Differential diagnostics: an early stage of helminthiases, dermatitises, HIV-infection (AIDS), brucellosis.
Laboratory diagnostics.
1. The microscopy of bloodless microscopic section of a skin from the parts with onchodermatitis is made in a drop of saline solution for the detection of microfilariae. Romanovsky–Gimza staining allows to identify a species.
2. Investigating of a sections of a cornea with definition of number of microfilariae.
3. Ophthalmologic research by a slit lamp with the detection of microfilariae.
4. Filtration of the large volumes of a blood and urine through milliporal filters with a microscopy is applied.
5. Mazotti’s test (in a low invasion) is allergic manifestations and increase of microfilariae in a skin after reception of 50 mg of ditrasine.
6. The immunological methods have secondary importance.
Treatment.
1. Diaetylcarbamazine citras (Ditrazin citras, DEC) - initial dose is 25 mg, then 6 mg/kg/day div. q8h. 10 days. It affects the microfilariae.
2. Then Antrypol (Suramin) 10% solution IV is used at first 1 ml then 10 ml 1 time per week 5-6 injections. It affects the macrofilariae. The control of urine must be carried out!
3. Then ditrasin is used for 10 days.
The universal preparation ivermectine (mectisan) is prescribed in a dose of 150 mg/kg PO 1 time per 6 months within 10-15 years.
In allergic reactions antihistamine and corticosteroids are applied.
Loasis - epidemiology, сlinics, diagnostics, treatment.
Loasis (Calabar swelling disease) is tropical tissue helminthiasis manifested by various allergic reactions, edema of soft tissues, impairment of serous membranes and conjunctiva. It is wide-spread in forest region of Western and Central Africa.
Causative organism is Loa loa, bisexual nematode having length up to 100 mm, the larva with the irregular twisted flexures has colourless cover.
Epidemiology. A source of an invasion and a final owner is a man and primates, intermediate owner and transmitting organism are gadflies Chrysops genus (places of a propagating are reservoirs with slow-moving water) they attack more often people with a dark skin. The day periodic form is typical. The way of transmission is transmissible.
Development cycle in a transmitting organism is following: during bloodsucking gadflies swallow microfilariae => they develop up to invasive stage in 7-10 days.
Development cycle in an organism of a man is: larvae take root into a skin during a bite of gadflies => they permeate into a hypodermic fat, under serous membranes and under the conjunctiva => they become puberal in 12 months => female gives birth to larvae (microfilariae) => microfilariae circulate in the blood.
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Pathogenesis:
1. Toxico-allergic reactions develop on products of metabolism and decay of helminths.
2. Mechanical damage of tissues (speed of a movement of helminths is 1 cm/min!).
3. An addition of a secondary infection leads to the development of abscesses.
4. Parasitizing in an eye causes a papilledema and pareses of muscles.
Clinics. Incubative period lasts from 4 months till one year.
1. Allergic signs are itch, urticarious rash, paresthesiae, subfebrile temperature, hypereosinophylia (60-90 %).
2. Typical signs are Kalabarous oedema (it is dense, painless, slowly disappeared oedema of the skin and hypodermic fat on local open parts of a body, the skin above it is pale, hot to touch, fossa does not remain during pressing, oedema is accompanied with high temperature, may appear in some years after departure from the hotbed of infection.
3. Destruction of helminths and an addition of a secondary infection leads to development of abscesses in muscles, axillary and inguinal lymphonodules.
4. Penetration under conjunctiva causes edema of eyelids, hyperemia of a conjunctiva, pain in the eyes, impairment of eyesight.
5. Migration under a mucous membrane of the urethra causes dysuric impairments, near nerve trunci it causes neuritises, penetration through capillaries of glomeruli leads to nephritis, in the CNS it leads to meningocephalitis.
Laboratory diagnostics:
1. Microscopy native and Romanovsky-Giemsa stained smears and thick drops of a blood.
2. It is possible to find helminths visually under a conjunctiva and under a skin.
Treatment:
1. Diaetylcarbamazine citras (Ditrazin citras, DEC) 2-3 mg/kg tid first 3 days (possibility of anaphylactic reactions) then up to 6 mg/kg 2-3 weeks.
2. Antihistamine preparations, glucocorticoids.
3. Surgical ablation of helminth from an eye.
Leishmaniasis
4. Visceral leishmaniasis - epidemiology, clinics, diagnostics, treatment.
Visceral leishmaniasis (Visceral leishmaniasis) is protozoal infection characterized by an impairment of internal organs with feverish reaction, splenomegaly, anemia, pancytopenia and chronic course. It is wide-spread in tropical, subtropical and partially in temperate zone of all continents.
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Causative organism is Leishmania donovani with four subspecies: L.d.donovani (Indian variant), L.d. infantum (Mediterranean-Central Asian variant), L.d.archibaldi (East African variant), L.d.chagasi (South American variant).
Epidemiology. There are three variants of visceral leishmaniasis (according to a geographic range, clinics and epidemiology):
1. Mediterranean-Central Asian is a zoonosis.
А) Enzootic natural hotbeds. A source of an invasion and reservoir are jackals, foxes, rodents; transmitting organism is Phlebotomus mosquito.
B) Village hotbeds. A source of an invasion and reservoir are dogs, saldom wild animals, transmitting organism is mosquito.
C) Urban (synanthropic) hotbeds. A source of an invasion are dogs and rats, transmitting organisms are mosquitoes. Mosquitoes infest from the sick person extremely rarely.
Children fall ill in foci more often, season of infection is summer.
2. Indian leishmaniasis (kala-azar) is anthroponosis.
Source of an invasion is a sick person, transmitting organism is mosquito female.
3. East African variant is zoonosis, but in a high morbidity it is anthroponosis.
Source of an invasion is wild mammalia and a man, transmitting organisms are mosquito females.
All leishmaniases have transmissible way of transmission, in Indian one hemotransfusion way is possible.
Development cycle in an organism of mosquito is the following: aflagellar amastigotes after blood sucking => flagelar form in a stomach (promastigotes) => reproduction, accumulation in 5-8 days in a pharynx.
Development cycle in an organism of the vertebral owner: promastigotes are accumulatedin a skin during a bite of mosquito => entering into the blood => dissimination in cells of RES => amastigote => reproduction by simple division (20-30 parasites in one cell) => destruction of cells.
Pathogenesis. There is a dense nodule with Leishmania in a place of penetration of causative organism => primary affect (it is absent in Indian leishmaniasis) => generalization of infection with reproduction in macrophagal cells of a spleen, liver, bone marrow, lymphonodules, wall of intestine, adrenal glands, kidneys, lungs => hyperplasia and degeneration in organs => immunopatological processes on autoantigens.
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Clinics. Incubative period is from 15-20 days till 10-12 months.
The initial period includes:
1. A primary affect in a place of a bite (it is not present in Indian leishmaniasis).
2. Toxinfectious syndrome.
3. Undulating fever.
4. Moderate increase of spleen.
The period of height of the disease (anemicosplenomegalous) lasts from 2 weeks till several months:
1. Irregular or remittant fever (sometimes subfebrile or hyperpyrexial). In 10-20% of pacients with Indian leishmaniasis it has twofold rise per day.
2. The typical sign is the splenomegaly even up to a pubic region, spleen is dense, painless (sometimes dull aches are present), reduces to norm after treatment.
3. Increased liver is dense and painless.
4. Lymphadenopathy (in Mediterranean-Central Asian leishmaniasis).
5. Portal hypertension, edemas, ascites are present.
6. Skin is dark, almost black (in Indian leishmaniasis), colourless, "«porcelain" in Mediterranean-Central Asian leishmaniasis .
7. Anemia, leukopenia, thrombocytopenia, agranulocytosis, increased ESR are found in the blood analysis.
8. The hemorrhagic syndrome is more often in Indian leishmaniasis.
The cachectic (terminal) period includes:
1. Cachexia, decrease of muscle tone.
2. Expressed hepatosplenomegaly.
3. Anemia (Нb 40-50 g/l).
4. Pancytopenia, uneosinophilia.
Lethal outcome is inevitable without timely treatment.
10 % of the patients after Indian and East African leishmaniasis have leishmanoids on a skin - nodules, papilloma or spots containing Leishmaniae - from some months till 1-2 years after a remission.
Differential diagnostics: malaria, brucellosis, typhoid fever, lymphogranulomatosis.
Laboratory diagnostics:
1. Microscopic examination of Romanovsky-Giemsa staining of print preparations of the bone marrow (sternal puncture, puncture of the ileal bone) .
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2. Microscopy of smears and thick drops of blood (Indian and East African leishmaniasis).
3. Microbiological assay of punctates of the bone marrow, liver, spleen in medium NNN
4. Bioassey (infestation of hamsters).
5. Serological tests (CFR, RIF, ELISA) have secondary importance.
Treatment:
1. 20 % Solusurminum (solustibosanum) solution IV or IM 100 mg/kg per day div. q12h 10-12 injections (first 2 days 1/4 of a dose must be prescribed).
2. Solustibosanum IM or IV daily or every other day. An initial dose is 6 ml, then dose is 12 ml/day. 120 ml are necessary for a course of treatment.
3. Pentostam IV or IM 6 ml daily 6-10 injections.
4. Glukantim IM 60-100 mg/kg/day 12-15 injections.
5. 10 % pentamidinum solution IM 4 mg/kg daily 10-15 injections (in a resistance to stibium).
Trypanosomiasis
5. African trypanosomiasis (Gambian and Rhodesian forms), epidemiology, pathogenesis, clinics, diagnostics, treatment.
African trypanosomiasis (Trypanosomosis africana, Sleeping sickness, tsetse-fly disease) is characterized by an irregular fever, rash, enlargement of lymphonoduls, edemas, sleepiness. It occurs ropical Africa only.
Causative organisms are microorganisms of Protozoa Trypanosoma brucei gambiense (Gambian trypanosomiasis or West African sleeping sickness) and T. brucei rhodesiense (Rhodesian trypanosomiasis (sleeping sickness)) class.
Epidemiology. A source and reservoir of invasion in hambian trypanosomiasis (anthroponosis) is a sick person or a carrier and sometimes domestic pigs, in Rhodesian trypanosomiasis (zoonosis) a source and reservoir of invasion are antelopes, rarely they are other animals and large cattle. The way of transmission is transmissible (a bite by the tsetse fly (Glossina)), in hemotransfusions, transplacental, direct mechanical transfer by sanguivorous flies from a sick person to other men. Fishermen and hunters fall ill more often.
Development cycle in a man - tripomastigotes multiply by binary division. The narrow, long forms with a garrot are in the blood of a patient, and short wide ones without a garrot develop in a transmitting organism.
Development cycle in a transmitting organism is tripomastigotes => epimastigotes => metacyclic trypanosomes in the organism of the man.
Pathogenesis. In a place of penetration of metacyclic trypanosomes inflammatory reaction (trypanosomic chancre) occurs => permeation into a blood, then in lymphatic vessels and nodes (reproduction and accumulation) => lymphogenous and hematogenic dissemination => the foci of a necrosis in a spleen, degeneration of liver cells, impairment of renal glomerules by cell-bound immune complexes, necrosises and hemorrhages in a myocardium, epicardium and endocardium, vasculitis with an occlusion of capillaries in the lungs, diffuse mesenchymal perivascular infiltrates in a brain, pia-arachnitis (leptomeningitis). Fibrosis in the heart, cardiomyopathy, demyelination, panencephalitis (autoantibody against nervous cells and myelin) develop in chronic stage.
Clinics. Incubative period is from 2 weeks till several months.
The early period (hemolymphatic):
1. Toxinfectious set of symptoms
2. Irregular fever (alternation of the feverish periods (some weeks) and the apyrexia (from several days till some months)
3. Trypanosomic chancre (red nodule surrounded by a waxy zone) is in a place of a bite.
4. On a skin of a chest, back there is an erythema like semirings, nodulous, papular with an itch called trypanides; edemas of the face and neck occur.
5. Lymphadenopathy (in Gambian forms) manifests on increase of posterior cervical lymph nodes (Winterbottome’s sign)
6. Hyperesthesia (Kerandel’s sign)
7. Hepatosplenomegaly
If patients survive the early period illness passes into late (meningoencephalitic) period in 2-10 months or in some years:
1. The increasing sleepiness up to a lethargy is characteristic.
2. Neurologic symptoms such as shuffling gait, stupor, cramps, paralyses, pareses , tremor, meningeal symptoms, ptosis, scrambled speech.
3. Hepatosplenomegaly
Causes of the death are cachexia, hyperpyrexia, purulent meningitis, pneumonia in the presence of a coma.
Features of the Rhodesian form are:
1. An acute course
2. The terms of a fever are long, and one of an apyrexia is short
3. Weakness, cachexia, thrombocytopenia, disseminated intravascular coagulation, impairment of the nervous system increase quickly
Death occurs in 3-9 months after the infestation, sometimes in some weeks.
Differential diagnostics is carried out with malaria, visceral leishmaniasis, tuberculosis, lepra, lymphogranulomatosis.
Laboratory diagnostics:
1. Microscopy of a chancre’s punctate, lymphonodules, the liquor, the bone marrow, blood (smear and thick drop)
2. Microscopy with enrichment (blood with Sodium citratum after a centrifugation)
3. Bioassey (infestation of rats)
4. Immunological methods (Reaction of immunofluorescence, ELISA, definition of Jg M in Gambian form)
5. The blood analysis (an acceleration of ESR) and liquor (increase of protein more than 0,25 g/l and lymphocytes in the second stage of illness).
Treatment:
In an early stage (without changes in the liquor):
1) 10 % suramin solution i/v 20 mg/kg (no more than 1 g) 1 time per week for 5-6 weeks (5 г on a course) in Gambian form; in Rhodesian form 1 g on the 1th, 3th, 7th, 14th, 21th day of treatment.
2) 10 % Pentamidin solution i.m. 3-4 mg/kg/day 5-10 injections. The courses are repeated.
3) Eflornithine 100 mg/kg 4 times a day i.v. fror 14 days or 75 mg/kg 4 times a day for 21-30 days.
These drugs can be combined.
In an early and late stage:
1) 3,6 % Arsobal (melarsoprol) solution i.v. some courses (it is given more often in the Rhodesian form)
2) 20 % Tryparsamide solution i.v. 30 mg/kg 10-12 injections.
3) Nitrofurason 0,5 х 3-4 times per day for 5-7 days (at relapses)
In a high parasitemia, serious fever and in the late stage of Rhodesian form suramin and then arsobal must be prescribed. Pentamidin 3 mg/kg i/m one time in 6 months is used for the prophylaxis of Gambian form.
6. American trypanosomiasis (Chagas disease) - etiology, epidemiology, pathogenesis, clinics, treatment.
American trypanosomiasis is a transmissible protozoan disease which is characterised by fever, lymphadenopathy, hepatosplenomegaly, serious impairment of the heart and nervous system.
The causative organism is Trypanosoma cruzi (zoonosis).
Epidemiology. A source and reservoir of causative organism are armadilloes, raccoons (2-17 %), anteaters, monkeys, bats, in village nidi - a man. Most often: dogs - 28%, cats - 20%. Disease is wide-spread in the countries of Southern and Central America.
The ways of transfer are transmissible (the bite of a Triatoma megista bug), causative organism gets into a wound with the feces of a bug), during hemotransfusions, with milk of a mother.
The development cycle in a man: tripomastigotes (in a blood) => amastigotes (in a cell) => the formation of pseudocysts => epimastigotes => tripomastigotes.
The development cycle in a body of a bug: tripomastigotes => spheromastigotes => epimastigotes => metacyclic trypanosomes => to man`s organism.
Pathogenesis. An acute inflammatory reaction of a skin (shagoma) in a place of penetration of a causative organism => percolation into the blood and dissemination (in 25 % of cases - secondary shagomes under the skin are present) => destruction of ganglionic cells of many organs (heart, nervous system, digestive tract, lungs) => dilation of hollow organs.
In the CNS there is an impairment of meninges, the foci of an infiltration in a brain; an inflammation of the adrenal glands, hyperemia and degeneration of hepatocytes in the liver, inflammation and dilation of the heart.
Clinics. The incubative period lasts for1-3 weeks.
An acute stage of illness:
1. Constant or remittent fever.
2. Shagoma on a skin (in 25 % secondary shagomas in a hypodermic fat appear then).
3. Conjunctivitis and edema of one of the eyes (Romanja`s sign) - in 50 % of cases.
4. Lymphadenopathy.
5. Generalized elastic edemas.
6. Macular eruption on a skin.
7. Hepatosplenomegaly.
8. Impairment of the heart - carditis (in 40 % there are changes in ECG)
9. The meningocephalitis and cardio-vascular insufficiency occur at the terminal stage.
Lethality is up to 10% of cases. Patients frequently die in the age of 50.
In 4-5 weeks the disease can pass into a chronic stage in survivors (in 10-20%):
1. Chronic cardiomyopathy
2. Enteromegaly (in 80 % - megaesophagus).
Differential diagnostics: leishmaniasis, malaria, rheumatic carditis, Crohn`s disease.
Laboratory diagnostics:
1. Microscopy (smear and "thick drop") of the blood, the liquor, punctates and lymphonodules, of the bone marrow and the lien.
2. Microscopy with enrichment (10 ml of the blood + 30 ml of ammonium chloride ) - the centrifugalized deposit is investigated.
3. Bioassey (mice)
4. Xenodiagnosis (feeding of a bug on the patient with the subsequent research of feces of a bug)
5. Serological tests - Reaction of Immunofluorescence, Reaction of Indirect Immunofluorescence,
In a chronic stage immunological methods are used:
1. Complement Fixation Test ( it is positive in 80% during the impairment of the heart and in 90 % during a impairment of the esophagus)
2. Microenzymes and immunosorbent assays
3. ELISA - rising of IgM in serum of a blood.
The treatment is effective frequently only in an acute stage:
1. Nifurtimox 8-10 мg\кg\d po div.4x/d p.c. for 4/12.
2. Benznidazole 7,5 мg\кg\d po div. 2x/d for 2/12.
Schistosomiasis
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