Liver function tests often increase bilirubin and transaminases
Introduction
Introduction Liver function tests for bilirubin and transaminase often increase the typical Q fever symptoms. Q fever is an acute natural epidemic infection caused by Rickettsia burneti (Coxiella burneti).
Cause
Cause
QHerlik's body enters the body from the respiratory mucosa. First, it propagates in the local reticuloendothelial cells, and then enters the blood to form rickettsialosis, sowing all tissues and organs of the whole body, causing tissue diseases such as small blood vessels, lung and liver. Vascular lesions mainly have swelling of endothelial cells and may have thrombosis. Pulmonary lesions are similar to viral or mycoplasmal pneumonia. There are exudates composed of fibrin, lymphocytes and large mononuclear cells in the bronchioles, and severe cases resemble lobar pneumonia. Recently, there have been reports of inflammatory pseudo-lung tumors caused by Q. The liver has extensive granulomatous infiltration. The heart can develop myocarditis, endocarditis and pericarditis, and can invade the valve to form neoplasms, or even lead to rupture of the main A sinus and perforation of the valve. Other spleen, kidney, testis can also occur lesions.
(1) Source of infection
Livestock is the main source of infection, such as cattle, sheep, horses, donkeys, dogs, etc., followed by wild rodents, birds (pigeons, geese, turkeys, etc.) and reptiles. In some areas, the infection rate of livestock is 20-80%, and the infected animals are healthy in appearance, while the secretions, excretions, and placenta and amniotic fluid all contain Q-Herlikon. The patient is usually not the source of infection, but the patient's blood and sputum can be separated from the Q rickettsia. There have been reports of hospital infections causing nosocomial infections, so it should be taken seriously.
(2) Ways of transmission
Animals are transmitted through ticks; humans are infected by:
Respiratory spread
It is the main route of transmission. Q Hot rickettsia is caused by animal feces, amniotic fluid and other excretions as well as sputum feces polluting dust or forming aerosols into the respiratory tract.
2. Contact propagation
In contact with sick animals and cockroaches, pathogens can invade the human body through damaged skin and mucous membranes.
3. Digestive tract spread
Drinking contaminated water and dairy products can also be contaminated. However, because the human gastrointestinal tract is not susceptible to this pathogen, and the contaminated milk often contains neutralizing antibodies, the virulence of the pathogen can be weakened without causing disease, so the chance of infection is less.
(3) Susceptibility to the population
Generally susceptible. In particular, slaughterhouse meat processing plants, milk factories, various animal husbandry, and tanning fur workers have higher rates of dyeing, and they are not necessarily infected after infection. Serological investigations have shown that the recessive infection rate can reach 0.5 to 3.5%. Immunity lasts after illness.
(4) Popular characteristics
The disease is distributed worldwide. More common in male youth. China's Jilin, Sichuan, Yunnan, Xinjiang, Tibet, Guangxi, Fujian, Guizhou and other more than a dozen provinces, municipalities and autonomous regions have this disease.
Examine
an examination
Related inspection
Liver function examination liver ultrasound examination
(1) Clinical diagnosis
For patients with fever, if there is a history of contact with livestock such as cattle and sheep, if there is a local disease, the possibility of Q fever should be considered. Those who are associated with severe headache, myalgia, pneumonia, hepatitis, and foreign Fibonacci test should be highly vigilant.
(2) Laboratory inspection
Blood picture
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 test
The acute Q-hot phase II antibody is elevated and the phase I antibody is at a low level. 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. Pathogen separation
Blood, sputum, urine or cerebrospinal fluid materials were injected into the abdominal cavity of guinea pigs. The serum complement-binding antibody was measured within 2 to 5 weeks, and the titer was increased. At the same time, the animals had fever and splenomegaly. The spleen tissue and spleen surface infiltration were taken by necropsy. Liquid 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.
Diagnosis
Differential diagnosis
Q fever differential diagnosis
Acute Q fever should be differentiated from influenza, brucellosis, leptospirosis, typhoid fever, viral hepatitis, mycoplasmal pneumonia, and parrot fever.
Q fever (headache) Q endocarditis should be differentiated from bacterial endocarditis: any endocarditis manifestations, blood culture multiple negative or accompanied by hyperbilirubinemia, hepatomegaly, thrombocytopenia (< 100,000/mm3) should consider Q endocarditis. 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.
Q heat diagnosis:
(1) Clinical diagnosis
For patients with fever, if there is a history of contact with livestock such as cattle and sheep, if there is a local disease, the possibility of Q fever should be considered. Those who are associated with severe headache, myalgia, pneumonia, hepatitis, and foreign Fibonacci test should be highly vigilant.
(2) Laboratory inspection
Blood picture
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. Pathogen separation
Blood, sputum, urine or cerebrospinal fluid materials were injected into the abdominal cavity of guinea pigs. The serum complement-binding antibody was measured within 2 to 5 weeks, and the titer was increased. At the same time, the animals had fever and splenomegaly. The spleen tissue and spleen surface infiltration were taken by necropsy. Liquid 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.
