Urinary schistosomiasis (epidemiology, clinics, diagnostics, treatment).
Urinary schistosomiasis (endemic hematuria, bilharziasis) is tropical tissue helminthiasis with a primary impairment of urogenital system.
Causative organism is bisexual helminth Schistosoma haematobium, the length of a male is 10-15 mm and of a female is 20-26 mm. Female produces 100-300 ova per day. The ovum has a terminal spine.
Epidemiology. The source of invasion and a final owner is a sick person (especialy children and teenagers), intermediate owner are molluscums.
The way of transmission is percutaneous (through a skin and mucosa). The workers of irrigated plantations, fishermen having a contact with the water of reservoirs (bathing, washing etc.) belong to the group of high risk.
Development cycle in an external environment consists of the next stages: ovum excreted with the urine of the patient => miracidium cames out in water and instils in a molluscum (sporocyst of the first stage, daughter sporocysts) => going out of Cercaria => their penetration through the skin or mucosa of a man.
Development cycle in an organism of a man consists of the next stages: Cercaria penetrates through the skin and loses a tail => schistosomula is formed and migrates along lymphatic and circulatory vessels to a liver => puberal Schistosoma migrats into veins of the wall of urinary bladder => helminthes lay the ova => the ova go out through tissues into urinary bladder and are excreted with the urine. Puberal helminths never leave the venous system. There are 45 days from the moment of infestation to the start of excretion of the ova. Prolongation of a parasitizing is from 5 to 10 years.
Pathogenesis. Sensibilization of an organism by the products of a vital activity of Cercaria and Schistosomula => eosinophilic infiltrations into lungs, liver, lien => the movement of the ova through the walls of the vessels with formation of granulomas (inflammatory, destructive, then proliferative reaction around the ova), a thrombosis and inflammation of vessels => a fibrosis of tissues, calcification of the ova => deformation of ureters, hydronephrosis, pyelonephritis, nephrolithiasis, renal insufficiency. An impairment of the prostate gland, spermatic cords, epididymises, testicles, polypous vegetations of the neck of the uterus. Bringing of ova into lungs is a cause of obliterating endarteritis, pulmonary heart. Bringing of the ova into the liver produces granulomatous hepatitis, in a brain - myelitis.
Clinics. Incubative period lasts for 4-16 weeks.
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Stage of infestation (about 2 months):
1. Acute dermatitis with temperature
2. Asthmatic cough
3. Hepatosplenomegaly
4. Lymphadenopathy
Stage of a maturation (8-10 weeks):
1. High fever with an eosinophilia
2. Toxinfectious syndrome
3. Dyspeptic set of symptoms
Stage of the developed invasion (3-7 years):
1. Toxinfectious syndrome
2. Terminal hematuria with a painful urination (urodynia) is the most typical sign
3. Impairment of a prostate gland is a cause of the pain in a perineum
4. Impairment of spermatic cords, epididymises and testicles lead to hydroscheocele
Stage of the late invasion (5-15 years):
1. Hydronephrosis
2. Edema of ureters
3. Pyelonephritis
4. Nephrolithiasis
5. Renal insufficiency, anuria.
An obliterating endarteritis of vessels of the lungs with development of pulmonary heart, granulomatous hepatitis, clinics of a tumour of a brain, paralyses can be present.
Complications are vesicointestinal, vesicovaginal fistulas, sepsis, uremia, obstruction of urinary bladder neck. The primary cancer of urinary bladder can develop.
Differential diagnostics: inflammatory and destructive diseases of the urinary tract.
Laboratory diagnostics:
1. Microscopy of urine after a centrifugation for detection of the ova.
2. Larvoscopy reveals miracidia in the urine.
3. Cystoscopy with a biopsy
4. X-ray inspection of the urinary bladder, excretory uro- and pyelography, retrograde pyelography, radioisotope renography.
5. The immunological methods (Complement Fixation Test, Reaction of Immunofluorescence, ELISA) during the late stage when ova are not excreted.
6. In autopsy ova are revealed in print preparations of various organs of the genitourinary system.
Treatment.
1. Biltricid (praziquantel) 20 mg/kg PO, q4h (2-3 doses).
2. Metrifonate, bilarcil 7,5-10 mg/kg /d po 1 dose.
3. Ambilhar 25 mg/kg/d div tid. 5-7 days.
4. Hycanthone, etrenol 2-3mg/kg/d i.m. 1 dose.
5. Amoskanat 7 mg/kg div. tid., repeat in 3-7 days.
8. Intestinal schistosomiasis - epidemiology, clinics, diagnostics, treatment.
Intestinal schistosomiasis (Bilharziasis mansoni) is tropical helminthiasis with a primary impairment of digestive organs. Schistosomiasis japonica (katayama disease), schistosomiasis intestinalis intercalatum and schistosomiasis mecongii have a similar pathogenesis and manifestation, therefore they are considered as intestinal schistosomiasises too.
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Causative organism Schistosoma mansoni is bisexual helminth; the length of a male is 10-15 mm and of female - 20-26 mm. Female produces up to 300 ova per day. The ova have a lateral spine. Illness is wide-spread in Africa and south America (Caribbean basin).
Epidemiology. A source of invasion and final owner is a man, rarely monkeys and gnawers (rats), intermediate owner are molluscums.
The way of transmission is percutaneous (through a skin and mucosa). Infestation takes place during a work on irrigated plantations, bathing in ponds.
Development cycle in an external environment consists of next stages: the ova excreted with a feces of the patient => miracidium cames out into water => miracidium instils in a molluscum (propagation) => going out of cercaria => their penetration through the skin and mucous of a man.
Development cycle in an organism of the man consists of next stages: cercaria penetrate through a skin, lose a tail => schistosomula => migration along lymphatic and circulatory vessels to a liver => puberal schistosoma => migration in inferior mesenteric and hemorrhoidal veins => helminthes lay ova => ova go out through walls of vessels, tissues of an intestine with a feces into external environment.
45 days pass from the moment of infestation till excretion of ova. Prolongation of a parasitizing is from 5 to 15 years (till 20-30 years).
Pathogenesis. In an early stage: sensibilization of an organism by products excreted by cercaria and schistosomula => eosinophilic infiltrates in lungs, liver, spleen => movement of ova through walls of vessels and tissues (granulomatous inflammatory reaction, necrosis, then - fibrosis, pseudopolyps in an intestine) => thrombosis and inflammation of vessels; in a chronic stage: ingress of ova in a portal system => a Simmers’s portal fibrosis, portal hypertension, endarteritis of a liver vessels; ingress of ova into the lungs => endarteritis of lung vessels, pulmonary heart; ingress of ova into a brain => paresises, paralyses, encephalitis.
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Clinics. Incubative period lasts for 4-16 weeks.
Stage of infestation (about 2 months):
1. Acute dermatitis with a high temperature
2. Asthmatic cough
3. Hepatosplenomegaly
4. Lymphadenopathy
Stage of maturation (8-10 weeks):
1. High fever with an eosinophilia
2. Toxinfectious syndrome
3. Dyspeptic syndrome
Stage of the developed invasion (3-7 years):
1. Toxinfectious syndrome
2. Dyspeptic set of symptoms (abdominal pain, irregular bloody stool with mucus, tenesmus, loss of appetite)
3. Polyposis and intestinal obstruction
4. Hepatosplenomegaly
5. In a drift of ova into a CNS convulsions, paraplegias occurs.
Stage of a late invasion (8-10 years):
1. Tubular-indurative Simmer’s fibrosis, fibrosis of a liver, portal hypertension - enlarged dense liver, splenomegaly, edemas, ascites, varicose phlebectasia of an esophagus may cause bleedings, anemia.
2. Pulmonary heart – thoracic pain, tachycardia, cyanosis, cough, breathlessness.
3. Hemorrhoids, polyposis of intestine, prolapse of the rectum.
Causes of the death are the bleeding from varicose enlarged veins of esophagus, cardiovascular insufficiency.
Schistosomiasis intestinalis intercalatum has benign course. The impairments of rectum and genitals (salpingites, endometrites) prevail.
Schistosomiasis japonica is the most serious one. The causes of heaviness are:
1. Helminths produce a maximum quantity of ova - up to 3000 per day
2. Long stay of helminths on one place with maximal production of ova and their calcification lead to extensive changes of an intestine down to an obstruction.
3. The necrosis with the subsequent fibrosis prevails in granulomas.
4. Drift of ova in to the nervous system is often - pareses, paralyses, encephalitises
5. Considerable impairment of liver with intralobular fibrosis occurs.
Schistosomiasis mecongii reminds that of Schistosomiasis japonica.
Differential diagnostics: schigellosis, nonspecific ulcerative colitis, amebiasis, impairment of liver, lungs, intestine caused by other causes.
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Laboratory diagnostics:
1. Microscopy of the feces (native smear, method of precipitation, thick Kato’s smear) sometimes with definition of the number of ova.
2. Larvoscopy (addition of water to the feces and detection of mobile miracidiums after being in a thermostat)
3. Rectoromanoscopy (hyperemia, erosions, ulcers) with a biopsy (detection of ova in puctate)
4. Punctate of a liver with detection of ova
5. Laparoscopy
6. X-ray examination
7. Immunological methods (CFR, reaction of immunofluorescence, ELISA) in late stage
8. Intracutaneous test.
Treatment:
1. Praziquantel 20 mg/кg q4h (only 2-3 doses).
2. Oxamniquine 10 mg/kg b.i.d. for 2 days IM and IV
3. Niridasol, Ambilhar 25 mg/kg/day in 3 receptions for 5-7 days
4. Hycanthone, Etrenol 2-3 mg/kg/day IM
Fevers
9. Phlebotomus fever (epidemiology, clinics, diagnostics, treatment)
Phlebotomus fever (Febris pappatasii, three-day fever, sandfly fever) is an acute arboviral disease transmitted by phlebotomus, characterized by a short-term fever, severe headache, pain in muscles, conjunctivitis and original hyperemia of scleras.
Causative organism is a virus of Bunyaviridae family.
Epidemiology. A source of infection is a sick person, transmitting organism is Phlebotomus pappatasii. Sandfly, rodents, birds may be reservoirs. The way of transmission is transmissible. Seasonal prevalence is May - June and July - August. Children fall ill more often. Disease is wide-spread in the countries of the Mediterranean sea.
Pathogenesis. The virus penetrates into a blood after a bite and reproduces in the reticuloendothelial system. It causes the changes in blood vessels, striated muscles, nervous system.
Clinics.
The incubative period lasts for 3-7 days.
1. The toxinfectious syndrome (frontal headache, weakness, pain in calfs and back, tenderness during the movement of the eyeglobes).
2. The increase of temperature is up to 39-40oC for 3 days (in 10 % of the patients for more than 4 days).
3. There is hyperemia of the face and the mucous of fauces, herpes labialis.
4. There are papulae on the skin after bites of infected sandflies.
5. Bradycardia and decrease of blood pressure are present.
6. The typical symptoms are severe pain when upper eyelid is raised up by fingers (first Taussig`s sign), morbidity during the pressure on the eyeglobe (second Taussig`s sign), hyperemia of a conjunctiva and sclera in a form of a tip near a cornea (Peak`s sign).
7. Macromacular exanthema.
8. Sometimes abdominal distention and fluid stool are present.
The course of the disease is favourable. If the course is severe hemorrhagic syndrom, meningeal signs (liquor`s supertension, the increase of protein) can be marked .
The differential diagnostics must be made with influenza, leptospirosis, louse-born typhus, relapsing fever and others.
Diagnostics.
1. Virologic method.
2. Serological method (Complement Fixation reaction, Indirect Hemagglutination Test) determines the increas of the antibody`s titer in the blood serum.
3. Blood analysis shows leukopenia, lymphopenia, shift of the formula to the left, aneosinophilia.
Treatment is symptomatic.
10. Dengue fever (epidemiology, pathogenesis, сlinics, diagnostics, treatment).
Dengue fever (Dandy-fever, Break-bone fever) is an acute viral nature-focal (endemic) bloody infection leasting with a high two-wave fever, intoxication, pain in muscles, arthralgia, exanthema, lymphadenopathy, leukopenia. It has classical and hemorrhagic forms.
The causative organism is a virus of Flavivirus genus.
Epidemiology. The source of infection is a sick person and sometimes monkeys, bats. The transmitting organism is Aedes aegypti mosquito. Virus can develop at the temperature of the air not lower than 22oC, therefore desease is wide-spread in the tropics. The way of transmission is transmissible.
Pathogenesis. There is an inflammation and reproduction of a virus in a place of a mosquito`s bite; 3-5 day virusemia and degenerative changes occur in the liver, kidneys, myocardium, musculs.
The hemorrhagic form appears in the aborigines after repeated contamination only. There is injury of small blood vessels and infringement of a permeability of large blood vessels (swelling of an endothelium, edema and infiltration), hemorrhages into endo- and pericardium, pleura, peritoneum, stomach, intestine, brain.
Clinics.
The incubative period lasts for 5-7 days.
1. The toxinfectious syndrome includes pain in the back, spine, sacrum, joints (especially in knees).
2. Fever increases up to 39-40oC within 3 days, then it decreases for 1-3 days and second feverish wave develops.
3. There is hyperemia and swollen face, conjunctivitis, enlargement of the peripheric lymphonoduses.
4. The replacement of tachycardia by bradycardia from the 2-3d days of the disease is typical.
5. Pains in the muscles and joints are severe (osteoalgic fever).
6. On the 3d-5th days maculo-papular or petechial rash with an itch appears on the hands, feet, trunk and limbs. Enanthema on a mucous of the mouth is present.
7. Hepatolienal set of symptoms.
The course of the classical form is favourable.
In the hemorrhagic form the course of the disease is severe: the sharply marked toxicosis, significant enlargement of the liver; hemorrhagic set of symptoms (petechia, hemorrhagic eruption, admixing of the blood in vomitive masses, nasal, uterine, gastric bleedings) occurs from the 2d day of illness; meningitis, meningocephalitis; kidney insufficiency; disseminated introvascular coagulation can be a complication; collapse appears in 20-40 % of cases .
Lethality is up to 5 % of cases.
Differential diagnostics must be made with malaria, yellow fever, sepsis, meningococcemia, phlebotomus fever and others.
Diagnostics.
1. Virologic method.
2. Serological method (Complement Fixation Test, Indirect Agglutination Test) determins increase of the antibody titer in the blood serum.
3. Blood analyses show leukopenia, relative lympho- and monocytosis, thrombocytopenia.
Treatment is symptomatic.
11. Yellow fever (epidemiology, pathogenesis, clinics, diagnostics, treatment).
Yellow fever is an acute bloody infection of the tropics, zooanthroponosis characterized by a hemorrhagic set of symptoms, hard intoxication, necrotic impairment of a liver, high lethality. It is quarantine infection.
The causative organism is a virus of Flavivirus genus.
Epidemiology. A source of infection is a sick person (urban type) or monkey and wild marsupial animals (rural or jungle type). The transmitting organism is Aedes aegypti (in the people) and A.africanus (in the monkeys) mosquito. Disease is wide-spread in South America, equatorial Africa. The way of transmission is transmissible, rarely is aerogenic one.
Pathogenesis. After a bite the virus invades the regional lymphnodes and multiplies there. There is then virusemia and the dissemination in a liver (fatty dystrophia, the necrosis - the more it is expressed the disease is more serious), in the kidneys (edema, hemorrhages, necrosis of the tubules), in the heart (toxic injury of a myocardium), in the brain (dystrophia of nervous cells, perivascular hemorrhages). There is a hemorrhagic set of symptoms (the immune complexes are significant).
Clinics.
The incubative period lasts for 3-6 days.
There are three periods in the clinics: initial (stage of hyperemia), the period of remission (during severe forms it absent is), period of intoxication (culmination).
The initial period lasts for 3-4 days.
1. The toxinfectious syndrome.
2. Fever is up to 39-40оC.
3. Hyperemia of the face, neck, upper half of the chest, scleras and conjunctivas.
4. Hepatosplenomegaly.
5. Tachycardia is replaced by a relative bradycardia in 2-3 day after the onset of the disease.
6. Hemorrhagic set of symptoms (eruption, bleeding sickness of the gums etc.) can be on the 3-4th day.
The period of remission lasts from some hours till 1-2 days: the state of a patient improves and the temperature decreases.
The period of an intoxication:
1. The rise of the temperature.
2. The sharply marked toxinfectious set of symptoms.
3. Hepatolienal set of symptoms.
4. Hepatic insufficiency, marked jaundice.
5. Renal insufficiency.
6. Hemorrhagic set of symptoms (hemorrhages, nasal, intestinal, uterine bleedings). A hematemesis is a bad prognostic sign.
7. Cardiovascular insufficiency. The replacement of a bradycardia by a tachycardia is a bad prognostic sign.
In 90 % of cases the course is moderate or severe. There can be mild or subclinical forms, variants with the expressed intoxication, but without jaundice; fulminant course with death on the 2-3d day of illness, variants with the expressed hemorrhagic set of symptoms, enlargement of a liver and insignificant injury of kidneys.
Differential diagnostics: viral hepatitis, sepsis, leptospirosis, hemorrhagic fevers.
Diagnostics.
1. Virologic method (intracerebral infestation of white mice or on the culture of the cells).
2. Serological method (neutralization test on white mice, Complement Fixation Test, Indirect Agglutination Test) with paired serums.
3. Blood analyses show leukopenia, neutropenia. The bilirubin, residual nitrogen are enlarged, ALT raises.
4. Intravital biopsy of a liver with histological research.
The treatment includes a plasma of convalescents (during the first 3 days of illness), symptomatic therapy. For prophylaxis alive vaccine is used.
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