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What is Q fever?


What is Q fever?

EPIDEMIOLOGY

'Query' or Q fever was first recognized as a disease of humans in abattoir workers in Queensland, Australia in the 1930s. With the notable exception of New Zealand, C. burnetii infections occur worldwide. The ability of C. burnetii to survive extreme environmental conditions for many years, and the low infective dose, results in ready transmission of infection, probably in most cases by inhalation of infectious aerosol particles. While cattle, sheep and goats are the most important animal reservoirs, C. burnetii has also been detected in fish, birds, rodents, marsupials, snakes, tortoises and many domestic animals, and has been recovered from ticks and other arthropods. Naturally infected cattle, sheep or goats carry large numbers of bacteria in blood and tissues, and they excrete viable organisms in milk. In most cases these animal infections are asymptomatic. While abortion occurs only rarely, the placenta of an infected animal frequently contains large numbers of organisms. It is contamination of the environment from these sources that usually precedes transmission to humans.

Because the minimum infective dose is a single viable organism, exposure need only be minimal. Most human cases of Q fever occur sporadically but outbreaks occur with high-risk occupations (farmers, hunters, workers in meat or milk processing plants, slaughterhouses, veterinary schools, etc.). Outbreaks have also been reported in such disparate groups such as inhabitants of a village through which infected sheep were herded, golf players on a course previously used as a sheep pasture, military personnel coming into contact with infected hay and poker players exposed to a parturient cat. Extracellular C. burnetii are extremely resistant to desiccation, low or high pH, disinfectants and ultraviolet light, and may remain infective in aerosols for up to 2 weeks and in the soil for as long as 5 months. Amebae may also be infected with C. burnetii and may be another reservoir for contamination of the environment. Ticks are probably important only in maintaining infections in small rodents and lagomorphs. There is little evidence for direct tick transmission to humans, but organisms may be excreted in large numbers in tick feces, leading to environmental contamination.

In addition to inhalation of viable C. burnetii in aerosols, infection may also occur through ingestion of infected milk and meat products. Most such infections result in seroconversion without symptoms, however. Coxiella burnetii has been isolated from the human placenta and breast milk, and transmission may also be from mother to child. Sexual transmission of Q fever has recently been reported.

PREVENTION

The extent to which Q fever organisms contaminate the environment, the ability of these organisms to survive harsh conditions and the low infective dose means that prevention through the use of environmental measures is difficult. Some measures, such as the avoidance of unpasteurized dairy products, may prevent some forms of transmission. Q fever can be prevented in animals using vaccines prepared from extracted subunits of phase I cells, and vaccines may also be useful for people at high risk when they can be identified. Vaccines prepared from phase II organisms have been shown to prevent abortion in animals, but vaccinated animals may still transmit infection to humans.

DIAGNOSTIC MICROBIOLOGY

The suspicion of acute Q fever is not dependent on a specific history of exposure to animals, since organisms persist in the environment for many years. Symptoms are not pathognomonic and may readily be confused with influenza or with other rickettsial diseases. Because organisms are highly infectious, all specimens from patients who have suspected Q fever should be handled with extreme care. Coxiella can be recovered from blood, urine and other body fluids during acute infection, using mice or vero cell lines, although only laboratories with adequate safety facilities should attempt this. The shell vial assay may improve recovery of organisms from patients who have endocarditis. A PCR assay, using primers derived from the htpAB-associated sequence, has been used to detect organisms in a variety of specimens, including heart valves and milk. Coxiella burnetii plasmid DNA has also been identified in human serum specimens by PCR.

Serologic diagnosis is more usual, and is especially useful in areas of high endemicity.

CLINICAL MANIFESTATIONS

The incubation period depends on the route of exposure, the inoculum dose and the age of the patient, but is usually about 3鈥? weeks. A variety of clinical manifestations may be recognized. The most frequent of these are mild fever (>99.5掳F (>37.5掳C)), headache, chills, sweating, cough, nausea and bradycardia relative to body temperature. A maculopapular rash develops in about 20% of acute infections. The fever usually subsides gradually during week 1, with recovery by week 3 of the illness. There is an inverse relationship between severity of disease and age, and infections in children may go unnoticed. Other frequently occurring presentations include pneumonia and hepatitis, and the prevalence of these may vary geographically. Possible reasons for this geographical variation include strain characteristics, the source, the route and the dose of infection and a variety of host factors.

Clinical recovery usually occurs by the third week but C. burnetii organisms may persist in the tissues much longer, and can be recovered from tissues years or even decades after primary infection. A post-Q-fever fatigue syndrome, associated with cytokine dysregulation and presenting with fatigue, myalgia, arthralgia, night sweats, mood change and sleep disturbance, may occur in up to 20% of patients. Chronic Q fever may result in osteomyelitis or encephalitis but there is a high risk of endocarditis, particularly in patients who have pre-existing valvular disease. Q fever endocarditis has a poor prognosis despite therapy. Myocarditis, splenic rupture, meningoencephalitis and pericarditis are all rare manifestation of acute Q fever.

MANAGEMENT

In-vitro studies have shown that rifampin, doxycycline and oxytetracycline and quinolones inhibit the growth of C. burnetii, although within the acidic environment of the phagolysosome other agents such as ceftriaxone and fusidic acid may be more effective. Prompt treatment of acute Q fever with doxycycline or tetracycline reduces the duration of fever, but it is not known whether this correlates with elimination of organisms. Combinations of doxycycline with either hydroxychloroquine, or ofloxacin taken daily for 18鈥?6 months has been recommended for chronic infections and may prevent development of endocarditis. The treatment of Q fever endocarditis is problematic. Prolonged regimens that include doxycycline and either rifampicin, trimethoprim-sulfamethoxazole or lincomycin have been reported to be effective but organisms can still be demonstrated in tissues months or even years later.

Q fever (Coxiella burnetii Infection) is a zoonotic disease caused by Coxiella burnetii, a species of bacteria that is distributed globally. In 1999, Q fever became a notifiable disease in the United States but reporting is not required in many other countries. Because the disease is underreported, scientists cannot reliably assess how many cases of Q fever have actually occurred worldwide. Many human infections are inapparent.

Cattle, sheep, and goats are the primary reservoirs of C. burnetii. Infection has been noted in a wide variety of other animals, including other species of livestock and in domesticated pets. Coxiella burnetii does not usually cause clinical disease in these animals, although abortion in goats and sheep has been linked to C. burnetii infection. Organisms are excreted in milk, urine, and feces of infected animals. Most importantly, during birthing the organisms are shed in high numbers within the amniotic fluids and the placenta. The organisms are resistant to heat, drying, and many common disinfectants. These features enable the bacteria to survive for long periods in the environment. Infection of humans usually occurs by inhalation of these organisms from air that contains airborne barnyard dust contaminated by dried placental material, birth fluids, and excreta of infected herd animals. Humans are often very susceptible to the disease, and very few organisms may be required to cause infection.

Ingestion of contaminated milk, followed by regurgitation and inspiration of the contaminated food, is a less common mode of transmission. Other modes of transmission to humans, including tick bites and human to human transmission, are rare.

Q fever is an acute or chronic disease caused by the rickettsial-like, Coxiella burnetii. Symptoms of acute disease are sudden onset of fever, headache, malaise, and interstitial pneumonitis. Chronic disease manifestations reflect the organ system affected. Diagnosis is confirmed by several serologic techniques, isolation of the organism, or Polymerase chain reaction (PCR). Treatment is with doxycycline or chloramphenicol.
Please see the web pages for more details on Q fever.

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  Radionuclide Scans   Radiography   Radiation Therapy   Radiation Exposure   Rabies   Quackery   Q Fever   Pyelonephritis   PXE   Pulmonary Fibrosis   Pulmonary Embolism   Puberty
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