Visceral leishmaniasis
Introduction
Introduction to visceral leishmaniasis Leishmaniasis is a parasitic disease caused by Leishmania. The clinical manifestations of leishmaniasis caused by different species are different. It can be divided into visceral leishmaniasis (VL), skin. Three types of cutaneous leishmaniasis (CL) and mucocutaneous leishmaniasis (ML), visceral leishmaniasis, also known as kala-azar, is caused by Leishmania donovani Systemic diseases, with long-term fever, hepatosplenomegaly, decreased peripheral white blood cell count and increased plasma globulin are the main clinical features. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: mosquito bites Complications: pneumonia
Cause
Etiology of visceral leishmaniasis
(1) Causes of the disease
The pathogens causing visceral leishmaniasis are the subspecies of Leishmania donovani, the subspecies of Leishmania donovani and the subspecies of Leishmania donovani. Some scholars believe that these three species are independent insect species. Recently, it has also been reported that tropical Leishmania (L.tropica) can also cause visceral leishmaniasis. The life history of leishmaniasis includes promastigote and amastigote (formerly known as Lido In the two phases, the former is found in the white scorpion and in the culture medium. The latter is found in the mammalian host. The anterior flagellum is conical, the front end is wider, and the rear end is sharper. The size is 15-25 m×1.5-3.5 m. There is a flagellum protruding from the front of the front part of the body, the core is located in the center, the moving base is located at the front, the flagellar body is elliptical, the size is 2.9 ~ 5.7m × 1.8 ~ 4.0m, inside the core and moving matrix, when white At the time of bite, the animal or the hostless body of the storage host enters the white sputum and transforms into the promastigotes. After 7 days of development and reproduction, the promastigotes enter the white sputum. When the bite is taken from a human or other animal host, the promastigotes enter In the body, it is phagocytized by phagocytic cells, transformed into an amastigotes and propagated, and is taken to various organs of the reticuloendothelial system to continue to multiply. The morphology of various Leishmania species is not significantly different except for the size. Identification of species based on isozyme electrophoresis and DNA analysis.
(two) pathogenesis
When the promastigotes of Leishmania donovani enter the human body from the white scorpion, it is engulfed by the host's phagocytic cells, and the glycoprotein Gp63 on the promastigotes can bind to the C3 receptor on the surface of macrophages. Another macromolecular phospholiposome (LPG) on the surface of the membrane activates complement, allowing C3 to settle on the surface of the worm and attaching the worm to the macrophage via the CR3 (C3biR) receptor. After being phagocytosed, the promastigotes are transformed into amoeto-free bodies and multiply in macrophages until the phagocytic cells burst, and the flagellates are swallowed by other phagocytic cells and continue to multiply, resulting in a large proliferation of the reticuloendothelial system. Lymph node enlargement and liver and splenomegaly.
The pathological changes are mainly liver enlargement, Kupffer cell proliferation, cytoplasm filled with a large number of amastigotes, often with plasma cell infiltration, splenomegaly, a large number of phagocytic cells and reticulocyte proliferation in the myelin, and plasma cell infiltration The sinusoidal endothelial cells proliferate, and there are a large number of mitochondria in the phagocytic cells. The number of spleen nodules is significantly reduced, the structure is unclear, and the atrophy is markedly atrophy. The lymphocytes in the thymus-dependent region around the central artery are almost completely lost, and the blood cells are reduced. Related to hypersplenism.
Prevention
Visceral leishmaniasis prevention
(1) Elimination of infectious sources: use pathogens or serological methods to detect sick dogs in endemic areas and kill them. The census patients were treated and found to be treated promptly.
(2) Elimination of the medium: spraying insecticides (such as dichlorvos, trichlorfon) in the endemic areas to eliminate white peony, 2.5% deltamethrin bath or spray dog body in the day of white peony (for each dog) 2-3 grams).
(3) Personal protection: Use mosquito nets during the day of chalking, pay attention to indoor sanitation, and if it is found to have white peony, it should be sterilized in time. Care should be taken when going out to work, and the repellent should be applied to the exposed parts of the skin to prevent mosquito bites.
Complication
Visceral leishmaniasis complications Complications pneumonia
Pneumonia is more common in children, the prognosis is poor, acute agranulocytosis is often seen in adult cases. If not treated in time, it will die within 2 weeks. Trauma or necrotizing stomatitis is a serious complication due to antibiotics. Widely used, it is now very rare.
Symptom
Symptoms of visceral leishmaniasis Common symptoms Abdominal pain Joint pain Fatigue macules Nasal bleeding Insufficient diarrhea Appetite deficiency Skin gradually dark black bloating
Incubation period
The incubation period of this disease is 3 to 3.5 months, and some can reach 5.5 months or longer.
2. Clinical symptoms and signs
The common symptoms of this disease are fever. The typical type is bimodal fever type, which may also be a relaxation heat type or a heat retention type, often accompanied by sweating, fatigue, general malaise and weakness, mild lymph node swelling and liver. Splenomegaly, the latter is particularly obvious, sometimes the skin may have maculopapular rash, erythema or hypopigmentation, scraper can find no flagellate, rash can also appear after treatment, the latter is called skin leishmaniasis after kala-azar (PKADL, post kala-azar dermal leishmaniasis), peripheral blood leukocytes are significantly reduced, followed by anemia, nosebleeds, gum bleeding or skin imperfections, patients with heavier infections, the skin of the limbs, etc. gradually dark black, so this The disease is also known as kala-azar.
3. Clinical type
Li Zongen and Zhong Huizhen (1935) divided the early clinical manifestations of the disease into the following clinical types:
(1) Tuberculosis type: slow onset, fever in the afternoon, night sweats, cough, lack of appetite, often misdiagnosed as tuberculosis.
(2) Typhoid type: About 1/3 of the cases have fever, headache and other symptoms, followed by body temperature rise to 39 ~ 40 ° C, continued non-return, and constipation and abdominal distension, splenomegaly and decreased peripheral blood white blood cell count Very similar to typhoid fever.
(3) Wave heat type: Sometimes the patient's heat type is wavy, sweating more, splenomegaly and the number of white blood cells in the peripheral blood are reduced, similar to brucellosis, but no joint pain.
(4) Malaria type: chills, fever and sweating, similar to the onset of malaria, can occur once a day or every day, usually only 2 to 3 days in a row, but it can last for several weeks.
(5) Bimodal fever type: About 1/3 of the early cases showed a bimodal fever type, that is, the body temperature had two rise and fall within 24 hours, one in the morning and the other in the afternoon or night.
(6) Respiratory tract infections: The initial symptoms of many cases are similar to upper respiratory tract infections, some of which may be similar to the flu.
(7) Gastrointestinal type: common in children, manifested as gastrointestinal discomfort, mild diarrhea, constipation, abdominal pain and so on.
Examine
Examination of visceral leishmaniasis
The number of white blood cells and neutropenia in the peripheral blood of the patient decreased, followed by the number of platelets and the number of red blood cells, and the amount of globulin in the plasma increased significantly. Therefore, the globulin water test was also positive, and the thymol turbidity test was also positive, and the erythrocyte sedimentation rate increased. .
Serum immunological examination
Commonly used are direct agglutination test (DAT), complement fixation test (CFT), indirect fluorescent antibody technology (IFAT) and enzyme-linked immunosorbent assay (ELISA), in which DAT, IFAT and ELISA are sensitive, ELISA and leprosy patients have crossover Response, detection of serum circulating antigen (CAg) is of great value for the early diagnosis and efficacy evaluation of this disease.
2. Molecular biology examination
The KDNA of Leishmania in patients was detected by PCR, which has high specificity and sensitivity, and can be used for early diagnosis and evaluation of curative effect.
Late spleen hyperfunction, B-ultrasound showed liver and spleen.
Diagnosis
Diagnosis and diagnosis of visceral leishmaniasis
diagnosis
The diagnosis of this disease is mainly based on:
1. The epidemiological history of patients with long-term fever from endemic areas should consider the possibility of the disease.
2. Clinical manifestations of long-term fever, hepatosplenomegaly, accompanied by a decrease in the number of peripheral blood leukocytes and a significant increase in plasma globulin, should be suspected and the disease for further examination.
3. Positive for serum immunology or molecular biology.
4. Parasitological examination of patients with Leishmania and no flagellate in the bone marrow smear is the main basis for the diagnosis of this disease. In clinically suspected cases and bone marrow smear negative, it can be used for spleen smear examination, the positive rate is higher Bone marrow puncture is high.
Differential diagnosis
The disease should be related to tuberculosis (usually tuberculosis in the lungs or other parts, anti-tuberculosis treatment is effective), typhoid fever (relatively slow pulse, obvious symptoms of poisoning, positive for fat, positive for blood culture), brucellosis (with cattle) , sheep, pigs and other livestock contact history, headache, joint pain, serum Brucella agglutination test positive) and other disease identification.
