the protein binding of sulfamethoxazole. (nih.gov)
  • Sulfonamide-induced reactions in desensitized patients with AIDS--the role of covalent protein haptenation by sulfamethoxazole. (umassmed.edu)
  • The metabolism of sulfamethoxazole occurs predominantly by N4-acetylation, although the glucuronide conjugate has been identified. (nih.gov)
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  • Genetic Toxicity Evaluation of Sulfamethoxazole in Salmonella/E.coli Mutagenicity Test or Ames Test. (nih.gov)
  • Urine concentrations of both sulfamethoxazole and trimethoprim are considerably higher than are the concentrations in the blood. (nih.gov)
  • With healthy, fullterm infants it appears acceptable to use sulfamethoxazole during breastfeeding after the newborn period. (nih.gov)
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  • Effect of long-term trimethoprim/sulfamethoxazole treatment on resistance and integron prevalence in the intestinal flora: a randomized, double-blind, placebo-controlled trial in children. (druglib.com)
  • Randomized controlled trial of pyrimethamine plus sulfadiazine versus trimethoprim plus sulfamethoxazole for treatment of toxoplasmic encephalitis in AIDS patients. (druglib.com)
  • Prospective randomized trial of trimethoprim/sulfamethoxazole versus pyrimethamine and sulfadiazine in the treatment of ocular toxoplasmosis. (druglib.com)
  • The effect of long-term intermittent trimethoprim/sulfamethoxazole treatment on recurrences of toxoplasmic retinochoroiditis. (druglib.com)
  • The following adverse reactions associated with the use of sulfamethoxazole and trimethoprim were identified in clinical trials, postmarketing or published reports. (medlibrary.org)
  • Approximately 70% of sulfamethoxazole and 44% of trimethoprim are bound to plasma proteins. (nih.gov)
  • Cefpodoxime-proxetil versus trimethoprim-sulfamethoxazole for short-term therapy of uncomplicated acute cystitis in women. (druglib.com)
  • Trimethoprim-sulfamethoxazole (TMP-SMX) is in pregnancy category C. TMP-SMX should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. (cdc.gov)
  • After tick removal, the area became inflamed, and the patient received trimethoprim/sulfamethoxazole (TMP/SMX) from a local urgent care center. (cdc.gov)
  • Herein, we report a case of vanishing bile duct syndrome following dapsone use in a patient with HIV infection and a recent history of trimethoprim/sulfamethoxazole-induced cholestasis. (nih.gov)
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  • Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection. (druglib.com)
  • Impact of trimethoprim-sulfamethoxazole prophylaxis on falciparum malaria infection and disease. (druglib.com)
  • Simultaneous determination of sulfamethoxazole and trimethoprim in biological fluids for high-throughput analysis: comparison of HPLC with ultraviolet and tandem mass spectrometric detection. (druglib.com)
  • Rapid and simultaneous determination of sulfamethoxazole and trimethoprim in human plasma by high-performance liquid chromatography. (druglib.com)
  • Use of sulfamethoxazole and trimethoprim at high doses and/or for extended periods of time may cause bone marrow depression manifested as thrombocytopenia, leukopenia and/or megaloblastic anemia. (medlibrary.org)
  • Detectable amounts of sulfamethoxazole and trimethoprim are present in the blood 24 hours after drug administration. (nih.gov)
  • During administration of 800 mg sulfamethoxazole and 160 mg trimethoprim b.i.d., the mean steady-state plasma concentration of trimethoprim was 1.72 μg/mL. (nih.gov)
  • During administration of 160 mg trimethoprim and 800 mg sulfamethoxazole b.i.d., the mean steady-state plasma concentration of trimethoprim was 1.72 mcg/mL. (nih.gov)
  • This graph shows the total number of publications written about "Sulfamethoxazole" by people in this website by year, and whether "Sulfamethoxazole" was a major or minor topic of these publications. (umassmed.edu)
  • The free forms of sulfamethoxazole and trimethoprim are considered to be the therapeutically active forms. (nih.gov)
  • The steady-state mean plasma levels of free and total sulfamethoxazole were 57.4 μg/mL and 68.0 μg/mL, respectively. (nih.gov)
  • Thirty percent of the total sulfonamide is excreted as free sulfamethoxazole, with the remaining as N 4 -acetylated metabolite. (nih.gov)
  • The steady-state minimal plasma levels of free and total sulfamethoxazole were 57.4 mcg/mL and 68.0 mcg/mL, respectively. (nih.gov)
  • It is followed by another antibiotic (such as trimethoprim - sulfamethoxazole ) taken by mouth for up to 1 year. (nih.gov)

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