Table of contents:
- Trypanosomes, trypanosomiasis
- Epidemiology of trypanas
- Trypanosome - etiology
- Trypanosome - diagnosis
- Clinical picture of trypanosomiasis
- Trypanosome - symptoms
- Trypanosomiasis treatment
Video: Trypanosome: Symptoms, Treatment, Diagnosis And Prevention
2023 Author: Riley Dean | [email protected]. Last modified: 2023-05-24 12:07
Trypanosome is the simplest unicellular organism that causes a serious parasitic disease in humans - trypanosomiasis. The carriers of this infection are flies and bugs. The incubation period of the disease in humans lasts up to a year. Trypanosomiasis is extremely difficult to tolerate, it is accompanied by symptoms such as fever, headache, insomnia, weakness, anxiety, skin reactions. In severe cases, damage to internal organs and death are possible.
The content of the article:
- 1 Trypanosomes, trypanosomiasis
2 Epidemiology of trypanas
- 2.1 African trypanosomiasis
- 2.2 American trypanosomiasis
- 3 Trypanosome - etiology
4 Trypanosome - diagnosis
- 4.1 African trypanosomiasis
- 4.2 American trypanosomiasis
5 The clinical picture of trypanosomiasis
- 5.1 African trypanosomiasis
- 5.2 American trypanosomiasis
- 6 Trypanosome - symptoms
7 Treatment of trypanosomiasis
- 7.1 African trypanosomiasis
- 7.2 American trypanosomiasis
Trypanosomiasis - tropical infections transmitted from pathogens belonging to the type of protozoa.
It was first described in 1902 in blood and in 1903 in a patient's cerebrospinal fluid. For her, a person is the main owner, and pigs may serve as an additional one. The flies Glossinapalpalis, Glossinatachinoides act as carriers. The Gambian form of African trypanosomiasis refers to anthroponosis (infections transmitted from person to person). The incidence can take the form of epidemic outbreaks, most often during the dry season of the year.
The Rhodesian trypanosome was described in 1909-1912. For her, the main reservoir is the forest antelope, the additional reservoir is various wild animals, sometimes cattle and humans. Flies Glossinamorsitans, Glossinapallidipes and others serve as vectors. Both types of parasites are morphologically identical. The body is curved, narrowed at both ends, equipped with a flagellum and an undulating membrane.
Trypanosome. Body length 15-40 μm, width 1.4-2 μm. The Rhodesian (East African) form of African trypanosomiasis is a zoonotic natural focal invasion. Infection of people occurs mainly during their stay in the territory of natural foci. Trypanosomes are dangerous parasites of humans and animals that cause serious diseases. Some types of trypanosomes cause sleeping sickness.
The carrier of African trypanosomiasis (as this disease is scientifically called) is the tsetse fly. This is a blood-sucking insect. The route of transmission is as follows: the tsetse fly bites an infected animal, its blood is full of parasites that cause disease. The fly drinks this blood and the parasites along with the blood enter the insect's intestines. There the parasites multiply and gradually move to the salivary glands and salivary ducts. When a healthy animal bites, parasites enter its bloodstream.
First, trypanosomes - the simplest unicellular organisms multiply at the site of the bite, then penetrate the bloodstream. Fever is observed, lymph nodes are enlarged. The parasites then enter the nervous system. And the most "fun" begins: severe headaches, confusion, drowsiness, and as a result - coma. Without the right treatment, almost one hundred percent death. Trypanosomes float and cause dangerous disease.
Epidemiology of trypanas
The blood-sucking tsetse flies are carriers of trypanosomes. The development of larvae and pupae occurs in moderately moist and shaded areas of the soil. Tsetse flies feed on human and animal blood. In insects, the trypanosome goes through a development cycle lasting about 20 days, ending in the formation of invasive (infectious) metacyclic forms of trypomastigotes.
Invasive flies transmit trypanosomes to humans through bloodsucking throughout their entire life, which lasts several months. One bite of an infected tsetse fly is enough for the development of the disease, since it secretes up to 40 thousand tons with saliva in one bite.
Transmission of infection is possible during blood transfusions (blood transfusions of trypanosome carriers to healthy people). The Gambian form of African trypanosomiasis refers to anthroponosis (infections transmitted from person to person); pigs may be an additional carrier and source of infection.
The carriers of the pathogen live in the so-called gallery forests and thickets along the banks of rivers and streams. The disease is common in West and Central Africa. The incidence can take the form of epidemic outbreaks, most often during the dry season of the year.
Trypanosome. The Rhodesian (East African) form of African trypanosomiasis is a zoonotic natural focal invasion. The main reservoir is the forest antelope, other wild animals, and sometimes cattle. The disease is common in the savannas of Eastern and Southern Africa. Infection of people occurs mainly during their stay in the territory of natural foci.
Usually, the Rhodesian form of trypanosomiasis is recorded in the form of isolated cases, but epidemic outbreaks have also been noted. More often men are ill. In recent years, outbreaks of trypanosomiasis caused by an animal parasite have been described among the population of Ethiopia. Importation of African trypanosomiasis to Russia is possible.
Bedbugs are the main vectors of American trypanosomiasis. Infection of bedbugs occurs when they feed on human or animal blood containing trypomastigotes. After 10-30 days, invasive (infectious) trypomastigotes appear in the rectum of the bug, excreted outside.
Once infested, bugs retain trypanosomes throughout their entire life (about 2 years). Trypanosomes enter the human or animal body when bitten with bugs' faeces. The alimentary route of infection (with food) and transmission of infection during blood transfusions are also possible.
The infection can also spread vertically (through the placenta). Known synanthropic (located near human habitation) and natural foci of Chagas disease. In the centers of the first type, bugs live in adobe houses, barns, poultry houses, and burrows of house rodents. In these foci, in addition to humans, the carriers of the pathogen are dogs, cats, pigs and other domestic animals.
In natural foci, the reservoirs of the pathogen are armadillos, anteaters, foxes, monkeys, etc. People are infected in the warm season when visiting these foci, when the carriers are most active.
Men are more often infected. Chagas disease is recorded throughout the year in all age groups, but more often in children. Isolated cases are more typical, but epidemic outbreaks are possible with a massive attack of triatom bugs on people. Chagas disease is widespread, it is detected in almost all countries of the American continent, especially significant foci are located in Latin American countries south of Mexico. The most frequent cases of the disease are registered in Brazil, Argentina, Venezuela. In other parts of the world, infection does not occur.
Trypanosome - etiology
Trypanosome - the causative agents of African trypanosomiasis - go through a complex development cycle with a change of hosts. Part of the cycle is carried out in the body of vertebrate hosts (humans, animals), the other part - in the body of insects.
Trypanosomes go through two stages of development - the tripomastigote stage and the epimastigote stage. In the causative agent of American trypanosomiasis, two more stages are described - the promastigote stage and the amastigote stage. Tripomastigotes parasitize only in humans and only in insects.
Trypanosome. Entering with blood into the body of the tsetse fly (a carrier of African trypanosomiasis), trypanosomes enter the salivary ducts and glands, where they turn into epimastigotes. After 2-5 days, the epimastigotes transform into trypomastigotes, and the flies become infectious. Getting into the organism of triatomaceous bugs (carriers of American trypanosomiasis) with blood, trypanosomes in the stomach of the insect turn into epimastigotes and multiply here for several days.
Then they pass into the posterior and rectum, where they return to the trypomastigous form. From this point on, bedbugs become infectious. African and American human trypanosomiasis are known.
- African trypanosomiasis: African trypanosomiasis, or sleeping sickness, is a vector-borne infection transmitted through blood-sucking vectors, in this case the tsetse fly, characterized by periods of irregular fever, skin rash, local edema and lymphadenitis, cachexia (wasting), and lethargy. It exists in two forms - Gambian and Rhodesian (East African), differing in epidemiology and characteristics of the clinical course. A detailed study of the phases of trypanosomiasis in the body of the tsetse fly was carried out in 1909. The second causative agent of sleeping sickness in Africa was described in 1909-1912;
- American trypanosomiasis: American trypanosomiasis is Chagas disease. In 1907, Chagas discovered a trypanosoma in the intestines of a bug, in 1909 he isolated a trypanosoma from a patient, identical to that found in a bug.
Trypanosome - diagnosis
The diagnosis is established on the basis of epidemiological, anamnestic, clinical and laboratory data. Decisive in the diagnosis is the detection of trypanosomes in the punctates of the lymph nodes, cerebrospinal (cerebrospinal) fluid, bone marrow, and also in the peripheral blood during the febrile period of the disease. Immunological diagnostic methods are used, of which the complement binding reaction is the most sensitive;
Trypanosome. The diagnosis is established on the basis of various data and is confirmed by the isolation of trypanosome from the primary affect, blood, cerebrospinal fluid, punctates of the lymph nodes, spleen, bone marrow and other organs. A biological test is carried out on guinea pigs. Serological tests are used (mainly in the chronic stage), most often RSK. An intradermal allergic test is used, as well as some other reactions.
The prognosis for severe Chagas disease (especially in children) is serious due to the frequent development of meningoencephalitis. In adults, the prognosis for life is more favorable, but questionable for recovery. Developing heart failure limits the patient's social activity, sharply reduces life expectancy.
Clinical picture of trypanosomiasis
The incubation period for the Gambian form of trypanosomiasis is 2-3 weeks, and for the Rhodesian form - 1-2 weeks. In the clinical picture, two stages are distinguished: early, or hemolymphatic, and late, or meningoencephalitic. At the site of the tsetse fly bite, after the incubation period, a red nodule 1-2 cm in size with a white waxy zone around (trypanosomal chancre) appears.
The incubation period for the Gambian form of trypanosomiasis is 2-3 weeks, and for the Rhodesian form - 1-2 weeks.
The chancre persists for several days and then disappears, leaving behind a pigmented scar. This is followed by a fever of the wrong type, lasting for weeks. The characteristic signs of the disease include skin rashes (trypanids) on the skin of the chest, back, face, legs. Sometimes patients have elements of a nodular type, as well as an itchy papular rash.
Trypanosome. Local edema is often observed, which is localized on the face, eyelids, neck, lasts a short time and disappears without a trace. Lymphadenitis is a persistent and early symptom of African trypanosomiasis. In the last stage of the disease, the most noticeable are the lymph nodes in the posterior triangle of the neck - a harbinger of the patient's death. The liver and spleen are usually enlarged.
The lesions of the central nervous system gradually develop - increased fatigue, insomnia, headaches, hyperesthesia (increased sensitivity to stimuli), mental disorders. Anemia develops. The early (hemolymphatic) stage lasts from several weeks or months to several years. If trypanosomiasis at this stage did not end in death or recovery, then the second, late (meningoencephalitic) stage, or sleeping sickness itself, begins.
The cardinal symptom of the meningoencephalitic stage is increasing sleepiness during the day, sleep can be very deep. As the pathological process develops, fibrillar twitching of the muscles of the face, tongue, trembling hands and feet appear. In the future, the trembling is replaced by convulsions and paralysis of the limbs. The numbness of the cervical muscles appears. In the terminal period, the patient lies, indifferent to everything around him. In parallel with lethargy, cachexia develops, from which the patient's death occurs.
Rhodesian and Gambian forms of African trypanosomiasis differ in some features of the clinical course. The Rhodesian form is more acute and quickly ends in death. The disease rarely lasts more than a year, loss of performance occurs from the very onset of the disease, febrile periods follow one after another. Severe cardiovascular disorders are characteristic. Often, patients do not live to see lethargy.
The Gambian form has a relatively more benign course, it can last for several years, patients remain able to work for a long time. But among Europeans, this form of trypanosomiasis is acute;
Trypanosome. The incubation period is 7-14 days. At the site of trypanosome insertion, a primary affect is formed - "chagoma" (an inflammatory dark red hard seal) with lymphangitis and an increase in regional lymph nodes.
At 4-6 weeks from the onset of the disease, the infection spreads. Malaise, headaches and muscle pains appear, body temperature rises to 38-40 ° C. Fever is persistent or remitting and persists for at least 2 weeks. Often, a small, patchy rash appears on the skin, which lasts 8-20 days. The lymph nodes are enlarged, painful.
The liver and spleen are enlarged. The cardiovascular system suffers, all signs of heart failure appear, which is the main cause of death in Chagas disease. The development of meningoencephalitis, which leads to the death of the patient in the early stages, is unfavorable in terms of the prognosis of the disease. The latent (latent) stage of the disease follows the acute one, if the latter ended in clinical recovery, but the pathogen did not get rid of.
There is no clinical symptomatology in patients with the latent form of American trypanosomiasis. In the chronic stage of American trypanosomiasis, two clinical forms are distinguished - cardiovascular and nervous. With the cardiovascular form, chronic damage to the heart muscle develops with severe circulatory failure.
With a nervous form, convulsions and paralysis develop. Cases of chronic American trypanosomiasis with insufficient thyroid function and the development of myxedema (widespread edema) have been described.
Trypanosome - symptoms
The incubation period is 2-3 weeks for African and 1-2 weeks for American trypanosomiasis. At the site of invasion of the pathogen, a "primary affect" is formed in the form of a nodule up to 2 cm in diameter with an infiltrated base, dark red in color. After 5-7 days, the nodule disappears, leaving behind skin pigmentation and sometimes a scar.
Trypanosome. The first period of the disease (up to a year) corresponds to the generalization of the infection and dissemination of the pathogen. Skin lesions are found with great consistency. Ring-shaped erythema, plaques with swelling of the skin around them, usually localized on the trunk and less often on the extremities are typical. These elements of the rash resemble those of tick-borne borreliosis (Lyme disease).
They evolve within a few weeks, reaching a diameter of 5 cm or more, disappearing without a trace after 1-3 months. Occasionally, a profuse itchy papular or pinpoint rash occurs. Catarrhal and hemorrhagic conjunctivitis is observed. In American trypanosomiasis, unilateral conjunctivitis with swelling of the eyelids (Roman symptom) often occurs. Regional lymph nodes increase, and then an increase in various groups of lymph nodes and generalized lymphadenopathy develops.
Simultaneously with skin lesions, there is a high fever of the wrong type with severe general intoxication, sometimes hyperesthesia and insomnia are noted. The duration of the febrile period is from a week to several months. On the part of the cardiovascular system, tachycardia, expansion of the borders of the heart, arrhythmias, and a decrease in cardiac output are characteristic.
Often, the phenomena of myocarditis are clinically weak, however, with little physical exertion, acute heart failure can develop with subsequent death.
Trypanosome. From the first days of the disease, an increase in the spleen and liver is revealed. The second period of the disease - actually "sleeping sickness" - corresponds to the penetration of the pathogen through the blood-brain barrier with damage to the brain substance. The first signs of damage to the nervous system are progressive weakness, apathy, lethargy, sleepiness during the day and insomnia at night.
Lethargic state and coma gradually develop. Signs of focal lesions of the nervous system are expressed insignificantly and are characterized by spontaneous tremor of the limbs and muscle paresis. The duration of this period is usually from 3 to 12 months. At this stage, spontaneous recovery does not occur.
In American trypanosomiasis, the peripheral nervous system is more involved in the process; Auerbach's nerve plexus is affected with paralytic disturbance of peristalsis and pathological expansion of various parts of the gastrointestinal tract.
In the early (hemolymphatic) stage, lomidine and suramin are used. The course dose of lomidine is 40 mg per kg of the patient's body weight, the drug is administered intramuscularly daily or every other day (for a course of 8-10 injections). As a rule, a second course of lomidine therapy is required. The drug is effective only in the Gambian form of African trypanosomiasis.
Suramin is administered intravenously at a daily dose of 20 mg per kg of body weight for adults and 10-15 mg per kg for children, the course of treatment is 5 injections with an interval of 3-7 days. If necessary, the course of treatment with suramin is repeated one month after the first course. In the late (meningoencephalitic) stage, treatment is carried out with arsenic-containing drugs. Arsobal is injected intravenously at 1.8-3.6 mg per kg of patient weight for 3 days. The course of treatment, if necessary, is repeated in a week. The drug is toxic.
Trypanosome. The drug trimelarsen is used - in two courses subcutaneously or intramuscularly, daily, in increasing doses (1 - 2 - 3 - 4 mg per kg of weight). Then, after a 7-day break, a second course is prescribed: within 4 days, the patient is injected with 4 mg of the drug per kg of body weight. Prevention consists in the timely diagnosis, isolation and treatment of patients, as well as in the prevention of human bites by the tsetse fly and in the destruction of flies.
In the area of distribution of the Gambian form of trypanosomiasis, successful chemoprophylaxis with lomidine is carried out (intramuscularly 1 time in 6 months, 3-4 mg per kg of body weight). Chemoprophylaxis of the Rhodesian form has not been developed;
Specific therapy for Chagas disease has not been sufficiently developed. Currently, nitrofuran derivatives are considered the most effective. Lampit (nifurtimox) is used in a daily dose of 8-10 mg per kg of body weight in three divided doses, the course duration is 3-4 months.
For the treatment of American tryponasomosis, lampit (nifurtimox) is used in a daily dose of 8-10 mg per kg of body weight in three divided doses, the course duration is 3-4 months
2-Nitroimidazole (Radonyl) has been developed and is being tested with encouraging results. Prevention is reduced to the destruction of bedbugs - carriers of Chagas disease and improvement of sanitary and living conditions. In focal areas, a mandatory examination of donors is carried out using the Mashado reaction in order to prevent the transmission of trypanosomes through blood transfusions.
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