Clinical varieties of cutaneous leishmaniasis. Leishmania: morphology and life cycle Visceral Mediterranean-Asian leishmaniasis

The group of protozoa of the genus Leishmania is the causative agent of leishmaniasis.

For humans, several types of Leishmania are pathogenic, which are similar in morphology, but

differ in epidemiology, geographical distribution, and cause the following diseases: visceral leishmaniasis(pathogen - Leishmania donovani and Leishmania infantum); cutaneous leishmaniasis(pathogen Leishmania tropica major et Leishmania tropica minor).

Morphology

Leishmaniasis exists in two forms: non-flagellated and flagellated.

Flagellaless form(amastigote) is formed in the body of vertebrate hosts, is located

intracellularly. The body is oval, rounded nucleus is located in the center and occupies up to 1/3 of the cell. The flagellum is absent, the main intracytoplasmic part of the flagellum is preserved -

kinetoplast in the form of a stick next to the nucleus. It reproduces by division in two.

Flagellar form (promastigote). It is formed in the body of an invertebrate host - a mosquito and on a nutrient medium. It has an elongated body with one flagellum. The end of the body, from which the flagellum departs,

pointed, opposite - rounded. Mobile, multiplies by longitudinal division.

Visceral Leishmania: Leishmania donovani - the causative agent of Indian leishmaniasis

(kala-azar) and Leishmania infantum- the causative agent of Mediterranean (children's) leishmaniasis.

Leishmania donovani - India, Pakistan, NE China, Nepal, Bangladesh.

Leishmania infantum - Mediterranean basin, Near and Middle East, Central and South America.

Life cycle Vertebrate hosts - humans, dogs, wolves, jackals, etc.

Invertebrate host and specific vector - mosquito of the genus Phlebotomus

infection of the vertebrate host occurs.

Invasive form- flagella.

Localization: cells of the liver, spleen, red bone marrow, lymph nodes

Ways of infection- transplacental, blood transfusion and percutaneous.

Indian leishmaniasis- anthroponosis, that is, the main source of infection- sick people.

Mediterranean leishmaniasis- anthropozoonosis. Basic source of infection- jackals,

dogs, foxes serving as reservoir hosts, rarely a sick person.

Pathogenic action: necrosis and degeneration of cells of affected organs with proliferation

connective tissue; damage to the red bone marrow, autoimmune processes lead to

pancytopenia.

illness; serological reactions

Prevention

Personal: protection against mosquito bites (use of repellents, mosquito nets),

preventive vaccinations.

Public: timely detection and treatment of patients; exterminating mosquitoes with

insecticides; destruction stray dogs in the foci of the Mediterranean form of visceral

leishmaniasis.

Cutaneous leishmania : Leishmania tropica minor- the causative agent of late ulcerative skin

urban leishmaniasis; Leishmania tropica major- the causative agent of acute necrotizing

rural cutaneous leishmaniasis; Leishmania brasiliensis- mucocutaneous causative agent

leishmaniasis; Leishmania mexicana- the causative agent of cutaneous leishmaniasis (Chiclero ulcer, Amazonian leishmaniasis).

Geographic distribution

· Leishmania tropica minor- Central and Western India;

· Leishmania tropica major- Central Asia, Northern Afghanistan, Iraq, Iran, Central Africa;

· Leishmania brasiliensis - countries of South America;

· Leishmania mexicana- Central and South America.

Life cycle

It differs little from the life cycle of other Leishmania.

Urban leishmaniasis - anthroponosis, source of infection sick people serve, rarely dogs

Rural leishmaniasis - anthropozoonosis.

Leishmania brasiliensis- - armadillos, rodents

Reservoir hosts are rodents (gerbils, ground squirrels, etc.).

The carrier of the disease is the mosquito; infection occurs when a mosquito bites, less often - through direct contact of damaged skin with infected material.

Invasive form- flagella

Localization: intracellularly (monocytes and macrophages) in skin cells.

Pathogenic action: severe inflammation at the site of the bite; formation of local (skin)

Prevention

Personal: protection against mosquito bites.

Public: extermination of rodents in the foci of cutaneous leishmaniasis, vaccinations.

causative agents of trypanosomiasis

Sleeping sickness (chronic version): the final owner is a man, monkeys. Pathogen - Trypanosoma brucei gambiense.Pathogenicity: Cervical swelling lymph nodes, fever, swelling of the distal parts of the limbs and around the eyes, meningoencephalitis, drowsiness. Carrier - flies of the genus Glossina(mainly from the group Glossina fuscipes).Invasive stage: trypomastigote form. Way of penetration: percutaneous, method - transmissible-inoculative. Widespread in tropical Africa.

Chagas disease: definitive owner - human, pets. Pathogen - Trypanosoma cruzi. Pathogenicity - fever, eyelid edema, meningoencephalitis, lesions of the gastrointestinal tract, myocardium, liver, central nervous system. Carrier - triatom bugs from the family of predators, primarily Triatoma infestans and Rhodnius prolixus.). Invasive stage: trypomastigous form. Way of penetration: percutaneous, method - transmissible-inoculative. Widespread in Latin America.

137. Malarial plasmodium. The fight against malaria, the tasks of antimalarial services at the present level. Types of malarial plasmodia.

Malaria prevention methods include drug therapy, exterminating mosquitoes and using various means to avoid insect bites. To date, a vaccine against malaria has not been invented, but active scientific research is underway in this direction.

Medicines used to prevent malaria include some drugs that are also used to treat the disease. Their dosage for prevention should be somewhat less than for treatment. Daily intake of such drugs is recommended. High cost and side effects drugs have made them popular only among visitors temporarily staying in areas with a high risk of contracting malaria. The local population prefers to manage with other preventive methods, including folk recipes. It should be added that medicines used for prevention become ineffective when treating a person who previously took them in small doses.

Medicines related to drugs of choice - various combinations with artimisinin - are not suitable for the prevention of malaria, they are used only for the treatment of the disease.

The oldest remedy for the prevention of malaria is quinine, it was prescribed for this purpose as early as the 17th century. AT modern medicine quinine is used only for treatment, for prevention today they recommend quinine, chloroquine, primaquine and a number of new drugs: mefloquine, doxycycline, atovaquone-proguanil hydrochloride.

It should also be taken into account that the effect of these drugs develops over time. They should be taken 1 to 2 weeks before visiting hazardous areas and continued for one week to one month after leaving areas with a high risk of malaria.

Malaria can be controlled by killing mosquitoes. In some regions, this preventive measure has been quite successful. With the drainage of swamps, the implementation of sanitary measures, and the treatment of patients, malaria left the United States and Southern Europe.

Malaria remains a pressing problem in developing countries, mainly in Africa.

DDT was once considered the most effective insecticide, it gained great popularity in developing countries, but was banned due to negative reviews. WHO in its recommendations addresses the topic of the return of DDT to the number of insecticides used to control malarial mosquitoes in some endemic areas.

Mosquito nets impregnated with insecticides also help in the fight against malaria, they act as protection against insect bites, reducing the number of infections. As a means of personal protection, it is recommended to wear closed clothing and use artificial or natural repellents.

Toxoplasma.

1. Kingdom Animals - Animalia

Subkingdom protozoa - Protozoa

Type Apicomplex - Apicomplexa

Class Sporoviki - Sporozoea

View Toxoplasma gondii- toxoplasma

The causative agent of toxoplasmosis was discovered in 1908. Sh.Nicollem and L.Manso

2.Latin name: Toxoplasma gondii

3. Disease caused: toxoplasmosis

4. Geographic distribution: worldwide

5. Morphology: Exist. in several stages: endozoite, pseudocyst, cyst, oocyst

In the human body exists in the form of a vegetative form (endosoid) and cysts

6. Localization: liver, spleen, lymphatic vessels, brain cells, cardiac and skeletal muscles, lungs, retina.

7. Invasive stage: endozoite, pseudocyst, cyst

8. Penetration:

Oral, transplacental, contact route

The method is alimentary, transmammary

9. Transmission factor: when oocysts get into the mouth from dirty hands, unwashed vegetables and fruits, cat hair, the use of poorly thermally processed meat and unboiled milk; through damaged skin when processing the meat of sick animals.

10. Source of invasion: a cat with toxoplasmosis

11. Development cycle: Complex, with the change of 2 hosts and the alternation of sexual and asexual reproduction.

Intermediate hosts - mammals (including humans), many species of birds, reptiles

Definitive host - mammals of the cat family, become infected by eating

12. Pathogenicity: destruction of host cells due to the reproduction of toxoplasma, heart, brain, eye structures. In the chronic period of invasion, it can lead to blindness and damage to the National Assembly.

13. Laboratory diagnostics: microscopy of blood smears, punctate of lymph nodes, centrifugate of cerebrospinal fluid, placenta, serological reactions, allergic tests

14. Prevention: -personal: boiling milk, term. Meat processing, hygiene, limiting contact with cats

Public: serological examination of pregnant women and their treatment

Balantidia

Balantidia (Balantidium coli) - pathogen balantidiasis.

Type of - Ciliophora

Class - Rimostomatea

View - Balantidium coli

Morphology: It exists in two forms: trophozoite and cyst.

trophozoite(vegetative form). The body is ovoid, covered with cilia. At the anterior end of the body is a cell mouth (cytostome) leading to the cell pharynx (cytopharynx). The cilia of the perioral space (peristome) are longer. Near the posterior end of the body is the anal pore (cytoproct). In the cytoplasm are digestive and 2 contractile vacuoles. In the endoplasm, 2 nuclei are a bean-shaped macronucleus, on the concave side of which there is a spherical micronucleus. The macronucleus regulates the vital activity of the cell, the micronucleus stores genetic information and participates in sexual reproduction. It feeds on carbohydrates, formed food particles, bacteria, leukocytes. Propagated by transverse division in two, conjugation is possible.

Cyst oval or spherical, covered with a two-layer shell. In the cytoplasm, a macro- and micronucleus is found, there is a posterior contractile vacuole.

Source of invasion - pigs, less often - humans, rats .

Invasive stage - cyst.

Penetration

-path oral, fecal-oral

-way alimentary

transfer factor- a person becomes infected through contaminated water or food, dirty hands.

Localization: large intestine (mostly caecum)

Pathogenic action: The formation of ulcers and necrosis of the mucous membrane of the colon; general intoxication, colitis (with acute balantidiasis).

Laboratory diagnostics: microscopy of a native smear of feces (detection of vegetative forms).

Prevention

Cutaneous leishmaniasis is a disease characteristic of those areas where the temperature can stay above 20 degrees for 50 days. However, isolated cases of infection can occur in any region. The causative agent of leishmaniasis is tropical leishmania.

Pathology according to the manifested symptoms is divided into 3 types:

Cutaneous leishmaniasis is characterized by a profuse rash on the epidermis in the form of pronounced papules.
Mucocutaneous leishmaniasis is characterized by the appearance of ulcers on the oral and nasal mucosa, in the pharynx.
Visceral leishmaniasis is characterized by the entry of the pathogen into the lymphatic vessels. Pathology spreads throughout the body along with the flow of fluid, affecting the internal organs. Basically, this form of leishmaniasis affects the heart muscle, spleen, liver, and lungs.

Cutaneous and visceral leishmaniasis can be transmitted from humans (anthroponotic form of pathology), from animals (zoonotic).

Pathogen vectors

Cutaneous leishmaniasis, depending on the pathogen, is divided into 2 types.

acutely necrotizing;
late-appearing.

Acute necrotizing pathology manifests itself depending on the season and has a close relationship with the presence of mosquitoes in the warm season. Basically, the disease begins to spread in the spring, its peak is observed in the summer, and a decrease in activity occurs in the beginning of winter.

Late-onset cutaneous leishmaniasis is characterized by a lack of attachment to any season. The disease can be diagnosed at any time of the year. The difficulty of diagnosis lies in the fact that animals and people are often carriers of an infection that does not show any symptoms.

The causative agent of visceral leishmaniasis is Donovan's leishmania.. The carrier of this pathology are mosquitoes phlebotomus.

Leishmania: life cycle

Further life cycle different forms pathologies are different. If a person is affected by cutaneous leishmaniasis, the pathogen begins to multiply at the site of a mosquito bite, as a result of which leishmaniomas are formed.

These pathogenic nodules contain:

macrophages;
fibroblasts;
endothelial cells;
lymphoid tissue.

Later, these nodules begin to gradually die off, and ulcers form in their place.

Symptoms

Various forms of leishmaniasis are characterized by individual symptoms, which can be used to determine the pathogen that affects the body.

Visceral pathology

This form of invasion has a long incubation period. From infection to onset primary symptoms Leishmaniasis usually resolves in 20-150 days.

Visceral leishmaniasis at the initial stage of development manifests itself with the following symptoms:

the appearance of general weakness;
apathy;
loss of appetite;
blanching of the epidermis;
slight enlargement of the spleen;
rise in temperature to 38 degrees.

In the absence of treatment for leishmaniasis, the primary symptoms include:

temperature increase up to 40 degrees;
cough;
enlarged lymph nodes;
pain in the liver area;
significant enlargement of the liver and spleen.

The neglected pathology makes itself felt:

severe deterioration in general well-being;
exhaustion;
severe enlargement of the spleen;
diarrhea
dryness of the epidermis;
pallor of the epidermis;
swelling of the lower extremities;
dizziness;
frequent heartbeat;
an increase in the abdominal region;
potency disorder.

The last stage of the pathology is characterized by:

swelling of the whole body;
decrease in muscle tone;
pale epidermis;
death of the patient.

With minimal damage to visceral leishmania internal organs often diagnosed with a chronic form of pathology, which does not manifest any symptoms.

Skin pathology

The incubation period of the disease of this form lasts 10–45 days. The initial stage of development is characterized by the following course:

The appearance on the epidermis of neoplasms similar to mosquito bites.
Later, these bites form into boils that look like a simple tubercle.
After 7–14 days, a black dead skin area appears in the center of the boil, signaling the onset of necrosis.
The furuncle forms into an ulcer, from the center of which pus begins to stand out, colored yellow-red.
Near the ulcer, secondary tubercles begin to appear.
After a while, they grow and merge together, forming a large wound.

The resulting wounds heal within 2-6 months if the patient has been treated for leishmaniasis.

mucocutaneous pathology

The symptomatology of this form is similar to skin pathology. The only difference is the spread of boils on the mucous membranes. In some cases, this disease can deform the face, which manifests itself:

runny nose;
nasal congestion;
difficulty in swallowing;
nosebleeds;
development of erosions and ulcers in the mouth and nose.

This form can provoke complications of 2 types:

when a secondary infection is attached, pneumonia may occur;
in defeat respiratory organs often results in death.

Treatment of skin pathology

Treatment of leishmaniasis mainly occurs with the help of drug therapy:

"Monomycin" is prescribed in the form of intramuscular injections three times a day every 8 hours at a dosage of 250,000 IU.
Glucantim injections are carried out at a dosage of 60 milligrams per kilogram of body weight.
"Seknidazol" use 500 milligrams four times a day for 3 weeks. After this period, the frequency of doses is reduced to 2 times a day for 3 weeks.
For the treatment of boils, Solyusurmin, Metacycline, Doxycycline are used, and other antimalarial drugs can be used.

In some cases, cryodestruction or laser therapy may be prescribed.

Treatment of visceral pathology

Visceral leishmaniasis is effectively treated with pentavalent antimony, pentamidine isothionate. Medicines based on antimony are used intravenously for 7-16 days. The dosage during treatment gradually increases.

If the medications were not effective, doctors prescribe Pentamidine at a dosage of 0.004 grams per 1 kilogram of body weight per day. The course of treatment consists of 10-15 injections given every day or every other day.

In addition to the specific drug treatment, pathogenetic therapy and prevention of bacterial deposits are prescribed.

To avoid the development of leishmaniasis of any form in humans, it is required to observe individual safety measures in places with a large concentration of insects. Especially such prevention is necessary in the spring-autumn period.

In winter, it is required to do preventive vaccinations, which consist in the introduction of 0.1-0.2 milliliters of liquid sulfur with a live weakened culture of the causative agent of tropical leishmania (major).

Such vaccinations provoke the development of pathology mild form, proceeding in the form of the formation of 1 boil and providing the formation of immunity to all types of diseases.

Leishmaniasis are protozoan vector-borne diseases occurring with damage to the skin and mucous membranes () or internal organs ().

Epidemiology of leishmaniasis.

The source of infection in urban cutaneous leishmaniasis is a human and presumably a dog; with rural-type cutaneous leishmaniasis - large and midday gerbils, fine-toed ground squirrel, etc. With visceral leishmaniasis, the source of infection is a sick person, dog, wild carnivores. infections - mosquitoes (see), which become infected with the blood of a sick person or animal.

Leishmaniasis diseases are common in the Mediterranean countries, South Asia and South America, in the USSR - in Transcaucasia and Central Asia.

Laboratory diagnostics. To detect the pathogen in cutaneous leishmaniasis, smears are prepared from the contents of the tubercles, in visceral leishmaniasis - from bone marrow punctate; in addition, do blood cultures. They put a skin allergic diagnostic test with killed cultures of leishmania (for cutaneous leishmaniasis) and: formol, antimony and with distilled water (for visceral leishmaniasis).

However, not all leishmaniasis are strict zoonoses, that is, animals will be the natural reservoir for them. Two types of the pathogen were also identified, which are purely anthroponotic infections (only people get sick with them). This zoonosis is characterized by a rather narrow distribution area. The incidence is mainly recorded on the territory of the African continent and in the countries of South America.. This is due to the fact that only limited species of animals can be the primary reservoir of the pathogen, and mosquitoes are carriers. The symptoms and treatment of leishmaniasis in people may differ depending on physiological characteristics organism.

The reasons

The presence of the pathogen infectious disease, which belongs to the genus of flagellated protozoa Leishmania.
The presence of natural foci of the pathogen. They are limited by the habitat of animals with this infectious pathology, and carriers - mosquitoes.
A sick person or animal will be epidemically dangerous to others for a long time. This period is limited by the time Leishmania is in the bloodstream and skin of the patient, that is, in fact, during all stages of leishmaniasis.
The least dangerous in the epidemic plan are patients with a visceral course of the infectious process, since in this case leishmania is the least accessible to blood-sucking insects.
Mosquito infection occurs as a result of the bite of a sick animal or person. When hit in intestinal tract insect, the causative agent of infection from the amastigote form passes into the promastigote. A week after infection, the mosquito becomes infectious to a susceptible animal or human body and remains so throughout its life.
In regions endemic for this infection, cases of human infection are also recorded when providing medical care for example, as a result of blood transfusion.
After the illness, immunity is developed, however, it is strictly specific. That is, when infected with another representative of the genus Leishmania, a person may re-develop a similar infection.

How does an infection develop?

Classification

There is no generally accepted classification for this infection. However, based on symptoms most authors distinguish two main clinical courses:

Cutaneous form, which is characterized by a predominant lesion of the outer integument of the patient's body.
With the visceral course of the disease, the infectious process covers the internal organs of the patient.

Depending on the main focus of the spread of infection, epidemiologists distinguish:

zoonotic pathologies, where the main reservoir will be a sick animal;
if the source of infection is a person, then they speak of an anthroponotic infection.

Symptoms of leishmaniasis in humans

Depending on the symptoms clinical course leishmaniasis infection is divided into visceral and cutaneous forms.

Visceral leishmaniasis is characterized by the following symptoms:

Incubation period with this form, it is quite long and can last up to six months.
It is characterized by a gradual increase in symptomatic manifestations. acute form is quite rare.
The first signs are the growing symptoms of acute intoxication with fever. However, short periods of remission are possible.
When examined during this period, an increase in regional lymph nodes is detected, which is not accompanied by algia.
The liver and spleen are greatly enlarged. On palpation, they are dense, but painless. The functioning of these organs is also impaired. Therefore, the detection or portal hypertension in leishmaniasis is not uncommon.
Symptoms of damage to the central nervous system and, in particular, the spinal cord may be detected.
The beginning of the terminal stage is characterized by the appearance of areas of dark pigmentation. skin, cachexia and symptoms of edematous-ascitic syndrome.

The cutaneous form of leishmaniasis has a shorter incubation period, lasting up to three weeks on average.

There are several clinical forms, which have their own symptomatic nuances, but they are all characterized by the presence of primary leishmanioma, which is formed at the site of the bite of an insect infected with the pathogen. From the tubercle formed after the bite, an ulcer is formed with serous-purulent discharge. It heals in the form of a scar.

Diagnostics

Leishmaniasis treatment

The patient is subject to hospitalization and must comply with bed rest.
To prevent the development of the mucous form of inflammation, a thorough treatment of the oral cavity is carried out.
The basis of therapy is Miltefosine (Impavido), which is prescribed for almost any form of infection.
In the visceral form of leishmaniasis, antimony preparations may be prescribed.
Chemotherapy with glucantim or amphotericin B.
Antibiotic therapy makes sense only when a secondary infection is attached. The causative agent of leishmaniasis very quickly becomes resistant to this treatment method.
If necessary, surgery can be performed.

Treatment of leishmaniasis in humans, as a rule, always ends successfully.

Prevention

Destruction various methods carriers of infectious diseases.
The local population living in endemic areas and people visiting these areas are advised to use protective equipment and repellents.
Patients should be promptly identified and treated.

Forecast

With timely diagnosis and appropriate treatment almost all patients recover.
In severe infections and the use of chemotherapy drugs, the mortality rate does not exceed 25%.
In the absence of adequate therapy, up to 90% of patients die.

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Diphyllobothriasis

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Leishmaniasis - vector-borne human or animal diseases caused by leishmania and transmitted by mosquitoes; characterized by damage to the internal organs (visceral leishmaniasis) or skin and mucous membranes (cutaneous leishmaniasis).

White mice, dogs, hamsters, ground squirrels and monkeys are susceptible to laboratory infection with Leishmania.

Epidemiology. The main sources of pathogens for visceral leishmaniasis are infected dogs, and for cutaneous leishmaniasis - ground squirrels, gerbils and other rodents. Mosquitoes of the genus Phlebotomus are carriers of pathogens. The transmission mechanism of pathogens is transmissible, through the bite of mosquitoes.

Pathogenesis and clinical picture . There are two forms of pathogens of cutaneous leishmaniasis: L. tropica minor - the causative agent of anthroponotic cutaneous leishmaniasis (urban type) and L. tropica major - the causative agent of zoonotic cutaneous leishmaniasis (rural type). With anthroponotic cutaneous leishmaniasis, the incubation period is several months. At the site of the mosquito bite, a tubercle appears, which increases and ulcerates after 3-4 months. Ulcers are most often located on the face and upper limbs. Sources of the pathogen are sick people and dogs. In zoonotic cutaneous leishmaniasis, the incubation period is 2-4 weeks. The disease is characterized by a more acute course. Ulcers are most often located on lower limbs. Leishmania reservoirs are gerbils, ground squirrels, and hedgehogs. The disease is common in Central Asia, the Mediterranean and Transcaucasia. L. braziliensis causes mucocutaneous leishmaniasis, characterized by granulomatous and ulcerative lesions of the skin of the nose and mucous membranes of the oral cavity and larynx. This form is found predominantly in South America. Visceral leishmaniasis (kala-azar, or black disease) is caused by L. donovani and is found in tropical and subtropical climates. The incubation period is 6-8 months. In patients, the liver and spleen are enlarged, affected Bone marrow and the digestive tract.

Immunity. Those who have been ill remain stable for life immunity.

Microbiological diagnostics. In the studied material (smears from tubercles, the contents of ulcers, stained according to Romanovsky-Giemsa), small oval-shaped Leishmania are found. Inoculations are also made on appropriate nutrient media to isolate a pure culture of the pathogen.

Treatment and prevention. For the treatment of visceral leishmaniasis, antimony preparations (solusurmin, neostibosan, etc.) and aromatic diamidines (stilbamidine, pentamidine) are used. In the case of cutaneous leishmaniasis, akrikhin, sublimate preparations, amphotericin B, monomycin, etc. are used. In order to prevent leishmaniasis, sick dogs are destroyed, rodents and mosquitoes are controlled. Vaccinations are carried out with a live culture of L. tropica major.