typhus
Introduction
Introduction to typhus Typhoid (typhus) is an acute infectious disease caused by rickettsia. It can be divided into epidemic typhus and endemic typhus. Epidemic typhus is caused by Platts rickettsia, which is transmitted by body lice, mostly in winter and spring. Local typhus typhus is caused by infection with rickettsial rickets, with rats and squirrels as the medium, and summer and autumn as the most. Local people are less ill than epidemic. The incubation period is 5 to 21 days, mostly 10 to 12 days. The table has an acute onset, chills, high fever, severe headache, muscle pain and tenderness, especially the gastrocnemius muscle, facial flushing, conjunctival hyperemia, neuropsychiatric symptoms such as insomnia, tinnitus, convulsions, mania, and even coma. There may be pulse increase or toxic myocarditis. More than the fifth day of the disease, the body appears congestive rash or maculopapular rash, which can later become hemorrhagic and have splenomegaly. Epidemic typhus still belongs to the human--human transmission of diseases, human beings are the only host, and body lice are the vectors of transmission. Endemic typhus is a natural epidemic disease caused by Rickettsia Mooseri. The rodent is the storage host. The mouse and the cockroach are the vectors and the human being is the victim. basic knowledge The proportion of illness: 0.006%-0.008% Susceptible people: no specific people Mode of infection: non-infectious Complications: myocarditis, bronchopneumonia
Cause
Cause of typhus
Platts rickettsial infection (80%)
Both P. striata and M. rickettsia have similar morphology, Gram-negative staining, weak resistance to the outside world, and easy to be killed by heat and general disinfectants. Strong resistance to dryness and low temperature. Human sputum is the only vector of epidemic typhus, which is dominated by body lice, followed by head lice. After sucking the patient's blood, the rickettsia invaded its intestinal epithelial cells to multiply, and after 5 days, the rickettsia was excreted with the sputum. When you bite a healthy person, the rickettsia can invade the body by itching skin scratches, causing spread. The sputum is the vector of endemic typhus. The pathogens multiply in the cells of the sacral wall and are excreted with the sputum. When the itch is inactive, the pathogen can enter the human body through the skin scar. When the rickettsia invades the human body, it multiplies in the endothelial cells of small blood vessels and capillaries. After the cells rupture, the rickettsia and the unique toxins circulate with the blood to various organs of the body, leading to various poisoning symptoms. At the same time, due to the invasion of rickettsia, it also causes small vasculitis and infiltration of inflammatory cells around the blood vessels, and forms typhus typhus nodules.
Pathogenesis
After a person is infected with a rickettsia cockroach or cockroach bite, the typhus rickettsia first propagates locally, then enters the bloodstream, produces rickettsialemia, and then reaches the body. Organ tissue, clinical manifestations of toxemia. Toxins released after the death of rickettsia rickettsia are the main cause of disease. It can cause papules, eschar and ulcers locally. It can cause lymphadenopathy in the whole body, and the lymph nodes near the eschar are particularly prominent. The center of the lymph nodes can be necrotic. Yellow-green exudate can be seen in the serosal cavity, such as the thoracic cavity, abdominal cavity, and pericardial cavity. The internal organs are generally congested, the spleen is often congested, can be swollen 2 to 5 times, the liver is also swollen, the myocardium can be focal or diffuse myocardial inflammation, and there may be focal hemorrhage or degenerative lesions. The lung may have hemorrhagic pneumonia or secondary bronchopneumonia. Meningoencephalitis can occur in the brain. The kidney can present a wide range of acute inflammatory lesions. The gastrointestinal tract is often extensively congested.
The histopathological changes of typhus are mainly in the vascular system, with focal or extensive vasculitis and perivascular inflammation, with lung, brain, heart and kidney being the most prominent. Monocytes, lymphocytes, and plasma cells are infiltrated around the blood vessels. In severe patients, vascular endothelial cell edema and vascular wall necrosis and rupture can be seen. It has been detected in vascular endothelial cells, macrophages and cardiomyocytes of various organs in patients with rickettsia.
Prevention
Typhus prevention
1. Control the source of infection is mainly rodent control. The masses should be mobilized and comprehensive measures should be taken to combine various mousetraps with drug-killing rodents. Commonly used rodenticides include zinc phosphide, ampoules and enemy mice.
2. Cut off the route of transmission to prevent biting by larvae, and avoid lying and lying on the grass during the season. When working in the wild area, you must tighten the cuffs and hem, and apply anti-insecticides such as diphenyl phthalate or benzyl benzoate.
3. Improve the disease resistance of the population There is no typhus vaccine for the population. Preliminary studies have shown that the membrane protein antigen with a molecular weight of 56×103 in rickettsia typhus has strong immunogenicity. The gene encoding this protein has been successfully expressed in E. coli and can be used as a vaccine for further study.
Complication
Typhus complication Complications Myocarditis bronchopneumonia
The more common complications are toxic hepatitis, bronchial pneumonia, myocarditis, meningoencephalitis and acute renal failure.
Symptom
Symptoms of typhus common symptoms rash fever with lymphadenopathy... lymphadenopathy splenomegaly
(1) Incubation period
The prevalence of epidemic typhus is 10 to 14 days. If the amount of infection is large, the onset time can be advanced. The prodromal symptoms are not obvious, and some are only low fever, headache and fatigue. The incubation period of endemic typhus is usually 5 to 15 days.
(two) symptoms and signs
The symptoms and signs of epidemic and endemic typhus are mainly four, namely fever, headache, rash and swollen lymph nodes.
(3) Physical inspection
The most common sign is splenomegaly.
(four) complications
Otitis media, mumps, and bacterial pneumonia are common complications, and some may have scrotal, penile, labia swelling and gangrene. Sometimes nerve irritation can occur, and some are coma, dull, stupid, and excited.
Examine
Typhus typhus
Laboratory inspection:
Blood picture
The number of white blood cells in the peripheral blood is reduced or normal, and the severe patients may be slightly increased. The classification often has a nuclear left shift phenomenon.
2. Serological examination
(1) External-Fiji reaction: The external-Fiji reaction is also called the Proteus agglutination test. The antibody against typhus typhus in the serum of the patient can agglutinate with the Proteus OXK antigen to provide a basis for diagnosis. On the first weekend of the disease, only a few (30%) were positive, 75% at the end of the second week, 90% at the third week, and the titer was 1:160 to 1:1280. It began to decline in the fourth week and turned negative in the eighth to the ninth week.
(2) Complement binding test: the positive rate is higher, the specificity is stronger, and the duration of continuous positive is longer, up to 5 years. It is necessary to use local rare strains as antigens, and multivalent antigens may also be used, because the antigenicity of rickettsia of different strains may vary greatly.
(3) Immunofluorescence antibody test: Indirect immunofluorescent antibody test (IFAT) was used to detect specific antibodies in the serum of patients, which appeared positive at the first weekend of the disease course, reached the peak on the 2nd to 3rd weekend, and gradually decreased after 60 days. But it can last for years. A report that was still positive after 10 years of illness.
(4) Dot enzyme immunoassay: using various serotypes of typhus rickettsia or part of protein as antigen, adsorbed on nitrocellulose membrane for dopase immunoassay (dot-EIA), detecting serum in patients Specific IgG and IgM antibodies for each serotype. The method has high sensitivity and specificity, and can distinguish various serotypes.
(5) Enzyme-linked immunosorbent assay and enzyme immunoassay: a protein with a molecular weight of 56×103 of typhus typhus expressed by genetic recombination technology as an antigen, enzyme-linked immunosorbent assay (ELISA) and enzyme immunization The enzyme (munition immunoassay, EIA) was used to detect IgG and IgM antibodies against rickettsial rickets in the serum of patients, with a sensitivity of 86% to 88% and a specificity of 84% to 90%.
3. Pathogen examination
(1) Pathogen isolation: Commonly used mice for typhus rickettsia separation. The patient's blood can be inoculated into the peritoneal cavity of the mice, each inoculated with 0.5 ml. Most cases occurred on the 7th to 9th day after vaccination. The mice that were dying were found to have congestion and edema in the lungs. The liver, spleen and lymph nodes were swollen and swollen, and pleural effusion and ascites appeared. Take ascites smear, peritoneum, mesentery, liver, spleen or kidney print, dry and then use Giemsa staining microscopy (1000-1600 times magnification), can find purple red in the cytoplasm of monocytes and macrophages, A plexiform distribution of typhus rickettsia. When a typhus rickettsia invades cells, it can multiply in the local cytoplasm under suitable conditions, so it is often clustered. If the anti-typhus rickettsia antibody is used as an immunofluorescence test, yellow-green fluorescence is observed in the cells under a fluorescence microscope.
(2) Molecular biological examination: According to the nucleotide sequence of the major membrane protein antigen whose molecular weight is 56×103, which is encoded by rickettsia typhus, a common and different primers were designed for each serotype. The nested-polymerase chain reaction (nested-PCR) detects the corresponding genes of five serotypes of Gilliam, Karp, kato, kawasaki and kuroki. It has high sensitivity and specificity and is considered to be useful for the diagnosis of typhus. And identify the serotype.
Other auxiliary inspections:
Severe complications of bronchial pneumonia, X-ray chest X-ray abnormalities.
Diagnosis
Diagnosis of typhus
diagnosis:
1. Epidemiological data should pay attention to whether it has been in the epidemic area of typhus within 4 to 20 days before the onset of illness, whether it has been working outdoors, camping in the open air or sitting and lying in the bushes. At the same time, attention should also be paid to the popular season. The prevalence of local typhus and so on.
2. Clinical manifestations of sudden onset, chills or chills, high fever, loss of appetite, facial flushing, superficial lymphadenopathy, hepatosplenomegaly, maculopapular rash, and characteristic eschar or ulcer. Patients with suspected typhus should pay great attention to finding eschar or ulcers. It is mostly located near the swollen, tender lymph nodes.
Differential diagnosis
1. Leptospira typhus typhus epidemic area is also often associated with leptospirosis. Moreover, both are more common in summer and autumn, all have fever, conjunctival hyperemia, lymphadenopathy, etc., so should pay attention to identification. Leptospirosis often has gastrocnemius pain, subconjunctival hemorrhage, early renal damage, and no rash, eschar or ulcer. Serological and pathogenic examinations can be performed if necessary, and the serum leptospirosis agglutination test is positive.
2. Typhus rash is more common in winter and spring and cold areas, with a history of mistletoe or a bite of rat bites, fever, maculopapular rash, skin ulcers and swollen lymph nodes. OX19 was positive in the agglutination of proteus, while OXK was negative.
3. There is often a history of eating unclean food before the onset of typhoid fever. Slow onset, body temperature gradually increased, relatively slow pulse, apathy, bloating, constipation, lower right abdomen tenderness, common rose rash. The total number of white blood cells decreased, and eosinophils decreased or disappeared. The fatda reaction can be positive, and blood and bone marrow culture can have typhoid bacillus growth.
4. Septicemia often has primary infections. Relaxation heat type and irregular heat type are common. Skin caused by Gram-positive bacteria often has rash or pattern-like changes, and those caused by Gram-negative bacteria are more likely to have shock. The total number of white blood cells in the blood increased, neutrophils increased, and there was a nuclear left shift. The external-Fiji reaction is negative, and blood and bone marrow culture may have pathogenic bacteria growth.
5. Dengue fever has been inhabited or stayed in dengue fever epidemic areas before the onset of dengue fever. There is a history of biting by Aedes mosquitoes during the day, more than in summer and autumn. Headache and body pain are more pronounced. More often, there are spots of rash and subcutaneous bleeding. The total number of white blood cells and platelets are often reduced. Dengue virus can be isolated from the serum of patients whose disease duration is shorter than 3 days. Serum anti-dengue virus antibody positive.
6. Epidemic hemorrhagic fever High fever, headache, low back pain and eyelid pain are more obvious, when the body temperature drops, shock occurs more frequently, subcutaneous hemorrhage, common ecchymoses, oliguria or no urine. The total number of white blood cells in the blood rises, and the atypical lymphocytes often exceed 10%, and the platelets are significantly reduced. Blood urea nitrogen and creatinine levels gradually increase with prolonged oliguria or anuria. The specific antibodies against the epidemic hemorrhagic fever virus in the serum are positive.
7. Others should also pay attention to the differential diagnosis of influenza, malaria, acute upper respiratory tract inflammation, malignant histiocytosis, lymphoma.
