Q fever pneumonia

Q hot pneumonia Sputum fever is an acute infectious disease caused by R. burnetii (also known as Burke rickettsia, Rick rickettsia). First discovered in Australia in 1935, because it is considered to be an unexplained disease (query is the meaning of doubt), it is hot. The main clinical manifestations are sudden fever, headache and body aches, and respiratory infections are the main route of transmission. Easy to cause lung disease (hot pneumonia, Q-feverpneumonia). Generally, there is no rash in the course of the disease, and the external Fiji reaction is negative, which is different from other rickettsial diseases. basic knowledge The proportion of illness: 0.005% Susceptible people: no specific population Mode of infection: respiratory transmission Complications: pleurisy

Q hot pneumonia cause

(1) Causes of the disease

Benarec parasitoids are parasitic in the cytoplasm of cells, mostly spherical or cuboid, and have strong resistance to physical and chemical factors. They survive at least 30 minutes at 50 °C and can be inactivated at 60-70 °C for 15-30 minutes. It can be stored for a long time at -70 ° C and freeze-dried, and can survive for several months to 1 year in contaminated soil. Therefore, the aerosol formed by inhaling contaminated soil is easy to cause disease, and the variation of Benarec has phase. The newly isolated pathogen in the animal or cockroach belongs to the first phase, and after the passage of the chicken embryo, it becomes the second phase, and only the second phase can undergo the complement-binding reaction with the recovery period and the early serum specimen, and the Bernard rickettsia against the guinea pig The voles and chicken embryos are pathogenic, with guinea pigs being the most commonly used experimental animals.

(two) pathogenesis

After invading the body, Benarec invades the body and then grows in local monocytes, then enters the blood circulation to form rickettsialosis, and involves small blood vessels and centripetal, liver, lung, kidney, brain and other organs. Spreading to form inflammation, individual cases due to serious death, confirmed by autopsy, lung lesions are diffuse inflammatory infiltration with large leaf distribution, similar to pneumococcal pneumonia, large leaf lung consolidation, only alveolar exudate rich Containing monocytes, lymphocytes, fibrin, containing only a small amount of neutrophils and red blood cells, can be distinguished from neutrophil-based bacterial pneumonia, alveolar macrophages (alveolar) Macrophage), Benarec corpuscles can be seen in alveolar macrophages, and histological sections show that rickettsia is mainly present in the vacuoles and cytoplasm of the cells, if fluorescein-labeled antibody is immunohistochemically It is more conducive to clear observation, due to the infiltration of macrophages, lymphocytes and plasma cells, the alveolar wall thickening, congestion and edema and alveolar septal necrosis can be seen, and the bronchiole mucosa can also be necrotic. Inflammatory infiltration.

Q hot pneumonia prevention

(1) Management of infectious sources: patients should be quarantined, and sputum and urine should be disinfected. Pay attention to the management of livestock and poultry, so that the pregnant animals are separated from the healthy animals, and the excreta, placenta and their polluted environment during the delivery period of the livestock are strictly disinfected.

(2) Cut off the route of transmission:

1. A slaughterhouse, a meat processing factory, a furry tannery, etc., and workers who have close contact with livestock must work in accordance with the protection regulations.

2. Destroy the rodent.

3. For suspected infected cattle and goat milk, it must be boiled for 10 minutes before drinking.

(3) Autoimmune: Vaccination can be given to workers who have more exposure to livestock to prevent infection. Livestock can also be vaccinated to reduce morbidity. The local vaccine of the dead vaccine is large; the attenuated live vaccine is used for scratching on the skin or oral administration of the sugar pill, and no adverse reactions are obtained, and the effect is good.

Q fever pneumonia complications Complications pleurisy

Combined with pleurisy.

Q hot pneumonia symptoms common symptoms relaxation heat high fever sore throat nausea diarrhea muscle soreness liver splenomegaly abdominal pain lung solid dry cough

The incubation period of hotness is generally 20 days, and the range is between 2 and 5 weeks. The clinical onset is acute, high fever, mostly relaxation heat with chills, severe headache and body muscle soreness. A few patients may still have pharynx. Pain, nausea, vomiting, diarrhea, abdominal pain and mental confusion, the respiratory symptoms caused by this disease are not obvious, may be related to the virulence of different regions and different strains, such as the occurrence of heat in Australia, causing pneumonia only 5 % to 9%, and in patients with fever in Nova Scotia or California in the western United States, pneumonia is typical, respiratory symptoms are prominent, and the incidence of pneumonia can reach 30% to 85%. In addition, respiratory pathogens are also inhaled. The number is related to the use of large doses of Benarec corpuscles to inhale the monkeys, resulting in the onset of pneumonia, while low-dose inhalation does not cause pneumonia, fever and pneumonia, most occur 4 to 5 days after onset Dry cough or a small amount of sticky, 15% to 45% of patients with pleural inflammation and chest pain symptoms, physical examination of the lungs can be heard and fine wet voice, sometimes with signs of lung consolidation, with relatively slow pulse And hepatosplenomegaly, etc., non-respiratory (such as liver, heart, eyes, blood vessels, etc.) caused by heat, a variety of performance, mainly depending on the different organs involved.

The incubation period is 12 to 39 days, with an average of 18 days. Most of the onset is rapid, and a few are slower.

(1) When the fever starts, the chills, headache, myalgia, fatigue, and fever rise to 39-40 °C within 2 to 4 days, and it is a relaxation heat type, lasting 2 to 14 days. Some patients have night sweats. In recent years, many patients have been found to have a regression heat profile.

(B) headache, severe headache is a prominent feature of this disease, more common in the forehead, after the eyelids and occipital, often accompanied by muscle pain, especially the psoas, gastrocnemius, can also be associated with joint pain.

(c) About 30 to 80% of patients with pneumonia have lung lesions. On the 5th to 6th day of the disease, dry cough and chest pain begin. A few have mucous sputum or bloody sputum. The signs are not obvious, and sometimes the small wet rales can be heard. X-ray examination often shows segmental or large-leaf blurred shadows around the lower lobe of the lungs, and texture thickening and infiltration around the lungs or bronchi, similar to bronchial pneumonia. Lung lesions were most prominent on the 10th to 14th day of the disease, and disappeared in 2 to 4 weeks. Even with pleurisy, pleural effusion.

(4) Hepatic liver love is more common. The patient had symptoms such as anorexia, nausea, vomiting, and upper right abdominal pain. The liver is swollen, but the degree is different. A few can reach 10cm under the costal margin, and the tenderness is not significant. Some patients have splenomegaly. Liver function tests for bilirubin and transaminase often increase.

(5) Endocarditis or endocarditis in about 2% of patients with chronic Q fever, showing long-term irregular fever, fatigue, anemia, clubbing, heart murmur, and difficulty in breathing. Secondary valvular lesions are more common in the aortic valve, and the mitral valve can also occur, which is associated with the original rheumatism. Chronic Q fever refers to patients with acute Q fever for several months or more, is a multi-system disease, can occur pericarditis, myocarditis, cardiopulmonary infarction, meningoencephalitis, myelitis, interstitial nephritis.

Q hot pneumonia check

1. The diagnostic value of routine blood tests for blood tests is not significant. The peripheral blood leukocytes in the acute phase are mostly normal, or mildly elevated with mild nuclear left shift, serum transaminase and alkaline phosphatase can be increased.

2. The sputum test sputum is stained by Gram, mainly showing a large number of monocytes, lymphocytes and a small amount of neutrophils, etc., and the sputum is separated into Benarec by the culture.

3. The pathogen examination depends on the separation of Benarec corpuscles from the blood, urine, sputum, cerebrospinal fluid and pleural fluid of the patient, and the clinical specimens are inoculated into guinea pigs, voles or chicken embryos. It takes 4-6 weeks for the animals to be inoculated. Specific antibodies appear, and there is a danger of causing infection at any time during the separation operation, so the conventional method is not used, and the operator should be properly protected if necessary.

Benarec corpuscles in tissues or macrophages can be directly observed using immunofluorescence-labeled antibody technology or by electron microscopy.

Patients with fever pneumonitis can obtain specimens by fiberoptic bronchoscopy lung biopsy and bronchoalveolar lavage, and perform Benarec detection on alveolar macrophages in biopsy tissue and lavage recovery fluid.

4. Serological examination The serological diagnosis method of phlegm-heating is simple and safe, and the result is reliable. It is often used clinically. Specific antibodies appear in the blood 2 to 4 weeks after the onset of the disease. The detection methods include complement-binding test and micro-blood agglutination test. , enzyme-linked immunosorbent assay (ELISA) and micro-immunofluorescence technology, the acute phase of IgG antibody is higher than the recovery period and more than 4 times more diagnostic, specific IgM antibodies can also be detected by ELISA, the antibody can be It lasts for more than 17 weeks after onset and has a certain diagnostic value.

The disease is negative for the external Filipino reaction, and is more easily distinguished from other common rickettsial diseases. In view of the phase variation of the Benarec corpuscle, the antibody level of the 2-phase antigen is significantly increased in the acute phase; The antibody titer of the phase antigen is increased, and its titer is 1:200.

5. Molecular biological testing DNA probe and PCR technology can be used to detect Benarec's DNA in specimens with high specificity, high sensitivity, and identification of acute and chronic infection of Bernard rickettsia.

6. Animal inoculation and isolation of pathogens 2 to 3 ml of blood from patients with fever are inoculated into the abdominal cavity of guinea pigs. The animals are sacrificed after fever and spleen smears are observed. The pathogens present in the cytoplasm can also be seen. Chicken embryo yolk sacs can also be used. Tissue culture and isolation of pathogens must be carried out in a conditional laboratory to avoid infection and dissemination.

7. X-ray examination: flaky blurred shadows scattered in the lungs, segmental and sub-segmental distribution, sometimes showing signs of large leafy consolidation, most of which occur in one or both sides of the lower lung.

Q thermal pneumonia diagnosis and identification

Q heat diagnosis

(1) Clinical diagnosis of patients with fever, if there is a history of contact with livestock such as cattle and sheep, local presence of this disease should consider the possibility of Q fever. Those who are associated with severe headache, myalgia, pneumonia, hepatitis, and foreign Fibonacci test should be highly vigilant.

(2) Laboratory inspection

1. The blood cell count is normal, the neutrophils are slightly shifted to the left, the platelets can be reduced, and the erythrocyte sedimentation rate is moderately increased.

2. Serology

(1) Complement binding assay The acute Q-hot phase II antibody was increased, and the phase I antibody was low. If the titer of a single serum phase II antibody has a diagnostic value of 1:64 or more, the serum titer of the double serum is increased by 4 times 2 to 4 weeks after the disease, and the diagnosis can be confirmed. Chronic Q fever, phase I antibodies are comparable or exceed II phase antibody levels.

(2) Microagglutination test The phase I antigen was converted to phase II antigen by trichloroacetic acid treatment, and stained with hematoxylin and then agglutinated with the patient's serum on a plastic plate. This method is more sensitive than the complement fixation test, and the positive rate (50% in the first week and 90% in the second week) can also be measured by capillary agglutination. However, the specificity is not as good as the combination test.

(3) Immunofluorescence and EliSA detection of Q heat-specific IgM (anti-II phase antigen), which can be used for early diagnosis.

3. The pathogen is separated from blood, sputum, urine or cerebrospinal fluid material, injected into the abdominal cavity of guinea pigs, and the serum complement-binding antibody is measured within 2 to 5 weeks, and the titer is increased. At the same time, the animal has fever and splenomegaly, and the spleen tissue is taken by necropsy. And spleen surface oozing smear staining microscopic examination of pathogens; rickettsia can also be isolated by chicken embryo yolk sac or tissue culture method, but must be carried out in a conditional laboratory to avoid infection in the laboratory.

Q fever differential diagnosis

Acute Q fever should be differentiated from influenza, brucellosis, leptospirosis, typhoid fever, viral hepatitis, mycoplasmal pneumonia, and parrot fever.

Q endocarditis should be differentiated from bacterial endocarditis: any endocarditis manifestations, blood culture multiple negative or accompanied by hyperbilirubinemia, hepatomegaly, thrombocytopenia (<100,000 / mm3) Q endocarditis should be considered. The combination test I phase antibody > 1/200 can be diagnosed. It has been reported in foreign countries that direct fluorescent detection of I and II phase IgA is highly effective and is used to diagnose Q endocarditis. Other manifestations of chronic Q fever should also be differentiated from the disease caused by the corresponding cause.

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