AMOEBIASIS SEMINAR ON PSM SUBJECT reading learning about the causative agent , understanding the disease clearly.

introduction to the topic
causative agent
understanding the disease
symptoms and signs
prevention and care
management and treatment

1. AMOEBIASIS MAHEK VERMA ROLL NO. 44 BATCH 2016 GUIDED BY – Dr. VIDYA RANI ma’am ( Professor )

2. CONTENTS INTRODUCTION HISTORY and EPIDEMIOLOGY EPIDEMIOLOGICAL DETERMINANTS INTRAINTESTINAL AMOEBIASIS EXTRAINTESTINAL AMOEBIASIS LAB DIAGNOSIS PREVENTION and CONTROL

3. INTRODUCT-ION T he term “AMOEBIASIS” has been defined by WHO – as the condition of harbouring the protozoan parasite Entamoeba histolytica with or without clinical manifestations. The symptomatic disease, occurs in <10% of infected individuals, is subdivided into – Intraintestinal and Extraintestinal amoebiasis. The Intraintestinal amoebiasis varies from mild abdominal discomfort and diarrhoea to acute fulminating dysentery. The Extraintestinal amoebiasis include involvement of liver, lungs, brain and spleen.

4. HISTORY The protozoan parasite ENTAMOEBA HISTOLYTICA was discovered by Losch in 1875. Losch demonstrated the parasite in the dysenteric faeces of a patient in St. Petersburg in Russia. In 1890, William Osler reported the case of a young man with dysentery, who later died of liver abscess. Councilman and Lafleur in 1891 established the pathogenesis of intestinal and hepatic amoebiasis.

5. EPIDEMIOL-OGY PREVALENCE IN THE WORLD Amoebiasis is a common infection of the human GI tract and has a worldwide distribution. It is a major health problem in the whole of CHINA, SOUTH EAST and WEST ASIA and LATIN AMERICA especially MEXICO. It is estimated that 50 million people carry E.histolytica in their intestinal tract and approx. 1/10 of infected people suffer from invasive amoebiasis. Invasive amoebiasis accounts for about 50,000 deaths in the world.

6. Prevalence rates vary from as low as 2% - 60% or more in areas devoid of sanitation. In areas of high prevalence, amoebiasis occurs in ENDEMIC forms as a result of high levels of transmission and constant reinfection. EPIDEMIC water-borne infections can occur if there is heavy contamination of drinking water supply.

7. PREVALENCE IN INDIA It is estimated that amoebiasis affects about 15% of Indian population. Prevalence rate is about 15% ranging from 3.6 - 47.4% in different areas. Epidemiologically, INDIA can be divided into three regions , depending on the prevalence of intestinal amoebiasis - HIGH PREVALENCE STATES MODERATE PREVALENCE STATES LOW PREVALENCE STATES >30% 10 – 30% < 10% Chandigarh, Tamil Nadu and Maharashtra Punjab, Uttar Pradesh, Bihar and Assam Haryana, Gujarat, Odisha and Sikkim

8. EPIDEMIOL-OGICAL DETERMINANTS

9. EPIDEMIOLO-GICAL DETERMINA-NTS AGENT FACTORS AGENT The amoebiasis is caused by potentially pathogenic strains of E.histolytica . Studies have shown that E.histolytica can be differentiated into 18 zymodemes. MORPHOLOGY E.histolytica occurs in three forms - 1.) Trophozoite 2.) Precyst 3.) Cyst

10. MORPHOLOGY of ENTAMOEBA HISTOLYTICA

11. LIFE CYCLE of ENTAMOEBA HISTOLYTICA

12. Reservoir of infection Man is the only reservoir of infection . The immediate source of infection is the faeces containing the mature quadrinucleate cysts. The cysts can remain viable under moist condition for about 10 days. Most individuals infected with E.histolytica remain symptom free and are healthy carriers of parasite. The carriers can discharge up to cysts daily. The greatest risk is associated with carriers engaged in the preparation and handling of food.  

13. Period of communicability As long as cysts are excreted ;this period may be several years, if cases are unrecognised and untreated. HOST FACTORS Amoebiasis may occur at any age. There is no sex or racial differences in the occurrence of the disease . Amoebiasis is frequently a household infection. When an individual in a family is infected, others in the family may also get affected.

14. Specific antiamoebic antibodies are produced when tissue invasion takes place. There is strong evidence that cell mediated immunity plays an important part in controlling the recurrence of invasive amoebiasis. ENVIRONMENTAL FACTORS Amoebiasis is more closely related to poor sanitation and socio-economic status than to climate. The use of night soil for agricultural purposes favours the spread of the disease. In countries with marked wet-dry seasons , infection rates are higher as cysts may survive longer

15. Epidemic outbreaks are usually associated with sewage seepage into the water supply. MODE OF TRANSMISSION 1.) Faecal-oral route This may readily take place through intake of contaminated water or food. 2.) Sexual transmission Oro-rectal contact is recognized among homosexual males. 3.) Vectors Flies ,cockroaches and rodents are capable of carrying cysts and contaminating food and drink.

16. Intestinal amoebiasis The lumen dwelling amoebae cause disease only when they invade the intestinal tissues, which occurs only in about 10% of cases of infection. The remaining 90% being the asymptomatic cases. Pathogenic strains Non- pathogenic strains For example- Entamoeba histolytica For example – Entamoeba dispar

17. Adherence Cytolysis Tissue necrosis Mucosal penetration Amoebic ulcer PATHOGENE-SIS OF INTESTINAL AMOEBIASIS

18. INTESTINAL AMOEBIASIS- amoebic ulcer in colon

19. CLINICAL FEATURES The clinical picture of intestinal amoebiasis covers a wide spectrum from non-invasive carrier state to fulminant colitis. The incubation period is highly variable from 1-4 months. The typical manifestation of intestinal amoebiasis is AMOEBIC DYSENTERY. Amoebic dysentery is insidious in onset and abdominal tenderness is less and localized.

20. Flask-shaped amoebic ulcer

21. Extraintestin-al amoebiasis The various extraintestinal lesions in amoebiasis are- Amoebic hepatitis Amoebic liver abscess Pulmonary amoebiasis Cerebral amoebiasis Splenic abscess Cutaneous amoebiasis Pericardial amoebiasis Genitourinary amoebiasis

22. LESIONS of EXTRAINTE-STINAL AMOEBIASIS

23. LAB DIAGNOSIS STOOL EXAMINATION Macroscopic appearance – the stool is foul smelling, copious, semiliquid, brownish –black in color and with blood and mucus. Microscopic appearance – 1.) Saline preparation - Cellular exudate is scanty and consists of PYKNOTIC BODIES, few pus cells, epithelial cells and macrophages. RBCs are clumped and yellow or brown –red in colour. CHARCOT-LEYDEN crystals are present .

24. CHARCOT- LEYDEN crystals

25. 2.) Iodine preparation For the demonstration of cysts or dead trophozoites, iodine mount is done to study the nuclear character. Stool culture – nelson’s, robinson’s and craig’s media are used. Mucosal scrapings Serodiagnosis – IHA, ELISA and Latex agglutination test. Molecular diagnosis – DNA probe, RT-PCR.

26. PREVENTION and CONTROL PRIMARY PREVENTION The measures aimed at primary prevention centre includes the preventing the contamination of food, water, vegetables and fruits with human faeces. Sanitation Water supply Food hygiene Health education Safe disposal of human excreta. Water filtration and boiling are most effective. Uncooked food disinfected with aq.soln.of acetic acid (5-10%) or vinegar. In the long term , a great deal can be accomplished through health education of public. Handwashing before eating and after defecation. Sand filters used for removing amoebic cysts. Food handlers are examined and treated periodically It includes basic knowledge of handwashing. Cysts are not affected with Cl treatment. Educated for food hygiene practices.

27. SECONDARY PREVENTION a.) EARLY DIAGNOSIS – Demonstration of trophozoites containing red cells is diagnostic. The trophozoites are seen in fresh mucus passed per rectum. Microscopy should be performed immediately before its cooling results. The absence of pus cells in stool is helpful in the differential diagnosis with shigellosis. Serological tests are negative in intestinal amoebiasis, but if positive than extraintestinal amoebiasis is assumed.

28. IHA is the most sensitive serological method. CIE and ELISA are newer methods used. b.) TREATMENT – 1.) METRONIDAZOLE Oral , dose – 30mg/kg/body wt. Dose is given after meals (3 times). Time – 8-10 days. Response in 48 hours. 2.) TINIDAZOLE. SYMPTOMATIC CASES

29. 1 .) In ENDEMIC areas – food handler (carrier) is treated ,not every persons because they have a high rate of reinfection. 2.) In NON-ENDEMIC areas – DIIODOHYDROXYQUIN oral , 650mg TDS(adults) and 30-40mg/kg/bogy wt.(children) for 20 days. DILOXANIDE FUROATE oral , 500mg TDS for 10 days (adults) CONTROL There is no acceptable chemoprophylaxis for amoebiasis. Mass examination and treatment are not a solution for amoebiasis. ASYMPTOMATIC CASES

30. References PARK’S TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE.( 25 th edition) PANIKER’S TEXTBOOK OF MEDICAL PARASITOLOGY

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