Scrub typhus

Introduction to tsutsugamushi Tsutsugamushidisease, also known as scrub typhus (scrubtyphus), is an acute infectious disease caused by Rickettsiatsutsugamushi. It is a natural epidemic disease, rodents are the main source of infection, and larvae are the vector. Its clinical features are acute onset, fever, rash, swollen lymph nodes, hepatosplenomegaly and eschar in the bite of larvae, and Jin Gehong has mentioned that the disease is prevalent in southern China more than 1600 years ago. It is called "sand heat". basic knowledge Sickness ratio: 0.001%-0.002% Susceptible people: no specific population Mode of transmission: insect vector transmission Complications: bronchial pneumonia pleurisy

The cause of tsutsugamushi disease

Rickettsia infection (90%)

Rickettsia is round, elliptical or short rod-shaped, the size is (0.3 ~ 0.6) m × (0.5 ~ 1.5) m, Gram staining is negative, Giemsa staining is purple, is an obligate intracellular parasitic Microorganisms, in smear staining microscopy, in the cytoplasm, especially in the cytoplasm of monocytes and macrophages, often found on the side of the nucleus is a cluster-like distribution of rickettsia rickettsia. Rodents are the main source of infection and storage, such as squirrels, yellow-breasted rats, house mice, and voles. Hares, rabbits, poultry and certain birds can also be infected with this disease. The larvae are the vector of the disease. There are more than 3,000 species of ticks, but those who can spread the disease are mainly scorpions, red carp and high lake carp. His life history includes eggs, larvae, nymphs, mites and adults. Only the parasitic life of the larvae camp needs to suck the body fluids of the animals, and the rest of the developmental stages are self-employed. Since the larva only bites the animal or the person once in the life, the larvae of the rickettsia are obtained from the mites infected with the ticks, and there is no chance of transmission in the present, and the larvae and pupa develop into adult worms to lay eggs. Rickettsia is passed on to the next generation (second generation) larvae. When the third generation of larvae licks animals or humans, rickettsia is introduced into the new host with saliva, so it is called intergenerational transmission.

Pathogenesis

After a person is bitten by an infected larvae, the rickettsia larvae first propagate locally, then enter the bloodstream, produce rickettsialemia, and then reach the body tissues of the body, clinical manifestations of toxemia, aphids The toxin released after the death of the rickettsia is the main cause of the disease. It can cause papules, eschar and ulcers in the local area, which can cause lymphadenopathy in the whole body. The lymph nodes near the eschar are particularly prominent. Necrosis, serosal cavity, such as chest, abdominal cavity, pericardial cavity visible yellow-green exudate, visceral hyperemia, spleen often hyperemia, can be swollen 2 to 5 times, liver is also swollen, myocardium can be focal or Diffuse myocardial inflammation, may have focal hemorrhage or degenerative disease, lung may have hemorrhagic pneumonia or secondary bronchial pneumonia, brain may have meningoencephalitis, the kidney may be a wide range of acute inflammatory lesions, the gastrointestinal tract is often extensive Congestive.

The histopathological changes of the disease are mainly in the vascular system. Focal or extensive vasculitis and perivascular inflammation can be seen. The lung, brain, heart and kidney are most prominent. Monocytes, lymphocytes and plasma cells infiltrate around the blood vessels. In severe patients, vascular endothelial cell edema and vascular wall necrosis and rupture can be seen. Rickettsia tsutsugamushi has been detected in vascular endothelial cells, macrophages and cardiomyocytes of various organs of patients.

Ascaria prevention

(1) Eliminating the source of infection is mainly rodent control, and the masses should be mobilized to use a combination of various rodent killers and drugs to eliminate rodents.

(2) Cutting off the route of transmission to eliminate weeds, transforming the environment, and eliminating the breeding ground is the most fundamental measure. When the field is in the field, the weeds within 50 meters of the surrounding area should be removed or incinerated, and then 1-2% of the dichlorvos should be sprayed. The ground can also be treated with a 40% dimethoate emulsion or a 5% malathion emulsion in a 1 solution at 20-25 ml/m2.

(3) Personal protection Avoid sitting on the grass on the side of the stream, drying clothes on the weed bushes, in the wild area military training, production labor, work activities, should tighten the cuffs, neckline and trousers, body exposed parts Rub 5% of dimethyl phthalate (ie, mosquito repellent), diphenyl phthalate, benzyl benzoate or potassium sulfide solution; to prevent cockroach larva bites, return to the camp area, bathe in time, change clothes If the larvae bite is found, it can be immediately picked up with a needle and coated with alcohol or other disinfectant.

(4) At present, there is no effective vaccine available for use. Those who enter the severely affected area can take doxycycline 0.1-0.2g or chloramphenicol 1g once every other day for 4 weeks.

Ascariasis complications Complications bronchial pneumonia pleurisy

There are bronchial pneumonia, encephalitis, pleurisy, otitis media, mumps, abortion, thrombophlebitis, DIC, septic shock, etc., occasional bleeding, intravascular hemolysis, etc., the domestic complications are less, to the bronchi Pneumonia and cardiovascular dysfunction are more common.

Symptoms of tsutsugamushi Common symptoms Severe headache, bleeding tendency, bacterial infection, maculopapular nosebleed, irregular heat conduction, block, hepatosplenomegaly, heart failure, ascites

The incubation period is 4 to 20 days, often 10 to 14 days.

The disease generally has no prodromal symptoms, and more sudden onset, body temperature rises rapidly, reaching 39 ~ 41 ° C, showing a continuous heat type, relaxation heat type or irregular heat type, lasting 1 to 3 weeks, while heating, more with Have chills or chills, severe headache, body aches, fatigue, lethargy, loss of appetite, nausea, vomiting, facial flushing, conjunctival congestion, photophobia, insomnia and cough, etc. Individual cases may also have eyelid pain, severe cases may occur Irritability, paralysis, hearing loss, tonic spasm, lethargy and coma, etc., can occur meningeal irritation and pathological nerve reflex.

The main signs include:

1. Anxiety and ulcers: the characteristics of this disease can be seen in 70% to 100% of patients. After being bitten by a larvae infected with rickettsial rickets, local red rash appears later, and it does not hurt. After the formation of blister, then necrosis and hemorrhage, followed by a black suede, called eschar, its edge protruding, surrounded by red, round or oval, varying in size, diameter can be 2 ~ 15mm, mostly 410mm; after the ecdysis falls off, it becomes an ulcer. The base part is light red granulation tissue. At first, there is often serum-like exudate, which is gradually reduced to form a smooth concave surface, occasionally secondary suppuration, most There are only 1 patient, occasionally 2 to 3 eschar or ulcers, and there are as many as 11 reports. Because larvae invade the human body, the odor is strong and the oppressed parts, the eschar is more common in the armpit. , scrotum, external genitalia, groin, perineum, perianal and belt compression, etc., but the head, neck, chest, back, abdomen, breasts and limbs are also found, because eschar is a bite of larvae, locust disease The gram body invades the part of the human body, so in theory Every tsutsugamushi patient should have eschar, about 30% of the patients in the bath, when changing clothes, you can find irritations that are not painful or itchy, and often found 1 to 2 weeks before the onset.

2. Lymph node enlargement: Lymph nodes near the eschar are often swollen, often accompanied by pain and tenderness. The superficial lymph nodes are also quite common. Generally, the older ones are like pigeon eggs, and the smaller ones are like broad beans, which can be moved. Found in the groin, underarms, behind the ear, etc., slow swelling, often in the recovery period of the disease can still be affected.

3. Skin rash: It occurs on the 2nd to 8th day of the disease course, and is more common on the 4th to 6th day. In a few cases, a rash may appear on the onset of the disease, or a rash may appear on the 14th day later. The incidence rate is different. 35.34%100%), may be related to the different stage of the disease at the time of the visit. The rash is mostly dark red congestive maculopapular rash, and there is also hemorrhagic, no itching, varying in size, 2 to 5 mm in diameter, and more scattered in the trunk. Department, development to the limbs, face rarely, palm and foot bottom less, a small number can be fusion measles-like rash, after 3 to 7 days, gradually subsided, no desquamation, but pigmentation, sometimes, in the course of disease A mucosal rash or bleeding point can be found on the soft, hard palate and buccal mucosa for ~10 days.

Some epidemic areas have mild patients with clinical manifestations of fever, headache, rash and swollen lymph nodes. These patients may have been cross-immunized by people who have been infected with serotypes of serotypes in the past.

4. Hepatosplenomegaly: hepatoma accounts for about 10% to 30%, splenomegaly accounts for about 30% to 50%, soft, smooth surface, no tenderness.

5. Others: tip of the tongue, often red, with white or yellow thick moss, conjunctival hyperemia is one of the common signs, while about 5% of patients may have subconjunctival hemorrhage, varicose veins visible in the fundus, blurred optic disc edge, edema, also visible Fundus hemorrhage, some patients with skin congestion, so there are facial and body skin flushing phenomenon, myocarditis is more common, heart rate can reach 120 times / min or more, heart sounds, pulse is weak, ECG can be T wave low or inverted, or conduction resistance Hysteresis, severe heart failure and circulatory failure may occur in patients with severe heart disease. The lung signs may vary depending on the condition. Lighter patients may have no obvious signs. Severe patients may develop interstitial pneumonia, mainly due to difficulty in breathing, and may develop cyanosis. There are secondary bacterial infections, which can be dry, wet voice, in addition, systemic hypersensitivity, testicular swelling and pain, scrotal swelling, low back pain and bloating.

Critical cases are severe multi-organ damage, heart, kidney failure, circulatory failure and bleeding, such as nosebleeds, gastrointestinal bleeding, etc., can also occur diffuse intravascular coagulation, if the patient's course of disease for more than 15 days, then The condition is often more severe, manifested as obvious multiple organ damage, heart, liver, kidney failure, shock, azotemia, bleeding tendency and coma.

Locust disease check

1. Blood: The number of white blood cells in the peripheral blood is reduced or normal. The severe patients can be slightly increased, and 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 tsutsugamushi rickettsia in the patient's serum can agglutinate with the Proteus OXK antigen to provide a basis for diagnosis. Only a few (about 30%) are positive, about 75% at the end of the second week, about 90% at the third week, and the titer can reach 1:160 to 1:1280. It begins to decline in the fourth week, and more than the 8th to 9th week. Turned negative.

(2) Complement binding test: high positive rate, strong specificity, and long-lasting positive time, up to 5 years, need to use local more common strains as antigen, also can use multivalent antigen, because of different strains The antigenicity of rickettsial rickets may vary widely.

(3) Immunofluorescent 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, peaked at the end of the second to third weekend, 60 days later. Gradually decline, but for several years, the report is still positive after 10 years of illness.

(4) Dot enzyme immunoassay: using various serotypes of tsutsugamushi rickettsia or part of protein as antigen, adsorbed on nitrocellulose membrane for dot enzyme immunoassay (dot-EIA), detecting patient serum The specific IgG and IgM antibodies of each serotype have 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, which is expressed by the genetic recombination technique, is used as an antigen, and enzyme-linked immunosorbent assays (ELISA) and enzymes are used. Immunoassay (EIA) was used to detect IgG and IgM antibodies against tsutsugamushi rickettsia in patients with serum, with sensitivity ranging from 86% to 88% and specificity ranging from 84% to 90%.

3. Pathogen examination:

(1) Isolation of pathogens: commonly used mice for tsutsugamushi rickettsia separation, the patient's blood can be inoculated into the peritoneal cavity of the mice, each inoculation 0.5ml, mostly on the 7th to 9th day after vaccination, dissecting the dying mice Can be found in both lung congestion, edema, liver, spleen, lymph node congestion and swelling, pleural effusion and ascites, ascites smear, peritoneum, mesentery, liver, spleen or kidney print, dry with Giemsa staining microscopy (enlarge 1000 to 1600 times), it can be found in the cytoplasm of monocytes and macrophages, and it is a cluster of tsutsugamushi rickettsia. When a tsutsugamushi rickettsia invades cells, it is suitable. Under the conditions of the local cytoplasm can be propagated into a mass, so it is often clustered. If the anti-mite disease rickettsial antibody is used for immunofluorescence test, under the fluorescence microscope, there is yellow-green fluorescence in the cells.

(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 tsutsugamushi, a common and different primers are 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 this disease. Diagnose and identify serotypes.

Severe complications of bronchial pneumonia, X-ray chest X-ray abnormalities.

Diagnosis and identification of tsutsugamushi disease

diagnosis

1. Epidemiological data: Should pay attention to whether you have been to the tsutsugamushi epidemic area within 4 to 20 days before the onset of illness, whether you have worked outdoors, open-air camping or sitting in the bushes, lying, etc. At the same time, you should also pay attention to the popular season, local The prevalence of the disease, etc.

2. Clinical manifestations: sudden onset, chills or chills, high fever, lack of appetite, facial flushing, superficial lymphadenopathy, hepatosplenomegaly, maculopapular rash, and characteristic eschar or ulcer, suspected of suffering from this disease Patients should pay great attention to finding eschar or ulcers, which are mostly located near the swollen, tender lymph nodes.

3. Laboratory inspection:

(1) Blood: The number of white blood cells in the peripheral blood is reduced or normal. The severe patients may increase slightly, and the classification often has a nuclear left shift phenomenon.

(2) Serological examination:

1Exo-Fif reaction: The exo-fibe reaction is also called the Proteus agglutination test. The antibody against tsutsugamushi rickettsia in the patient's serum can agglutinate with the Proteus OXK antigen, providing a basis for diagnosis. Only a few of the first week of the disease (30% or so) positive, about 25% at the end of the second week, about 90% at the third week, the titer can reach 1:160 ~ 1:1280, began to decline in the fourth week, and turned to the eighth to the ninth week negative.

2 Complement binding test: high positive rate, strong specificity, and long-lasting positive time, up to 5 years, need to use local common strain as antigen, can also use multivalent antigen, due to different strains of tsutsugamushi The antigenicity of rickettsia can vary considerably.

3 Immunofluorescent 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. However, it can last for several years and reports that the test is still positive after 10 years of illness.

4 spot enzyme immunoassay: using various serotypes of tsutsugamushi rickettsia or part of protein as antigen, adsorbed on the nitrocellulose membrane for dot enzyme immunoassay (dot-EIA), detecting the serum in each patient The serotype-specific IgG and IgM antibodies have high sensitivity and specificity, and can distinguish various serotypes.

5 enzyme-linked immunosorbent assay and enzyme immunoassay: a gene encoding the tsutsugamushi rickettsia protein with a molecular weight of 56×103 as an antigen, using enzyme-linked immunosorbent assays (ELISA) and enzymes Immunoassay (EIA) was used to detect IgG and IgM antibodies against tsutsugamushi rickettsia in patients with serum, with sensitivity ranging from 86% to 88% and specificity ranging from 84% to 90%.

(3) Pathogen examination:

1 pathogen isolation: commonly used mice for tsutsugamushi rickettsia separation, the patient's blood can be inoculated into the mouse abdominal cavity, each inoculation 0.5ml, more on the 7th to 9th day after vaccination, dissecting the dead mice can be found Double lung congestion, edema, liver, spleen, lymph node congestion and swelling, pleural effusion and ascites, ascites smear, peritoneum, mesentery, liver, spleen or kidney print, dried with Giemsa staining microscopy (magnification 1000 ~ 1600 times), in the cytoplasm of monocytes and macrophages, purple-red, plexiform distribution of rickettsia rickettsia, when a tsutsugamushi rickettsia invades cells, in suitable conditions Under the local cytoplasm can be propagated into a mass, so it is often clustered. If the anti-mite disease rickettsial antibody is used for immunofluorescence test, under the fluorescence microscope, there is yellow-green fluorescence in the cells.

2 Molecular biological examination: According to the nucleotide sequence of the major membrane protein antigen with a molecular weight of 56×103, which is encoded by Rickettsia tsutsugamushi, 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 strong specificity and is considered to be useful for the diagnosis of this disease. Identify serotypes.

Differential diagnosis

1. Leptospirosis is also often associated with leptospirosis, and both are more common in summer and autumn, with fever, conjunctival hyperemia, lymphadenopathy, etc. The disease often has gastrocnemius pain, subconjunctival hemorrhage, early renal damage, no rash, eschar or ulcer, serological and pathogenic examination if necessary, serum leptospirosis agglutination test 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, but no eschar, no lymphadenopathy, OX19 is positive for agglutination of proteus , while OXK is negative.

3. Before the onset of typhoid fever, there is often a history of unclean food eating, slow onset, gradually rising body temperature, relatively slow pulse, indifferent expression, abdominal distension, constipation, tenderness in the lower right abdomen, common rose rash, decreased total white blood cells, eosinophils Reduce or disappear, the fatda reaction can be positive, blood, bone marrow culture can have typhoid bacillus growth.

4. Septicemia often has primary infection lesions, relaxation heat type, irregular heat type is common, skin caused by Gram-positive bacteria often rash or pattern-like changes, caused by Gram-negative bacteria Frequent shock, increased white blood cell count, neutrophil enlargement, nuclear left shift phenomenon, foreign-Fiji reaction negative, blood, bone marrow culture may have pathogenic bacteria growth.

5. Dengue fever has lived or stayed in dengue fever epidemic area before, and there is a history of biting by Aedes mosquitoes during the day, more than the incidence of summer and autumn, headache, body pain is more significant, more often at the same time there are maculopapular and subcutaneous hemorrhage, total white blood cells And platelets are often reduced, dengue virus can be isolated from the serum of patients with a disease duration of less than 3 days, and the serum is positive for anti-dengue virus antibodies.

6. Epidemic hemorrhagic fever, high fever, headache, low back pain and eyelid pain are more obvious, when the body temperature drops, shock is more common, subcutaneous hemorrhage, common ecchymosis, oliguria or auria is common, blood leukocyte count is increased, atypical lymphocytes often More than 10%, platelets are significantly reduced, blood urea nitrogen and creatinine levels gradually increase with the prolongation of oliguria or anuria, serum specific antibodies against epidemic hemorrhagic fever virus.

7. Others should also pay attention to the differential diagnosis of influenza, malaria, acute upper respiratory tract inflammation, malignant histiocytosis, lymphoma and the like.

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