Typhus rickettsial pneumonia

Introduction to typhus rickettsia pneumonia Typhus has epidemic typhus and endemic typhus. The former is transmitted by human sputum by Platts rickettsia, and bronchopneumonia is second only to Q-heat pneumonia. The latter is also called plaque. Muriontyphus is an acute infectious disease transmitted by rickettsia variabilis. The clinical features are similar to those of epidemic typhus, but the disease is mild, and bronchitis is more common, and those with concurrent pneumonia are more common. less. basic knowledge The proportion of illness: 0.055% Susceptible people: no specific people Mode of transmission: spread through humans Complications: myocarditis, pneumonia, otitis media

The cause of typhus rickettsia pneumonia

(1) Causes of the disease

The pathogen of epidemic typhus is Plasmodium rickettsia, which is a microbiccobacteria, 0.3-0.6 m long and 0.3 m wide. It is usually parasitic in the vascular endothelial cells of patients and the intestinal epithelial cells of the body. The pathogen is extremely sensitive to heat, ultraviolet rays and general chemical disinfectants. It is killed at 56 ° C for 30 min or 37 ° C for 5 to 7 h. It has strong tolerance to low temperature and dryness. It can be stored for a long time under -20 ° C. The sputum can retain vitality for several months, and the resistance of Moritz rickettsia in form, dyeing and heat disinfectant is the same as that of Priscilla rickettsia, but it is indistinguishable, but it is against guinea pigs, rats and The mice are extremely sensitive. After injection, the guinea pigs are feverish, the scrotum is highly red and swollen, and the mice are caused by fever and death. The scrotum reaction of guinea pigs caused by Platts rickettsia is far more than that caused by rickettsia. Weak, it lacks pathogenicity to mice and rats, so it is vaccinated with guinea pigs, mice or rats to distinguish between Platts and Mori.

(two) pathogenesis

Rickettsia first grows and propagates in local cells, which in turn creates creatinemia and invades tissues and organs to form typical proliferative, thrombotic or necrotizing vasculitis and perivascular inflammatory granuloma (also known as maculopathy). Typhoid nodules), this lesion affects the whole body, especially the skin of the dermis, myocardium, lung, brain, liver, kidney, adrenal gland, etc., causing various clinical symptoms, the toxins released by the pathogen cause various poisoning symptoms 2 weeks after the onset, the most prominent vascular lesions, such as increased capillary permeability, vascular embolism and ecchymoses, may be related to secondary delayed allergic reactions, the pathological changes of bronchial pneumonia in the lungs, mainly as Local congestion, edema, alveolar exudation, consolidation, enriched with monocytes, lymphocytes, plasma cells, red blood cells and a small number of neutrophils, Giemsa or Gram stained tissue sections, showing alveolar interstitial hyperplasia with a large number Mononuclear cell infiltration, a large number of rickettsia in the bronchial epithelium, monocytes, if secondary bacterial infection, pneumococcal is more common, epidemic typhus and Pathology and pathogenesis of typhus side is substantially the same, but the latter vascular lesions less.

Typhus rickettsia pneumonia prevention

Starting from the management of infectious sources and cutting off the channels of transmission, we have carried out extensive patriotic health education and various activities, vigorously carried out activities to eliminate cockroaches, prevent cockroaches, eliminate rodents and eliminate cockroaches, and enhance the awareness of health and disease prevention among the people. In the epidemic areas of epidemic typhus Inhabitants can be inactivated vaccination, and endemic typhus is mostly distributed.

Complications of typhus rickettsial pneumonia Complications Myocarditis Pneumonia otitis

Common bronchitis, pneumonia, myocarditis, abnormal lung function, other visible stomatitis, otitis media, severe heart failure, pulmonary edema symptoms and signs.

Typhus rickettsia pneumonia symptoms common symptoms cyanosis dry cough, abdominal pain, chills, bloating, reaction, nausea, fever

The incubation period of this disease is 5 to 15 days. Most of the onset is rapid, high fever, chills, headache, muscle aches and body rash, often accompanied by slow reaction, paralysis, tremors such as hands and nausea, vomiting, bloating, abdominal pain, Constipation and other digestive symptoms, lung involvement can form typical rickettsial bronchopneumonia, manifested in a significant number of coughs after a few days of onset, mostly dry cough or a small amount of sticky sputum, with chest tightness and shortness of breath, respiratory growth rate becomes shallow, with Aggravation of the disease can occur in the lips and nail bed, chest auscultation can be heard and wet voice or sputum pronunciation, some patients due to milder conditions, only manifested as bronchitis changes, which is more likely to occur in endemic typhus, serious Symptoms and signs of heart failure and pulmonary edema.

Examination of typhus rickettsial pneumonia

1. Blood test: The white blood cell count is mostly in the normal range, a few are higher than 10×109/L, and occasionally below 5×109/L, the platelet count is decreased, and eosinophils are significantly reduced or disappeared.

2. Serological test:

Foreign Filipino reaction: Epidemic typhus patients can produce a higher-cost agglutination reaction to Proteus OX19 strain, especially at the peak of the onset of 2 weeks (between 1:320 and 1:5120), endemic typhus A similar agglutination reaction can also occur, but the agglutination potency is lower, mostly between 1:160 and 1:640.

Complement binding assay: The complement-binding assay with granular rickettsial antigen not only has group specificity, but also specificity, which can be used to distinguish between epidemic typhus and endemic typhus.

The positive reaction of the Rickettsia agglutination test is earlier than that of the external Fiji, and has a high group specificity to distinguish other rickettsial diseases such as tsutsugamushi, Q fever, and local typhus. The reaction is relatively weak.

3. Molecular biological examination: DNA probe technology or PCR method for detection of P. striata-specific DNA in specimens is fast, sensitive and specific, but it is suitable for experimental research and is difficult to be routine in clinical practice. Carry out.

4. Animal vaccination: guinea pigs are sensitive to Platts rickettsia. Patients with early onset of blood are inoculated into the abdominal cavity of male guinea pigs. After 7-10 days, guinea pigs have fever. A large number of pathogens can be found in the cytoplasm of peritoneal scraping. The scrotum of guinea pigs is only light. Redness, no obvious swelling, to distinguish from endemic typhus.

There is no characteristic change in chest X-ray examination, which can show the shadow of the lungs with spotted or patchy exudative density, with general pneumonia or bronchial pneumonia images, occasional leaves, and segmental lung consolidation shadows.

Diagnosis and identification of rickettsia pneumonia

The diagnosis is based on epidemiology, heat history, rash, chest symptoms and signs and external Fiji reaction. It is based on the epidemic season, the severity of symptoms, the nature of rash, the test of complement fixation, and the scrotal reaction of guinea pigs.

It must be differentiated from other diseases such as typhoid fever, leptospirosis, ascariasis, lobar pneumonia, influenza and other rash acute infectious diseases.

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