Q FEVER

Q fever is a zoonotic disease caused by the rickettsia Coxiella burnetii. The disease is called so because the etiologic agent was not identified (Q for query) when the disease was described. It is also known as nine mile fever.

Etiology:  
C. burnetii is very small, 0.2-0.5 μm, rod-shaped, coccoid or diplococci gram negative bacillus. However, it cannot be demonstrated by Gram stain. It is an obligate intracellular parasite associated with reticuloendothelial (RE) and vascular endothelial cells. Coxiella replicates only in the phagolysosome. This is a highly fastidious organism that can only grow within other cells. Coxiella burnetii is resistant to pasteurization by holder method but may be killed by flash method.

Epidemiology:  
C. burnetii is extremely stable in the environment and has "spore-like" characteristics. It infects a wide range of animals including goats sheep cattle and cat, where it produces no symptoms. The organism is found in the placenta and in the feces of infected livestock. Sheep, cattle, and goats are the principal reservoirs for human infection. C. burnetii is also maintained in nature through an animal-tick cycle. The organisms persist in contaminated soil and is a focus for infection. It is also passed in milk. It is found worldwide and infection is common in ranchers, veterinarians, abattoir workers and others associated with cattle and livestock.

Mode of infection:  
Q fever is acquired via inhalation (aerosol) or ingestion of contaminated milk or food. 

Pathogenesis:  
C. burnetii infects macrophages and survives in the phagolysosome where they multiply. The bacteria are released by lysis of the cells and phagolysosomes. The organism multiplies in the lungs and is disseminated to other organs.

Clinical features:  
The incubation period varies from 9 to 28 days and averages 18 to 21 days. Unlike other rickettsial diseases, Q fever is not associated with skin eruptions. The disease can be mild and asymptomatic. The disease can be acute or chronic. In acute Q fever the patient presents with headache, fever, chills and myalgia. Atypical pneumonia, relative bradycardia, hepatomegaly and splenomegaly may be observed. Pneumonia and granulomatous hepatitis are observed in patients with severe infections. Granulomas can be seen in histological section of most patients with Q fever. Chronic Q fever typically presents as endocarditis generally on a damaged heart valve. Prognosis of chronic Q fever is not good. In chronic disease immune complexes may play a role in pathogenesis. Phase variation occurs in the LPS of C. burnetii. In acute disease antibodies are produced against the phase II antigen. In chronically infected patients antibodies to both phase I and phase II antigens are observed. Cellular immunity is important in recovery from the disease.

Laboratory diagnosis:  
Diagnosis is made using serological tests such as complement fixation test, agglutination test and fluorescent antibody tests. Antibodies to Phase II antigen are detected in acute cases and antibodies to both Phase I and II antigen are detected in chronic cases. Agglutination tests are more sensitive than CF tests. C. burnetii may be identified by immunofluorescence. Routine blood cultures are always negative. It can be grown in yolk sac of chick embryo and various types of cell-cultures. A shell-vial technique can be employed to isolate the bacterium.

Treatment:  
Antibiotics used in treatment are tetracycline or chloramphenicol.