What is Q Fever?
Q fever is an acute infectious disease caused by Benacox and is a natural epidemic disease. Clinically, the onset of illness is acute, and the fever is high. Most of them are relaxation fever with chills, severe headache, and muscle soreness. A few patients may still present with sore throat, nausea, vomiting, diarrhea, abdominal pain, and insanity. No skin rash, often accompanied by interstitial pneumonia, liver function damage, etc., the external test was negative. Acute and chronic Q fever are caused by different strains of Benacox body respectively.
- Visiting department
- Respiratory Medicine
- Common causes
- Cattle, horse, sheep, ticks and other pathogens
- Common symptoms
- High fever, relaxation fever with chills, severe headache, and muscle soreness, etc.
Basic Information
Q fever etiology
- The epidemic of the disease is worldwide and its distribution is quite extensive in China.
- Source of infection
- Domestic animals such as cattle, horses, sheep, donkeys are the main sources of infection, and other poultry such as mule, camel, dog, pig, rodent and pigeons, swallows can be naturally infected. Most infected animals look healthy, and pathogens are present in the feces for a long time. Patients are usually not the source of infection, but the pathogens contained in their sputum can occasionally infect the surrounding population.
- 2. Ways of transmission
- Ticks are a vector of transmission, and pathogens are transmitted by ticks in livestock and wildlife. Q fever pathogens can exist in ticks for a long time and can be passaged by eggs. Tick feces also contain a large number of pathogens.
- (1) Respiratory tract transmission The respiratory tract is the main route of transmission, and 10 pathogens can cause disease. Pathogens can be turned into aerosols after they are automatically discharged from the body, and dry tick faeces can also contaminate dust and invade the human body from the respiratory tract to cause disease.
- (2) Contact transmission is another important transmission method. Such as veterinarians, herders, slaughterhouse workers, tannery workers, laboratory workers, etc., as well as dairy meat, fur processing factory workers and sick animals (its amniotic fluid, placenta, vaginal secretions, etc. are particularly contagious), fetal animals, Contaminated organs, animal products, pathogen cultures, etc. have many opportunities to contact. Pathogens can enter the body from damaged skin or mucous membranes. The puppet is bitten by ticks. Pathogens in tick faeces can invade through the wound.
- (3) Digestive tract milk from infected animals often contains pathogens, which cannot be completely killed by pasteurization, so drinking milk, especially raw milk, can also get sick. May also be infected by drinking raw water. Digestive tract transmission has not been confirmed. Perhaps the pathogen did not invade the human body from the digestive tract, but the person caused the disease by inhaling an aerosol formed when the contaminated milk or water was dumped.
- 3. Susceptible
- The population is generally susceptible to Q fever pathogens. The incidence of young adults and the above occupational population is higher than that of the general population. There are many hidden infections in endemic areas, and they have lasting immunity after illness.
- The disease has no obvious seasonality, and the incidence in spring is higher in farming and pastoral areas due to the relationship between the litter size of livestock.
Q fever clinical manifestations
- The clinical manifestations of Q fever are diverse and mainly depend on the number of pathogens entering the body, strains, individual immunity, and underlying diseases. The incubation period is 9-30 days, with an average of 17-20 days.
- Self-limiting fever
- The most common clinical manifestation of Q fever. Only fever, no pneumonia, self-limiting course of disease, usually 2 to 14 days.
- 2.Q fever pneumonia
- Clinically, there are three forms of atypical pneumonia, rapidly progressing pneumonia, and asymptomatic pneumonia. Onset is mostly acute and slow onset. Almost all patients have fever, accompanied by chills or chills, and the body temperature rises from 39 ° C to 40 ° C within 2 to 4 days, showing a relaxation type; most patients have obvious headaches; In addition to fever and headache, there are still muscle pain (especially the psoas and gastrocnemius muscles), congestion of the face and eyes, diarrhea, fatigue, sweating, and exhaustion. Occasionally, there is pain after the eyeballs, joint pain, and no rash.
- Respiratory symptoms were not prominent. The patient developed dry cough, chest pain, and a small amount of sticky sputum or blood in the sputum after 3 to 4 days. At the time of the physical examination, the lungs can be smelled and a few wet murmurs can be heard. The signs of lung consolidation soon follow the progress of pneumonia. Most patients have no respiratory symptoms. The course of this type of Q fever is generally 10 to 14 days.
- 3. Chronic Q fever
- The increasing number of cases deserves attention. Fever often lasts for more than several months, and the clinical manifestations are diverse. In addition to prone to endocarditis, pneumonia, and hepatitis, it can also be accompanied by pulmonary infarction, myocardial infarction, interstitial nephritis, arthritis, and osteomyelitis. Or appear in conjunction.
- 4. Other
- Patients with Q fever may have aseptic meningitis or (and) encephalitis, often with severe headaches, but brain tissue lesions are not significant. Meningitis or (and) encephalitis caused by Q fever is rare, and white blood cell counts in the cerebrospinal fluid may increase, ranging from tens to hundreds or even thousands, mainly mononuclear cells. Protein levels are usually elevated and glucose levels are normal. Other neurological complications include muscle weakness, recurrent meningitis, blurred vision, and abnormal behavior. Q fever patients occasionally develop spinal osteomyelitis, bone marrow necrosis, and hemolytic anemia.
Q heat check
- Routine hematuria
- The white blood cell count is more normal, and only a small number of patients may have an increased white blood cell count. ESR is often increased, especially in patients with chronic Q fever, mild proteinuria may occur during fever, and microscopic hematuria may occur in patients with Q fever endocarditis.
- 2. Serum immunological test
- Serum immunology tests are very specific. Complementary tuberculosis test (CF), microagglutination test, capillary agglutination test, indirect immunofluorescence test, and enzyme-linked immunosorbent test (ELISA) are commonly used. Patients in the acute phase of Q fever generally only produce antibodies to phase II antigens, and a low titer of phase I antibodies appears after several weeks of fever. Q zealous endometritis can show high titer Phase I CF antibodies. The foreign test was negative. Acute Q fever can be diagnosed when seroconversion of phase antibody to or antibody seroconversion or 4-fold increase.
- 3. Molecular biology testing
- At present, DNA probe technology and PCR technology can be used to detect Benacox body-specific DNA in specimens with strong specificity and high sensitivity. It is helpful to identify acute and chronic infections of Benacox body.
- 4. Animal vaccination and pathogen isolation
- Take 2 ~ 3ml of blood from patients with fever during inoculation in the peritoneal cavity of guinea pigs. Animals will be killed after fever, and spleen embossing smear will be performed. Pathogens can be found in cytoplasm. Chicken embryo yolk sac or tissue culture can be used to isolate pathogens.
- 5. Other
- There may be mild abnormalities in liver function, and T-wave and ST-segment changes in ECG. In the case of Q-heart endometritis, echocardiography can detect neoplasms. Liver biopsy is of great value in the diagnosis of Q fever granulomatous hepatitis.
- The culture method isolates Rickettsia, but it must be performed in a conditional laboratory to avoid causing laboratory infection.
Q fever diagnosis
- The diagnosis of Q fever depends on epidemiology, clinical manifestations, and serology. Resident history and occupation in the affected area have important reference value for diagnosis. Patients with low cellular immune function, previous history of heart valve disease, and history of heart valve replacement have bacterial culture negative endocarditis, and the possibility of Q warm endocarditis should be considered. The diagnosis depends on serological tests and / or molecular biology tests, which often require certain conditions and equipment. If necessary (conditional units) do animal inoculation and pathogen isolation. Q fever's negative Fei Fei test is conducive to distinguish Q fever from other rickettsial diseases.
Q fever treatment
- Doxycycline is the most effective treatment drug. The course of treatment should not be too short to prevent recurrence. Recurrence is still effective. General and symptomatic treatment is the same as typhus. Tetracycline and chloramphenicol are also quite effective for this disease. It usually goes away after 48 hours. Clinical trials have also confirmed that macrolides and fluoroquinolones are also quite effective.
- Chronic Q fever is generally treated with a combination of at least two effective drugs. Doxycycline combined with rifampicin can be used. It has now achieved certain results and the course of treatment is several years (generally at least 3 years). Another alternative treatment option is doxycycline combined with hydroxychloroquine. Q-heart endometritis can use hydroxychloroquine combined with doxycycline. The course of treatment is 18 to 36 months, which can be adjusted according to the level of serological testing. Replacement therapy can be treated with doxycycline and ofloxacin for 3 years or more. When unsatisfactory treatment with antibacterial drugs requires simultaneous artificial valve replacement. Antibacterial treatments should be performed every 6 months during antimicrobial treatment. Treatment can be discontinued when the phase I IgA antibody titer is 1:50 and the phase I IgG antibody titer is 1: 200. Antibodies should be reviewed every 3 months for the first 2 years after discontinuation of treatment. When the treatment is effective, the erythrocyte sedimentation rate gradually decreases, and anemia and hyperglobulinemia can be corrected.