African trypanosomiasis
Introduction
Introduction to African trypanosomiasis African trypanosomiasis, also known as African sleep sickness or sleepiness encephalitis, is a disease transmitted by parasitic single-celled trypanosomes through tsetse bites. It is raging in sub-Saharan Africa, and some of the prevalence areas are as high as 80%. Symptoms such as fever, rash, edema, and swelling of the lymph nodes may occur at the beginning of the patient, and inflammation may occur in the brain and meninges. The condition of East African trypanosomiasis can deteriorate rapidly, and the affected condition of the brain is earlier and more than that of West African trypanosomiasis. In the late stage of trypanosomiasis, other nervous system problems may occur slowly, and the situation of lethargy will continue to increase, eventually leading to coma and death, and the name of sleepy encephalitis is also named. Patients with high fever should be diagnosed and treated early, usually through appropriate drugs and treatment, can be cured. basic knowledge The proportion of illness: 0.001% - 0.002% Susceptible people: no special people Mode of infection: contagious Complications: malnutrition, epilepsy
Cause
Causes of African trypanosomiasis
Pathogen infection (45%):
The pathogen is Trypanosoma brucei, which extensively invades wild animals and livestock. Three subspecies can cause disease to humans, namely Tbgambiense, Tbrhodesiense, Brinell. Tbbrucei, the former causes Gambia trypanosomiasis, the second causes Rhodesia trypanosomiasis, the latter mainly causes wild animals and livestock (bovine-based) nagana disease, rarely caused Clinical cases, so it is not detailed.
The extracellular parasitic worms of the Trypanosoma brucei are closely related in their subspecies. Therefore, there is a nucleus in the center of the worm body, and there is a moving matrix at the back end. The flagella attaches to the moving matrix and reaches the worm along the wavy membrane of the worm body. After the front end of the body is free, the shape of the trypan worm is variable, and the shape is long spindle-shaped. It has a slender shape (length 20 ~ 40 m, free flagella length of 6 m) or a thick short type (length 15 ~ 25m, width 3.5m, free Flagella is shorter than 1 m or flagella is not free. Slim is more common in peripheral blood and is fusiform; thick and short are more common in tissues.
Its life history is divided into the teetee fly, which belongs to the genus Glossinae and the human body. When the tsetse sucks the patient or the sick animal (beast) blood, the trypanosome enters the fly with the blood. The midgut divides and multiplies, penetrates the intestinal wall and swims to the anterior stomach to enter the esophagus, forms the upper flagellate body in the parotid gland, and finally forms an infectious flagellate. This stage takes about 12 to 30 days and makes the flies live for three months. It is contagious. In the human body stage, when the infective tsetse bites the human body, the trypan worm enters with the saliva, enters the bloodstream after local division and reproduction, and is mainly slender during the climax of worm. When the body produces immunity, it is more common in the form of thick and short.
The three subspecies of Trypanosoma are very similar. In the past, they mainly relied on their virulence, biochemical characteristics (isozymes) in certain animals, their breeding in the fly, clinical characteristics and popular areas. In recent years, they have been used. Molecular biology techniques to identify.
Pathogenesis:
When the fly maggot bites, it often causes subcutaneous hemorrhage. The trypanosome develops and breeds here, causing an inflammatory reaction, sometimes causing a hard squat. Later, the trypanosome enters the blood circulation and the lymphatic system, continues to divide and multiply, spreads the whole body, and forms a lymphatic blood phase (phase I). Trypanosoma can cause the body to produce antibodies, and its reproduction is also limited by antibodies. However, due to the mutated nature of the glycoprotein antigen on the surface of trypanes, the parasites evade the host's immune response, that is, "immune evasion", resulting in a large amount of IgM in the host. While trypanosomes can still survive in the human body for a long time, and manifest as fluctuations in parasitemia, antigen-antibody reaction is also a factor causing disease. Long-term infection, trypanosome can cause meningoencephalitis in the central nervous system (phase II) ).
Early lymph nodes and spleen enlargement, lymph node biopsy is positive for trypanosomiasis, cell infiltration more than 6 months after the disease and connect with connective tissue, intracardiac, adventitia can be seen spotted and massive bleeding, myocarditis is more common, manifested as heart Hypertrophy, pericarditis and effusion, central nervous system lesions, early meningeal lymphocytes, plasma cells and macrophage infiltration, late encephalitis, brain tissue congestion and scattered bleeding, and can be found in trypanosomes After 1 to 2 years, the basal ganglia, the midbrain, the diencephalon, the white matter, the gray matter and the peripheral nerves are demyelinated, and finally cause subcortical atrophy, hepatic bleeding, congestion and focal necrosis.
Prevention
African trypanosomiasis prevention
The main measures to combat trypanosomiasis include the discovery, treatment of patients and the elimination of tsetse flies. Change the environment of insect insects, such as clearing shrubs and spraying insecticides. The therapeutic drug suramin has a good effect on various early stages of sleeping sickness. Other drugs include pentamidine and melatonol (mela arsenic alcohol), etc., and the curative effect is good. For cases involving the central nervous system, organic arsenic should be used for treatment.
The basis for controlling Gambia trypanosomiasis is to census and treat a large number of asymptomatic infected persons, especially those with enlarged lymph nodes. At the same time, to treat patients and strengthen management of livestock, the "fragrance" trapping machine can be used to kill tsetse flies once. It can kill thousands of grams, which is a very effective way to reduce the threat of tsetse flies; and because the tsetse fly is easy to repeat, it takes 1 time / 6 months, because the incubation period of Gambia trypanosomiasis is long, so it is difficult to see in time. The effect of reduced morbidity has recently been used in the epidemic area of Rhodsia in Uganda, and it has been successful in collecting tsetse fuzzing machines. Because of the short incubation period of Rhodesia trypanosomiasis, it can be seen in time. The effect of the control.
Complication
African trypanosomiasis complications Complications malnutrition epilepsy
Complications are highly malnourished, secondary infections in the lungs, status epilepticus or heart failure.
Symptom
Symptoms of African trypanosomiasis common symptoms amenorrhea myalgia coma reaction dull secondary infection weak ataxia gait instability sensation senile diarrhea
The severity and development process of two types of trypanosomiasis are different. For example, the Gambian type is asymptomatic after infection, and it can last for several months or even several years. About half of this stage has cervical lymphadenopathy, and there is no squat in the initial stage. Lymphatic blood stage symptoms are mild, meningoencephalitis appears later, and progress is slow. Rhodessia type incubation period is 2 to 3 weeks. The incidence is acute, the condition is heavy, and there are many symptoms of acute poisoning, such as high fever, obvious weight loss, rapid failure, and There are secondary infections or myocarditis, but the lymphadenopathy is mild. Natural processes often die from toxemia within 6 to 9 months. Meningoencephalitis can occur early and progress rapidly, but there are also typical sleep symptoms. Those who have not yet appeared, the trypanosomiasis is divided into three phases according to the course of the disease:
1. Initial: After 2 to 3 days of infective tsetse bites, local skin redness and swelling, accompanied by pain and tenderness, the texture is hard, that is, the trypanosomal "squat", its diameter is about 3 ~ 10cm, the formation of ulcers is rare, often There is a local lymph node enlargement, and the "squat" is dissipated by itself after 2 to 4 weeks, and the "squat" is squeezed. In the extruded edema fluid, trypanosomes can sometimes be found, but only a few patients are treated at this stage.
2. Lymphatic blood phase: (In the period of trypanosomiasis, the latent period of phase I is generally 10 days to 3 weeks, and individual cases can be as long as 5 years. When the trypanosome enters the blood circulation through the lymphatic system, irregular or intermittent high fever may occur. With severe progressive headache, fatigue, itchy skin, myalgia and joint pain; and progressive lymphadenopathy, which may be localized or systemic, Gambian type is more common in the neck, especially in the posterior triangle, called Winterbottom The Rhodesia type is mainly on the clavicle, the armpit and the groin, and its location may be related to different tick and bite habits. The enlarged lymph node is 1 to 2 cm in diameter, soft and no tenderness, and can be active. More often.
The fever period lasts for 1 week or more, that is, intermittently. With the mutation of the trypanosome antigen, the immune escape occurs and the fever is re-started regularly. The worm is obvious in this period, and the fever can be very light, especially the Gambian type. The temporary rash can be used. Patients found in superficial skin are more common in the chest and upper abdomen. They usually appear 6 to 8 weeks after the onset of the disease. They are oval, ring-shaped, and reddish. After a few days, the fever subsides. As the disease progresses, the fever gradually decreases. Very rare, during this period can occur different organ damage, such as fatal myocarditis, prominent in the Rhodesian type, moderate swelling of the spleen accounted for about 25% to 50%, liver can be swollen and serum AST and ALT is elevated, patients are prone to secondary bronchopneumonia, iridocyclitis, optic atrophy, periodic diarrhea, mucus and blood, anemia, peripheral edema, ascites, pericardial effusion and Pulmonary edema, in addition to men with impotence, women of childbearing age can amenorrhea or abortion.
3. Meningoencephalitis (sleeping, late, stage II): The central nervous system symptoms are mainly advanced, at this time the patient's weight is significantly reduced, and soon can not afford normal work, headache becomes persistent, response Slow, drowsiness, and progressive deterioration, with the exception of nighttime insomnia, clinically causing meningoencephalitis, Rhodesian type seen 2 to 6 weeks after the disease, rapid progress, Gambian type seen in the months after the disease months, several years, cone The worm first invades the brainstem and the diencephalon, and then the cortex. The symptoms are personality changes, indifferent to the surrounding things, expressionless, slow-moving, speech-through, slow-sensing hypersensitivity (lightly pinching the deep muscles of the patient, it takes a little while to feel pain , the degree of pain is heavier than normal, ie kerandel sign), lip and tongue tremor, muscle tremor, gait instability, reverie, mania, obvious mental illness, and epilepsy convulsions, etc., chorea-like movements and ataxia are more common in children As the disease progresses, muscle rigidity, lethargy, followed by lethargy, coma, accompanied by generalized itching, cerebrospinal fluid examination at this stage can see an increase in white blood cell count, usually >100 × 106 / L, the end of the death from high malnutrition, secondary infection of the lungs, status epilepticus or heart failure.
People from African endemic areas have found that the trypanosomal "squat", irregular fever, severe headache, lethargy, lethargy, swollen lymph nodes, and tachycardia are helpful for diagnosis. The diagnosis depends on the discovery of pathogens.
Examine
African trypanosomiasis
The increase of macroglobulin in anemia and blood is the most prominent. The early IgM increases, which can reach 8-12 times of normal value within 15 days after onset. The increase of IgM in cerebrospinal fluid is also earlier, and it is earlier than the increase of white blood cells and protein. It is 100 mg/L.
Acute Rhodesia type, especially fever, can be found in peripheral blood or tissue fluid, and can be found by wet specimens or Giemsa staining. Gambia type is generally difficult to find pathogens, in the early "squat" or enlarged lymph nodes (such as posterior neck knot) Section) Puncture aspirate, may find pathogens, thick blood smear or blood concentration, bone marrow smear and cerebrospinal fluid after centrifugation may be positive, can also be used for animal inoculation, Rhodesia type can be inoculated in large, white mice; Gambia type The monkey should be inoculated, and the blood of the inoculated animal should be inspected after 2 weeks, and it can also be cultured in NNN medium.
Patients with trypanosomiasis must be tested for cerebrospinal fluid because their treatment depends on whether they have meningoencephalitis. At this time, the pressure of cerebrospinal fluid is often increased, the number of cells, especially lymphocytes, is increased, the protein is slightly increased, and IgM is significantly increased. Centrifugal cerebrospinal fluid may be Find the pathogen.
Immunodiagnostic test: The most commonly used antibodies are specific antibodies detected by IFAT and ELISA. They are commonly used for screening, especially for large-scale screening. However, pathogens must be searched before treatment, and trypanosomal antigen of serum or cerebrospinal fluid can be detected by monoclonal antibody ELISA. .
Examination of cerebrospinal fluid during meningoencephalitis showed an increase in white blood cell count, usually 7100 × 106 / L.
Diagnosis
Diagnosis and identification of African trypanosomiasis
The trypanosomal "squat" should be differentiated from other insect bites, cellulitis or coke. The lymphatic phase should be differentiated from feverous diseases such as malaria, typhoid fever, relapsing fever, viral hemorrhagic fever, and late stage cerebral malaria. Viral encephalitis, acute phase of bacterial meningitis, tuberculous meningitis, neurosyphilis and cerebrospinal fluid in the differentiation of various meningitis or meningoencephalitis with mononuclear cells, should pay attention to the occasional syphilis serum Test positive.
