Coxiella
Coxiella burnetii
Q Fever
Goats
Complement Fixation Tests
Endocarditis, Bacterial
Rickettsia
Zoonoses
Rickettsia rickettsii
Blotting, Southwestern
Seroepidemiologic Studies
Vacuoles
Transfer Agreement
National Institute of Allergy and Infectious Diseases (U.S.)
Waste Management
Databases, Protein
National Institute of General Medical Sciences (U.S.)
Survival of Mycobacterium avium and Mycobacterium tuberculosis in acidified vacuoles of murine macrophages. (1/167)
Despite the antimicrobial mechanisms of vertebrate phagocytes, mycobacteria can survive within the phagosomes of these cells. These organisms use various strategies to evade destruction, including inhibition of acidification of the phagosome and inhibition of phagosome-lysosome fusion. In contrast to mycobacteria, Coxiella burnetii, the etiologic agent of Q fever, inhabits a spacious acidified intracellular vacuole which is prone to fusion with other vacuoles of the host cell, including phagosomes containing mycobacteria. The Coxiella-infected cell thus provides a unique model for investigating the survival of mycobacteria in an acidified phagosome-like compartment. In the present study, murine bone marrow-derived macrophages were infected with either Mycobacterium avium or Mycobacterium tuberculosis and then coinfected with C. burnetii. We observed that the majority of phagocytosed mycobacteria colocalized to the C. burnetii-containing vacuole, which maintained its acidic properties. In coinfected macrophages, the growth of M. avium was not impaired following fusion with the acidified vacuole. In contrast, the growth rate of M. tuberculosis was reduced in acidified vacuoles. These results suggest that although both species of mycobacteria inhibit phagosome-lysosome fusion, they may be differentially susceptible to the toxic effects of the acidic environment in the mature phagolysosome. (+info)Infectivity, transmission and 16S rRNA sequencing of a rickettsia, Coxiella cheraxi sp. nov., from the freshwater crayfish Cherax quadricarinatus. (2/167)
A rickettsia-like organism isolated from infected, farm-reared Cherax quadricarinatus was cultured in the yolk sac of developing chicken eggs, but could not be cultured in 3 continuous cell lines, bluegill fry (BF-2), fathead minnow (FHM), and Spodoptera frugiperda (Sf-9). The organism was confirmed by fulfilling Koch's postulates as the aetiological agent of mortalities amongst C. quadricarinatus. When C. quadricarinatus was inoculated with the organism, mortality was 100% at 28 degrees C and 80% at an ambient temperature of 24 degrees C. Horizontal transmission with food and via the waterborne route was demonstrated, but mortalities were lower at 30 and 10% respectively over a 4 wk period. The 16S rRNA sequence of 1325 base pairs of the Gram-negative, obligate intracellular organism was 95.6% homologous to Coxiella burnetii. Of 18 species compared to this rickettsia, the next most closely related bacterium was Legionella pneumophila at 86.7%. The suggested classification of this organism is Order Rickettsiales, family Rickettsiaceae, tribe Rickettsieae, within the genus Coxiella. We suggest it should be named Coxiella cheraxi sp. nov. (+info)Detection of long-term cellular immunity to Coxiella burneti as assayed by lymphocyte transformation. (3/167)
Delayed hypersensitivity to the antigens of Coxiella burneti, Nine Mile strain, was demonstrated in human subjects with various past histories of exposure to the organism by using lymphocyte transformation assays. Individuals with histories indicating exposure to C. burneti up to 8 years before the study demonstrated marked lymphocyte transformation in vitro to whole-cell antigens consisting of formalin-killed C. burneti phase I and phase II. These individuals also demonstrated a marked lymphocyte response to the trichloracetic acid-soluable phase I antigen. One individual who acquired Q fever during the study and one individual who received an experimental Q fever vaccine 4 years earlier were also evaluated by the lymphocyte transformation assay. It was also found that phase I trichloroacetic acid-soluble material was capable of acting as an antigen in the assay, whereas the phase II trichloroacetic acid-soluble material did not contain any antigenic material capable of causing lymphocyte transformation. The complete phase I trichloroacetic acid-soluble antigen, which was found to consist of protein and carbohydrate, was chemically fractionated into monospecific fractions. The fraction treated to eliminate carbohydrate was the only fraction found to elicit an in vitro response. (+info)Changes in buoyant density relationships of two cell types of Coxiella burneti phase I. (4/167)
Coxiella burneti phase I, purified from a formalin-inactivated yolk-sac vaccine, was separated into two bands of morphologically distinct cell types when subjected to sucrose gradient centrifugation. Recycling of the less dense, rod-shaped cells in unbuffered sucrose gradients (pH 5.5 to 6.0) resulted in the formation of bands having the location and appearance of the original two bands. Recycling of the denser band of larger ovoid-shaped cells yielded a single band, suggesting that the larger cell type arose from the smaller cell. In contrast to vaccine-derived rickettsiae, live, cell culture-propagated phase I organisms formed a single band in unbuffered sucrose gradients, at the same density as the upper band of the vaccine preparation. Centrifugation of cell culture-derived rickettsiae for 26 to 48 h in sucrose gradients of pH 5.5 resulted in the formation of a second band, at the same density as the lower band of the vaccine preparation. This did not occur in gradients of pH 7.0. Treatment of cell culture-propagated rickettsiae with formalin or germicidal ultraviolet radiation induced a total shift of the less dense cell population to a zone of higher density when centrifuged isopycnically in CsC1 gradients. This density change did not occur in sucrose gradients, suggesting a difference in the effect of these treatments on the permeability of the cell membrane to sucrose and CsC1. (+info)Glomerulonephritis associated with Coxiella burnetii endocarditis. (5/167)
A patient with endocarditis associated with chronic Coxiella burnetii infection is described in whom glomerulonephritis developed with granular deposits containing immunoglobulins and complement in the glomeruli. The serum was notable for the variety of circulating antibodies detected, which included antibodies directed against native DNA. (+info)Studies on the physiology of Rickettsiae. IV. Folic acids of Coxiella burnetii. (6/167)
Mattheis, Martha S. (University of Kansas, Lawrence), M. Silverman, and D. Paretsky. Studies on the physiology of rickettsiae. IV. Folic acids of Coxiella burnetii. J. Bacteriol. 85:37-41. 1963.-Yolk, yolk sac, and embryo tissues of uninfected eggs, and those infected with Coxiella burnetii, were analyzed for folic acid derivatives by employing diethylaminoethyl (DEAE)-cellulose column chromatography. Infected tissues contained quantitatively less folate, but the elution profiles of both infected and uninfected tissues were identical. Purified C. burnetii contained some types of folate apparently unique to these rickettsiae, and not found in infected tissue. The major folate fraction of C. burnetii was partially characterized by (i) elution position from DEAE columns; (ii) treatment with conjugase; (iii) growth response by Lactobacillus casei, Streptococcus faecalis R, and Pediococcus cerevisiae; and (iv) response to oxidation, reduction, and formylation. (+info)CONVERSION OF THE PHASE I ANTIGEN OF COXIELLA BURNETII TO HAPTEN BY PHENOL TREATMENT. (7/167)
Anacker, R. L. (Rocky Mountain Laboratory, Hamilton, Mont.), W. T. Haskins, D. B. Lackman, E. Ribi, and E. G. Pickens. Conversion of the phase I antigen of Coxiella burnetii to hapten by phenol treatment. J. Bacteriol. 85:1165-1170. 1963.-Trichloroacetic acid extracts of Coxiella burnetii are converted to hapten by treatment with phenol. Such extracts react, like the original trichloroacetic acid extract, at high dilution in the complement-fixation test and produce zones of precipitate with specific antibody in gel diffusion tests; but, unlike the parent extract, injection of the phenol-treated extract neither induces resistance to challenge in guinea pigs nor antibody formation in guinea pigs, rabbits, or mice. This loss of antigenicity is correlated with removal of protein from the original product. (+info)STUDIES ON THE PHYSIOLOGY OF RICKETTSIAE. V. METABOLISM OF CARBAMYL PHOSPHATE BY COXIELLA BURNETII. (8/167)
Mallavia, L. (University of Kansas, Lawrence) and D. Paretsky. Studies on the physiology of rickettsiae. V. Metabolism of carbamyl phosphate by Coxiella burnetii. J. Bacteriol. 86:232-238. 1963.-Preparations of disrupted Coxiella burnetii catalyze synthesis of citrulline from ornithine and carbamyl phosphate at an optimal pH of 7.0 to 7.5. Rickettsial synthesis of the pyrimidine precursor, ureidosuccinate, is demonstrated and confirmed by isolating C(14)-labeled ureidosuccinate from reaction mixtures of carbamyl phosphate and labeled aspartate. The data suggest a further rickettsial synthesis of orotate and imply rickettsial competence for host-independent pyrimidine synthesis. (+info)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.
1. Caprine arthritis-encephalitis (CAE): A viral disease that affects the joints and central nervous system of goats.
2. Caseous lymphadenitis (CLA): A bacterial infection that causes abscesses in the lymph nodes and other organs.
3. Contagious ecthyma (Orf): A viral disease that causes skin lesions and scarring.
4. Goat pox: A viral disease that causes fever, weakness, and skin lesions.
5. Pneumonia: A bacterial or viral infection of the lungs that can be caused by a variety of pathogens.
6. Scabies: A parasitic infestation that causes skin irritation and hair loss.
7. Tetanus: A neurological disorder caused by a bacterial toxin that affects muscle contractions.
8. Toxoplasmosis: A parasitic infection that can cause fever, anemia, and other symptoms in goats.
9. Urinary tract infections (UTIs): Bacterial infections of the urinary system that can affect both male and female goats.
10. Vitamin deficiencies: Deficiencies in vitamins such as vitamin A, D, or E can cause a range of health problems in goats, including skin conditions, poor appetite, and weakness.
Goat diseases can be diagnosed through physical examination, laboratory tests, and imaging studies. Treatment depends on the specific disease and may involve antibiotics, antiviral medications, or supportive care such as fluid therapy and nutritional supplements. Prevention is key in managing goat diseases, and this includes maintaining good hygiene, providing clean water and a balanced diet, and vaccinating goats against common diseases.
Sheep diseases can be caused by a variety of factors, including bacteria, viruses, parasites, and environmental factors. Here are some common sheep diseases and their meanings:
1. Scrapie: A fatal neurological disorder that affects sheep and goats, caused by a prion.
2. Ovine Progressive Pneumonia (OPP): A contagious respiratory disease caused by Mycobacterium ovipneumoniae.
3. Maedi-Visna: A slow-progressing pneumonia caused by a retrovirus, which can lead to OPP.
4. Foot-and-Mouth Disease (FMD): A highly contagious viral disease that affects cloven-hoofed animals, including sheep and goats.
5. Bloat: A condition caused by gas accumulation in the rumen, which can lead to abdominal pain and death if not treated promptly.
6. Pneumonia: An inflammation of the lungs, often caused by bacteria or viruses.
7. Cryptosporidiosis: A diarrheal disease caused by Cryptosporidium parvum, which can be fatal in young lambs.
8. Babesiosis: A blood parasitic disease caused by Babesia oviparasites, which can lead to anemia and death if left untreated.
9. Fascioliasis: A liver fluke infection that can cause anemia, jaundice, and liver damage.
10. Anthrax: A serious bacterial disease caused by Bacillus anthracis, which can be fatal if left untreated.
Sheep diseases can have a significant impact on the health and productivity of flocks, as well as the economy of sheep farming. It is important for sheep farmers to be aware of these diseases and take appropriate measures to prevent and control them.
Causes and risk factors:
The most common cause of bacterial endocarditis is a bacterial infection that enters the bloodstream and travels to the heart. This can occur through various means, such as:
* Injecting drugs or engaging in other risky behaviors that allow bacteria to enter the body
* Having a weakened immune system due to illness or medication
* Having a previous history of endocarditis or other heart conditions
* Being over the age of 60, as older adults are at higher risk for developing endocarditis
Symptoms:
The symptoms of bacterial endocarditis can vary depending on the severity of the infection and the location of the infected area. Some common symptoms include:
* Fever
* Chills
* Joint pain or swelling
* Fatigue
* Shortness of breath
* Heart murmurs or abnormal heart sounds
Diagnosis:
Bacterial endocarditis is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
* Blood cultures to identify the presence of bacteria in the bloodstream
* Echocardiogram to visualize the heart and detect any abnormalities
* Chest X-ray to look for signs of infection or inflammation in the lungs or heart
* Electrocardiogram (ECG) to measure the electrical activity of the heart
Treatment:
The treatment of bacterial endocarditis typically involves a combination of antibiotics and surgery. Antibiotics are used to kill the bacteria and reduce inflammation, while surgery may be necessary to repair or replace damaged heart tissue. In some cases, the infected heart tissue may need to be removed.
Prevention:
Preventing bacterial endocarditis involves good oral hygiene, regular dental check-ups, and avoiding certain high-risk activities such as unprotected sex or sharing of needles. People with existing heart conditions should also take antibiotics before dental or medical procedures to reduce the risk of infection.
Prognosis:
The prognosis for bacterial endocarditis is generally good if treatment is prompt and effective. However, delays in diagnosis and treatment can lead to serious complications such as heart failure, stroke, or death. Patients with pre-existing heart conditions are at higher risk for complications.
Incidence:
Bacterial endocarditis is a relatively rare condition, affecting approximately 2-5 cases per million people per year in the United States. However, people with certain risk factors such as heart conditions or prosthetic heart valves are at higher risk for developing the infection.
Complications:
Bacterial endocarditis can lead to a number of complications, including:
* Heart failure
* Stroke or brain abscess
* Kidney damage or failure
* Pregnancy complications
* Nerve damage or peripheral neuropathy
* Skin or soft tissue infections
* Bone or joint infections
* Septicemia (blood poisoning)
Prevention:
Preventive measures for bacterial endocarditis include:
* Good oral hygiene and regular dental check-ups to reduce the risk of dental infections
* Avoiding high-risk activities such as unprotected sex or sharing of needles
* Antibiotics before dental or medical procedures for patients with existing heart conditions
* Proper sterilization and disinfection of medical equipment
* Use of antimicrobial prophylaxis (prevention) in high-risk patients.
Emerging Trends:
Newly emerging trends in the management of bacterial endocarditis include:
* The use of novel antibiotics and combination therapy to improve treatment outcomes
* The development of new diagnostic tests to help identify the cause of infection more quickly and accurately
* The increased use of preventive measures such as antibiotic prophylaxis in high-risk patients.
Future Directions:
Future directions for research on bacterial endocarditis may include:
* Investigating the use of novel diagnostic techniques, such as genomics and proteomics, to improve the accuracy of diagnosis
* Developing new antibiotics and combination therapies to improve treatment outcomes
* Exploring alternative preventive measures such as probiotics and immunotherapy.
In conclusion, bacterial endocarditis is a serious infection that can have severe consequences if left untreated. Early diagnosis and appropriate treatment are crucial to improving patient outcomes. Preventive measures such as good oral hygiene and antibiotic prophylaxis can help reduce the risk of developing this condition. Ongoing research is focused on improving diagnostic techniques, developing new treatments, and exploring alternative preventive measures.
Definition:
Veterinary abortion refers to the intentional termination of a pregnancy in an animal, typically a farm or domesticated animal such as a dog, cat, horse, cow, or pig. The procedure is performed by a veterinarian and is usually done for reasons such as unwanted breeding, disease or genetic disorders in the fetus, or to prevent overpopulation of certain species.
Types of Veterinary Abortion:
1. Spontaneous Abortion (Miscarriage): This occurs naturally when the pregnancy is terminated by natural causes such as infection or trauma.
2. Induced Abortion: This is performed by a veterinarian using various methods such as injection of drugs or surgical procedures to terminate the pregnancy.
Methods of Veterinary Abortion:
1. Drug-induced abortion: This method involves administering medication to the animal to cause uterine contractions and expulsion of the fetus.
2. Surgical abortion: This method involves surgical intervention to remove the fetus from the uterus, usually through a small incision in the abdomen.
3. Non-surgical abortion: This method uses a device to remove the fetus from the uterus without making an incision.
Complications and Risks of Veterinary Abortion:
1. Infection: As with any surgical procedure, there is a risk of infection.
2. Hemorrhage: Excessive bleeding can occur during or after the procedure.
3. Uterine rupture: In rare cases, the uterus may rupture during the procedure.
4. Incomplete abortion: In some cases, not all of the fetus may be removed, leading to complications later on.
5. Scarring: Scars may form in the uterus or abdomen after the procedure, which can lead to reproductive problems in the future.
Prevention of Unwanted Pregnancies in Animals:
1. Spaying/neutering: This is the most effective way to prevent unwanted pregnancies in animals.
2. Breeding management: Proper breeding management, including selecting healthy and fertile breeding animals, can help reduce the risk of unwanted pregnancies.
3. Use of contraceptives: Hormonal contraceptives, such as injection or implants, can be used in some species to prevent pregnancy.
4. Behavioral management: In some cases, behavioral management techniques, such as separation or rehoming of animals, may be necessary to prevent unwanted breeding.
Ethical Considerations of Veterinary Abortion:
1. Animal welfare: The procedure should only be performed when necessary and with the intention of improving the animal's welfare.
2. Owner consent: Owners must provide informed consent before the procedure can be performed.
3. Veterinarian expertise: The procedure should only be performed by a licensed veterinarian with experience in the procedure.
4. Alternative options: All alternative options, such as spaying/neutering or rehoming, should be considered before performing an abortion.
Conclusion:
Veterinary abortion is a complex issue that requires careful consideration of ethical and practical factors. While it may be necessary in some cases to prevent the suffering of unwanted litters, it is important to approach the procedure with caution and respect for animal welfare. Owners must provide informed consent, and the procedure should only be performed by a licensed veterinarian with experience in the procedure. Alternative options, such as spaying/neutering or rehoming, should also be considered before performing an abortion. Ultimately, the decision to perform a veterinary abortion should be made with the intention of improving the animal's welfare and quality of life.
Zoonoses (zoonosis) refers to infectious diseases that can be transmitted between animals and humans. These diseases are caused by a variety of pathogens, including bacteria, viruses, parasites, and fungi, and can be spread through contact with infected animals or contaminated animal products.
Examples of Zoonoses
Some common examples of zoonoses include:
1. Rabies: a viral infection that can be transmitted to humans through the bite of an infected animal, typically dogs, bats, or raccoons.
2. Lyme disease: a bacterial infection caused by Borrelia burgdorferi, which is spread to humans through the bite of an infected blacklegged tick (Ixodes scapularis).
3. Toxoplasmosis: a parasitic infection caused by Toxoplasma gondii, which can be transmitted to humans through contact with contaminated cat feces or undercooked meat.
4. Leptospirosis: a bacterial infection caused by Leptospira interrogans, which is spread to humans through contact with contaminated water or soil.
5. Avian influenza (bird flu): a viral infection that can be transmitted to humans through contact with infected birds or contaminated surfaces.
Transmission of Zoonoses
Zoonoses can be transmitted to humans in a variety of ways, including:
1. Direct contact with infected animals or contaminated animal products.
2. Contact with contaminated soil, water, or other environmental sources.
3. Through vectors such as ticks, mosquitoes, and fleas.
4. By consuming contaminated food or water.
5. Through close contact with an infected person or animal.
Prevention of Zoonoses
Preventing the transmission of zoonoses requires a combination of personal protective measures, good hygiene practices, and careful handling of animals and animal products. Some strategies for preventing zoonoses include:
1. Washing hands frequently, especially after contact with animals or their waste.
2. Avoiding direct contact with wild animals and avoiding touching or feeding stray animals.
3. Cooking meat and eggs thoroughly to kill harmful bacteria.
4. Keeping pets up to date on vaccinations and preventative care.
5. Avoiding consumption of raw or undercooked meat, particularly poultry and pork.
6. Using insect repellents and wearing protective clothing when outdoors in areas where vectors are prevalent.
7. Implementing proper sanitation and hygiene practices in animal housing and husbandry.
8. Implementing strict biosecurity measures on farms and in animal facilities to prevent the spread of disease.
9. Providing education and training to individuals working with animals or in areas where zoonoses are prevalent.
10. Monitoring for and reporting cases of zoonotic disease to help track and control outbreaks.
Conclusion
Zoonoses are diseases that can be transmitted between animals and humans, posing a significant risk to human health and animal welfare. Understanding the causes, transmission, and prevention of zoonoses is essential for protecting both humans and animals from these diseases. By implementing appropriate measures such as avoiding contact with wild animals, cooking meat thoroughly, keeping pets up to date on vaccinations, and implementing proper sanitation and biosecurity practices, we can reduce the risk of zoonotic disease transmission and protect public health and animal welfare.
Coxiella
Coxiella burnetii
Coxiella (bacterium)
Coxiella (gastropod)
Phagosome
Gamasoidosis
Atypical pneumonia
Inflammatory myofibroblastic tumour
Pneumonia
Coccobacillus
Bacterial cellular morphologies
Lake Galilee (Queensland)
Intracellular bacteria
Amblyomma gervaisi
Coxiellaceae
Johnston Atoll
Legionella clemsonensis
Paul Fiset
Haemaphysalis leporispalustris
Rickettsia akari
Q fever
Intracellular parasite
Valérie Belin
Pomatiopsidae
Bremetennacum
List of sequenced bacterial genomes
Edwin Herman Lennette
Tick
Axenic
Pasteurization
Coxiella - Wikispecies
Coxiella burnetii genotyping - PubMed
Taxonomy browser (Coxiella-like endosymbiont of Argas persicus)
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Adverse Pregnancy Outcomes and Coxiella burnetii Antibodies in Pregnant Women, Denmark
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Q Fever (Coxiella burnetii)| CDC
Robert Heinzen, Ph.D. | NIH: National Institute of Allergy and Infectious Diseases
Coxiella-Burnetii Rickettsia - The Epinhood (TEH)
A simple method for enrichment of phase I Coxiella burnetii. | J Microbiol Methods;211: 106787, 2023 08. | MEDLINE
SSQFEV C
Coxiella burnetii - how deadly could be the Q fever? - McKesson BioServices
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Bacterial Pneumonia: Practice Essentials, Background, Pathophysiology
Complement fixation test to C. burnetii: MedlinePlus Medical Encyclopedia
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Zoonoses
Q Fever, Scrub Typhus, and Rickettsial Diseases in Children, Kenya, 2011-2012 - Volume 22, Number 5-May 2016 - Emerging...
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Q Fever: Practice Essentials, Background, Pathophysiology
Burnetii23
- Coxiella burnetii and Rickettsia are two types of bacteria that can cause severe illness in humans. (epibiodev.blog)
- Coxiella burnetii can cause a disease known as Q fever, which can cause flu-like symptoms and in severe cases can be fatal. (epibiodev.blog)
- Q fever is a zoonotic disease with acute and chronic stages caused by the rickettsia-like organism Coxiella burnetii. (cdc.gov)
- Subsequent blood tests indicated that the hepatitis was caused by Coxiella burnetii , the organism which causes Q fever. (cdc.gov)
- To date, a total of 191 clinical cases of acute Q fever (Figure 1) have been serologically confirmed at the VCL by a fourfold or greater rise in Q fever complement fixation phase II antibody titer or by a 1:20 or greater Coxiella burnetii-specific immunoglobulin M (IgM) titer using an indirect immunofluorescence test on a single serum specimen. (cdc.gov)
- Q-fever is an underreported disease caused by the bacterium Coxiella burnetii, which is highly infectious and has the ability to disperse great distances. (nau.edu)
- Coxiella burnetii is a Gram-negative obligate intracellular bacterium. (bvsalud.org)
- To screen convalescent-phase serum samples, we used a Coxiella burnetii ImmunoDot assay (GenBio, San Diego, CA, USA) according to the manufacturer's instructions. (cdc.gov)
- So tell me David, what is Coxiella burnetii ? (cdc.gov)
- Dr. David Swerdlow] Coxiella burnetii is an intracellular bacterium that causes Q fever. (cdc.gov)
- Infection with Coxiella burnetii can be asymptomatic, acute, or chronic. (cdc.gov)
- Coxiella burnetii is a category B bioterrorism agent because it is highly infectious, rather resistant to heat and drying, and can become airborne and inhaled by humans. (cdc.gov)
- Dr. David Swerdlow] If there were an intentional spread of Coxiella burnetii , we didn't know who should be given preventative treatment, called post-exposure prophylaxis or PEP, to prevent illness. (cdc.gov)
- Pregnant women are also at high risk following exposure to Coxiella burnetii . (cdc.gov)
- It is crucial to know who should be treated and how, following an intentional release with possible BT agents, including Coxiella burnetii . (cdc.gov)
- The complement fixation test to Coxiella burnetii ( C burnetii ) is a blood test that checks for infection due to bacteria called C burnetii , which causes Q fever . (medlineplus.gov)
- Hartzell JD, Marrie TJ, Raoult D. Coxiella burnetii (Q fever). (medlineplus.gov)
- Q fever is caused by the bacteria Coxiella burnetii . (healthlinkbc.ca)
- Sheep are a major reservoir for Coxiella burnetii. (cdc.gov)
- Q fever is a disease caused by the bacterium Coxiella burnetii, which can be transmitted to humans from animals such as sheep, goats, and cattle. (cdc.gov)
- Coxiella burnetii study was to describe the clinical, microt and Brucella spp. (who.int)
- Detection of antibodies to Coxiella burnetii, the causative agent of Q fever, by complement fixation. (tamu.edu)
- Phylogenetic inference of Coxiella burnetii by 16S rRNA gene sequencing. (cdc.gov)
Bacteria1
- Coxiella bacteria may also be present in raw milk from infected animals. (healthlinkbc.ca)
Legionellales1
- Three other CSIs suggest that members of the genera Coxiella and Rickettsiella shared a common ancestor exclusive of other Legionellales. (mcmaster.ca)
Molecular1
- Twenty four, 7 and 6 CSIs are uniquely shared by members of the genera Legionella, Coxiella and Aquicella, respectively, identifying these groups in molecular terms. (mcmaster.ca)
Bacterial1
- In addition, overexpression of the active GTPase -defective mutant (GFP-Rab1b Q67L) affected the development of the Coxiella -replicative compartment inhibiting bacterial growth . (bvsalud.org)
Details1
- Coxiella - Taxon details on National Center for Biotechnology Information (NCBI). (wikimedia.org)
Present2
- In this report , we present evidence that the Coxiella -replicative vacuoles (CRVs) also interact with the secretory pathway . (bvsalud.org)
- Le present travail a consiste en l'etude sur systeme HLA de classe II dans la population congolaise. (bvsalud.org)
Intracellular2
- Because PV biogenesis, host cell maintenance, and generation of developmental forms adapted to intracellular replication and extracellular resistance are central to Coxiella pathogenesis, we are conducting studies to better understand the molecular and cellular biology of these processes. (nih.gov)
- Rescue of Coxiella from an obligate intracellular lifestyle has enabled our development of complete set of genetic tools are now allowing fulfillment of molecular Koch's postulates for suspected Coxiella virulence genes. (nih.gov)
Fever1
- Coxiella -like bacteria have been associated with infection cal signs (fever, skin eschar, local lymph node enlargement) in birds ( 4 , 5 ). (cdc.gov)
Ticks4
- To explore pathogenicity to humans, we used and if a removed tick was positive for Coxiella -like bacte- molecular techniques targeting Coxiella- like bacteria to ria according to qPCR but no skin biopsy was sampled or retrospectively analyze skin biopsy samples and ticks col- when serologic results were positive. (cdc.gov)
- Ticks were identified by matrix-assisted la- for the Coxiella -like bacteria associated with R. sanguin- ser desorption/ionization time-of-flight mass spectrom- eus , R. turanicus , and H. pusillus ticks to be Candidatus C. etry (Bruker Daltonics, Billerica, USA) ( 6 ). (cdc.gov)
- On the basis of the aligned rrs (55%) Dermacentor marginatus , 7 (35%) R. sanguineus , gene sequences of Coxiella -like bacteria, we developed 1 (5%) R. bursa , and 1 (5%) Ixodes ricinus ticks. (cdc.gov)
- Coxiella- a specific qPCR to detect the DNA of all Coxiella spe- like bacteria were found significantly less commonly in I. cies and degenerated primers aimed to amplify a 659-bps ricinus ticks (p = 0.002, relative risk = 0.5). (cdc.gov)
Virulence3
- Moreover, we are investigating the extent and relevance of Coxiella strain diversity and developing genetic methods to dissect the virulence of this refractory pathogen. (nih.gov)
- Our comparative genomics studies revealed genetic heterogeneity among Coxiella strains and predicted strain-specific virulence factors. (nih.gov)
- Functional characterization of these effector proteins and their cellular targets will provide important insight into Coxiella virulence mechanisms. (nih.gov)
Infection1
- 11. Unrecognized pre-transplant disseminated Coxiella burnetti infection diagnosed in a post-transplant heart-kidney recipient. (nih.gov)
Genetically1
- Vero cells infected with genetically transformed Coxiella expressing mCherry red fluorescent protein. (nih.gov)
Molecular1
- In addition to providing needed information on pathogen biology, our research goals are aimed at development of new Coxiella countermeasures, such as rationally designed subunit vaccines and tools for molecular epidemiology. (nih.gov)
Category1
- Coxiella is also a recognized category B biothreat with potential for illegitimate use. (nih.gov)
Techniques1
- Using contemporary cell biology techniques, we are characterizing the Coxiella PV to define both bacterial and host factors that mediate its formation. (nih.gov)
Host2
- Moreover, metabolic pathway reconstructions based on genome data helped us develop a medium that supports robust host cell-free (axenic) growth of Coxiella . (nih.gov)
- Our results indicate that modulation of host cell functions by Coxiella proteins is required for PV formation and pathogen growth. (nih.gov)
