Coxiella burnetii

Chapter 42 Coxiella burnetii


Coxiella burnetii was originally named Rickettsia burnetii, and it shares rickettsial characteristics, including obligate intracellular growth, failure to stain by Gram’s method, and transmission, in some cases, by ticks. Recent 16S rRNA gene sequencing has demonstrated that these bacteria are more closely related to the genera Francisella and Legionella than to the family Rickettsiaceae, with which they are taxonomically placed.


The organism is the cause of “Q fever” (query fever) that was first described as a cause of febrile illness in abattoir workers in Queensland, Australia, in 1937. Burnett and Freeman, working in Nine Mile, Montana, described a febrile illness in guinea pigs following tick exposure, and in 1938, the “Ninemile agent” was found to be identical to the agent of Q fever. Rickettsia burnetii was subsequently reclassified into the new genus Coxiella, in honor of Herald R. Cox, who initially isolated the organism in the United States.


Coxiella burnetii is a small pleomorphic rod-shaped bacterium (0.2-0.4 μm wide and 0.4-1 μm long) with a cell membrane similar to that of gram-negative bacteria. The organism multiplies in phagolysosomes of infected cells and can undergo phase variation, with antigenic changes in the lipopolysaccharide (LPS). Phase I is the highly infectious, natural phase; a complex carbohydrate on its surface blocks antibody interaction with surface proteins. LPS is modified upon in vitro cultivation, and the organism enters phase II, exposing surface proteins to antibodies and producing a less virulent form.



DISEASES AND EPIDEMIOLOGY


Q fever is a zoonotic disease that is endemic throughout the world, except for New Zealand. Coxiella burnetii is widely distributed in nature and has been identified in arthropods, birds, reptiles, fish, and mammals, including humans. All reservoirs of C. burnetii have not been identified, although livestock, such as ruminants, are primary reservoirs and pet cats and dogs have been linked to urban outbreaks of Q fever. Intermittent shedding may occur in vaginal discharges, feces, urine, milk, and birth products. Arthropods facilitate a sylvan life cycle in reservoir animals, and transmission by ticks and other arthropods to domestic animals and rarely to humans has been documented.


Disease may follow respiratory or digestive exposure. Domestic animals and humans are most commonly infected by inhalation of contaminated aerosols of dried placental materials, birth fluids, and excreta of infected animals. Humans are often very susceptible, and the infectious dose is perhaps as low as one organism. Within herds, infection may also be maintained by inhalation of contaminated dust or through contact with fomites. Consumption of raw cow’s or goat’s milk may result in asymptomatic infection in humans.


The extraordinary stability of C. burnetii outside the host is associated with the small sporelike forms observed by electron microscopy. The bacterium is resistant to elevated temperatures, ultraviolet light, desiccation, and disinfectants such as 0.5% sodium hypochlorite, quaternary ammonium compounds, and phenolics. Environmental survival favors wind-borne transmission, often over long distances. These factors also make C. burnetii a putatively attractive target for use in biological warfare and bioterrorism.


Q fever is an occupational disease of farmers, veterinarians, and abattoir workers. It became a notifiable disease in the United States in 1999, but reporting is not required in many other countries; accurate estimates of worldwide incidence are not available, and underestimation seems likely in light of the frequently insidious nature of the disease.


Acute Q fever is less common. The incubation period is 2 to 4 weeks, and the resulting disease is a self-limited flulike syndrome, with severe headache, malaise, fever, myalgia, and chills. Complications such as pneumonia, hepatitis, pericarditis, myocarditis, meningoencephalitis, gastroenteritis, pancreatitis, optic neuritis, lymphadenopathy, and skin rash are uncommon. Mortality is usually low in the absence of complications. The route of infection may determine the predominant manifestation of acute disease.


Endocarditis may develop years after acute infection. Chronic illness occurs in approximately 5% of patients, and most frequently involves not only the heart but also arteries, bones, and liver. Patients at risk for chronic disease include those with preexisting cardiac valve defects, transplant recipients, patients with cancer, and those with chronic kidney disease. The case fatality rate for chronic Q fever may be as high as 65%. Contracting Q fever during pregnancy may result in abortion or premature birth, and intrauterine transmission may occur.


Coxiella burnetii usually causes inapparent or mild disease in domestic animals. Sporadic abortions have been reported in sheep, goats, and cattle. Infertility or birth of weak offspring is a rare sequel to ruminant infection. Companion animals may be infected, but rarely exhibit clinical disease; however, abortion in cats and the birth of weak puppies have been described. Human illness has resulted from exposure to infected, pregnant, or parturient queens and bitches.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Coxiella burnetii

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