Q fever is an acute or chronic disease that is caused by the pathogens Coxiella burnetii rickettsienartigen. An acute illness begins suddenly with fever, headache, malaise, and interstitial pneumonitis. Chronic manifestations occur depending on the organ affected system. The clinical diagnosis can be confirmed by various serological techniques, pathogen isolation or PCR. For therapy, doxycycline or chloramphenicol is.
Coxiella burnetii is a small intracellular pleomorphic bacterium that is no longer expected to Rickettsiaickettsien. Because molecular biological studies, it was as proteobacteria in the same group as Legionella sp. reclassified.
Q fever is an acute or chronic disease that is caused by the pathogens Coxiella burnetii rickettsienartigen. An acute illness begins suddenly with fever, headache, malaise, and interstitial pneumonitis. Chronic manifestations occur depending on the organ affected system. The clinical diagnosis can be confirmed by various serological techniques, pathogen isolation or PCR. For therapy, doxycycline or chloramphenicol is. Coxiella burnetii is a small intracellular pleomorphic bacterium that is no longer expected to Rickettsiaickettsien. Because molecular biological studies, it was as proteobacteria in the same group as Legionella sp. reclassified. Q fever can be acute therapy Chronic Acute course is accompanied by a febrile illness that often affects the respiratory tract and sometimes the liver is involved. During pregnancy infected women have an increased risk of spontaneous abortion and premature birth. Chronic fever occurs in 5% of patients. Usually, it is manifested by a endocarditis or hepatitis; it can also lead to osteomyelitis. Q fever is common worldwide and is mainly used as an inapparent infection in domestic animals and livestock before. The main reservoir for human infections are sheep, cattle and goats. C. burnetii persists in stool, urine, milk and tissues (particularly the placenta), so it is easy to contamination of objects and the formation of infectious aerosols. C. burnetii is maintained in nature by an animal tick cycle, but arthropods are not involved in human infection. Etiology There may be work-related cases of rickettsial disease in people who have close contact with farm animals and their products due to their activities. To a transfer occurs mostly through inhalation of infected aerosols, but the disease can also be acquired by ingestion of contaminated raw milk. C. burnetii is very virulent, resists inactivation and remain capable of reproduction in dust and chair for months; even a single bacterium can cause an infection. Because of these properties C. burnetii is a potential biologischr warfare agent. Very rarely the disease from person to person is. Symptoms and signs The incubation period is on average 18-21 days (9-28 days). Some infections are associated with minimal discomfort; However, most patients have influenza-like symptoms. The onset is abrupt with fever, severe headache, chills, malaise, myalgia, anorexia and sweating. The fever can be up to 40 ° C rise and over 1 persist to> 3 weeks. 4-5 days after onset there is respiratory symptoms (a dry non-productive cough, pleuritic chest pain). These symptoms may be particularly pronounced in elderly or debilitated patients. On physical examination often a pulmonary crackles noticeable and there may be signs of lung consolidation exist. Unlike Rickettsioses there is not a rash at Q-fever. Acute hepatic involvement occurs in some patients and is reminiscent of viral hepatitis with fever, malaise, hepatomegaly with pain in the right upper quadrant, and possibly jaundice. Headaches and respiratory symptoms are often missing. Chronic Q fever can manifest itself within a few weeks to several years after the initial infection. Hepatitis may manifest as FUU. A liver biopsy can show granulomas that of other causes of Lebergranulomen (z. B. tuberculosis, sarcoidosis, histoplasmosis, brucellosis, tularemia, syphilis) must be differentiated. Endocarditis subacute bacterial endocarditis resembles a by viridans streptococci; often the aortic valve is affected, but growths may occur at each door. Finger clubbing, arterial emboli, hepatomegaly, splenomegaly and a purple rash may occur. The mortality rate is only 1% of untreated patients, but is higher in patients with endocarditis. Some patients with neurological involvement, there is permanent damage. Diagnosis immunofluorescence assay or PCR of infected tissue Sometimes acute and ongoing serological examinations symptoms do not immediately close to the diagnosis. In the early stages of Q fever is reminiscent of many infections (eg. As influenza, other viral infections, salmonellosis, malaria, hepatitis, brucellosis). Later, there is reminiscent of many forms of bacterial, viral and mykoplasmenbedingter and other atypical pneumonia. Clinical history of contact with animals or animal products are diagnostically important. Diagnostic method of choice is the immunofluorescence assay (IFA) of the infected tissue; Alternatively, an enzyme-linked immunosorbent assay (ELISA) can be performed. Acute and course of serum samples (in particular, complement fixation) can be performed. Antibodies against antigens of phase II can be used to diagnose an acute disease, and antibodies against antigens of both phase I and phase II are used to diagnose a chronic disease. By means of PCR of the pathogen can be detected in biopsy samples. C. burnetii can be isolated from clinical samples, but only in specialized research laboratories; routine cultures of blood and sputum are negative. In patients with respiratory symptoms or signs of disease, a chest X-ray must be made; it can be found atelectasis, pleurabasierte opacities, pleural effusion and Lappenkonsolidation. The overall impression of the lung may recall a bacterial pneumonia seen histologically but the finding is more like a psittacosis and some viral pneumonia. In acute Q fever, the blood may be normal, but about 30% of patients have a leukocytosis. Alkaline phosphatase, AST and ALT are elevated in typical cases only mediocre on the 2- to 3-fold standard value. If a liver biopsy performed in diffuse granulomatous changes are often visible. Doxycycline therapy in acute Q fever, the drug of first choice is doxycycline 200 mg p.o. 1 times a day, followed by 100 mg 2 times daily until clinical improvement occurs, the patient of about 5 days is afebrile and has received a therapy for at least an additional 7 days; normalerqweise a 2 to 3 weeks, continued treatment is required. A tetracycline resistance has not been documented. In endocarditis the duration of treatment must be extended (by month over years to lifelong), typically for at least 18 months. Doxycycline 100 mg p.o. 2 times täglichj plus hydroxychloroquine 200 mg p.o. all 8 hours is recommended at this time. Clinical findings, ESR, blood count and antibody titers should be monitored to determine to help when the treatment can be stopped. The consultation of a specialist in infectious diseases can help with the complexity of the disease and its treatment deal. Treatment with antibiotics is only partially effective common and damaged valves must be replaced surgically generally, although it already has been some healing without surgery. For chronic granulomatous hepatitis, the optimal therapy has not been determined. Prevention vaccines are effective and in Australia, where a Q fever vaccine is commercially available, vaccination is recommended to protect people at risk in the workplace (eg. As slaughterhouse and dairy rendering plants where shepherds Wollsortierern, farmers) , Prior to vaccination, screening with skin and blood tests should be performed to determine a possibly existing immunity against Q fever because the vaccine in people with pre-existing immunity can cause severe local reactions.