Medical Parasitology :

2. MedicalParasitology • Medical Parasitology: • that branch of medical sciences that deals with parasites of medical importance to man. • Parasites: • organisms that live in or on a host (temporarily or permanently) deriving food and shelter from that host.

3. Parasitism - a way of life • Symbiosis: “Any two organisms living in close association, commonly one living in or on the body of the other, are symbiotic, as compared with free living.” Symbiosis may be: • Commensalism: Sharing the table. One partner benefits but the other is not hurt. • Mutualism: Both partners benefit. • Parasitism: One partner (the parasite) harms and lives on the expense of the other (host).

4. Types of Hosts • Definitive host: • In which the adult or sexually reproducing form of the parasite lives. • Intermediate host: • In which the parasite lives during its larval stage or asexually reproducing form. • Reservoir host: • An animal harboring the same adult or sexually reproducing forms of the parasite like in human. Reservoir hosts represent a potential source of infection to man.

5. I like to present my self as insects and my allies Simply called Worms Medical Parasitology includes the study of 3 major groups of parasites: Protozoa Arthropods Helminths Hi I am a protozoa called One-celled organisms e.g. Musca domestica e.g. Giardia lamblia e.g. Ascaris lumbricoides

6. Helminths Helminths (Worms) Platyhelminths Nematodes (Flat worms) (Round worms) Trematodes Cestodes (Flukes) (Tape worms)

7. Suggested Text Book

8. Websites of Interest • There are thousands of reading resources on internet providing information and images on parasites, not all of them are as trustworthy. • Two excellent sites to look for general information and visual illustrations: • CDC (Division of Parasitic Diseases) http://www.cdc.gov/ • WHO (Tropical Diseases Research Program) http://www.who.int/en/ • Published papers: NCBI (Pubmed) http://www.ncbi.nlm.nih.gov/pubmed

9. Gastrointestinal Module Some Gastrointestinal Parasites Causing Dysentery

10. Parasites causing dysentery [1] Entamoeba histolytica &Amoebic dysentery [2] Balantidium coli & Balantidial dysentery [3] Trichuris trichiura &Trichuriasis Learning Objectives 1- Know the Definition of Dysentery, its mechanism & List the parasites causing it. 2- In each parasitic infection: A) Understand Life-cycle & Mode of transmission. B) Correlate the Pathogenesis with the Clinical Picture & complications C) Identify the appropriate methods for Diagnosis. D) Mention the drug of choice. E) List the different methods used for Prevention & Control. 3- Differentiate between pathogenic and commensal amoebae. 4- Understand the role of pigs in transmission of Balantidiasis.

11. Page numbers of the studied parasites in: Medical parasitology, 9th Edition. Markell & Voge's [1] E. Histolytica & Amoebic dysentery: Page; 22-36 [2] Balantidium coli & Balantidial dysentery: Page; 62-65 [3] Trichuris trichiura & Trichuriasis. Page; 263-266

12. Dysentery Painful frequent evacuation of small quantities of stool containing blood and mucus. It is usually a manifestation of large intestine affection.

13. Parasites Causing Dysentery 1-Entamoeba histolytica >Amoebic dysentery 2-Balantidium coli > Balantidial dysentery 3-Trichuris trichiura > Trichuriasis + 4-Schistosoma mansoni 5-Plasmodium falciparum 6-Leishmania (visceral) 7-Strongyloides stercoralis [heavy infection]

14. Amoebae Phylum: Sarcomastigophora Subphylum: Sarcodina Amoebae are either: a-Parasitic in man or b-Free living in water & soil Parasitic amoebae may be: a-Pathogenicorb-Non pathogenic [commensal] The only pathogenic amoeba of man is Entamoeba histolytica

15. 1- Entamoeba histolytica Disease: Amoebiasis or Amoebic dysentery. Distribution: Worldwide, endemic in tropical and subtropical countries. Habitat: Large intestine, mainly in the caecum, rectum & in the flexures. Definitive Host: Man. Reservoir host: Monkeys and rodents caecum

16. Morphology 1- Trophozoite Itis actively motile by pseudopodia. -Size: about20 µm (12–60 µm). -Cytoplasm: will differentiated into ectoplasm & endoplasm -Nucleus: spherical -Nuclear membrane: lined by fine regular chromatin granules. -Karyosome: small & central -Food vacuoles: leucocytes, bacteria, may be RBCs.

17. 2- Precyst It round in shape & smaller than trophozoite 3- Cyst: It may be A: uninucleate, B: binucleate or C: Quadrinucleate (=mature) cyst. Quadrinucleate cyst [= infective stage] Size:15 um in diameter, rounded with well developed cyst wall & contains four 4 nuclei.

18. Mode of infection Man is infected by ingestion of the quadrinucleated cysts through a- Ingestion of food or drink contaminated with infected faecal matter directly or through mechanical transmission of cysts by flies or cockroaches. b- Food handlers [chronic asymptomatic cyst carriers]. Autoinfection (Faeco-oral route)

19. Ingestion of contaminated food & water Life cycle:

20. Life cycle • Excystation of ingested mature (4N) cysts occurs in the small intestine. A nuclei division occurs, released trophozoites migrate & colonize the large intestine. • Trophozoites multiply by binary fission and produce cysts. Both stages are passed in feces. • Trophozoites can invade the intestinal wall (intestinal disease) or extraintestinal sites such as liver, brain & lung (extraintestinal disease).

21. Cycle of Quadrinucleate cyst of E.hitolytica within GIT Precyst Uninucleate cyst Binucleate cyst Pass out in stool In the lumen Quadrinucleate cyst Enter with food Attached to mucosa Binary fission trophozoite Mucosa of large intestine

22. Encystation of Trophozoite into>>>Cyst

23. Pathogenesis of amoebiasis Pathogenesity depends on: 1- Virulence of the infective strain of the parasite, e.g. 2- Host factors: General condition, immunity, drugs, debilitating states. 3- Intestinal condition: Some factors ↑ extent of intestinal invasion as injury, excess carbohydrate diet, stasis, bacteria flora. Pathological lesions are either: 1-Primary in the large intestine or 2- Secondary in extra-intestinal tissues. === E.dispar.

24. Pathogenesis Trophozoites secrete histolytic enzymes that cause >>necrosis of mucosa >>>>>>> ulcer with a wide base & narrow opening (undermined or flask-shaped ulcer). trophozoites Flask-shaped ulcer Ulcer formation is followed by: Fibrous thickening of intestinal wall, 2ry bacterial infection. Extra-intestinal invasion by trophozoites via portal blood.

25. Clinical picture: A- Intestinal Amoebiasis [1]- Asymptomatic infections (85-95% ):Cyst passers. [2]- Symptomatic infections (5-15%): Invasion of the intestinal mucosa  Flask-shaped ulcers. (A) Acute amoebic dysentery [Dysenteric Colitis]: Gradual onset, low grade fever, colic, dysentery (4-8/day). (B) Chronic amoebic colitis [Non Dysenteric Amoebiasis]: Intermittent diarrhea (1-4/ day) alternate with relative normality, abdominal pain, flatulence and loss of weight. On examination: Tenderness [localized usually over the caecum, sigmoid colon or on flexures of transverse colon]. Colonis thickened and palpable.

26. Clinical picture: B- Extra-Intestinal amoebiasis Spread of trophozoitesbydirect spread from primary intestinal lesion to the surrounding tissues or by via portal blood. Mainly to: Liver[producing amoebic hepatitis or abscess] usually of right lobe. other organs (e.g. lung, brain, spleen, and kidney)amoebic abscesses Skinproducing cutaneous amoebiasis. In extra-intestinal amoebiasis, there are: Fever, leucocytosis& clinical picture that varies according to the affected organ. Amoebic liver abscess

27. Complications of intestinal amoebiasis 1-Invasion of the appendix > Appendicitis. 2- Perforation of an ulcer > Peritonitis. 3- Strictures: due to healing by fibrosis. 4- Haemorrhage: due to erosion of a large blood vessel in the wall of the ulcer. 5-Amoeboma: It is an inflammatory thickening in the wall around the ulcer.

28. Pathogenesis & Complications

29. Diagnosis of intestinal amoebiasis 1- Clinical: History & clinical picture. 2- Laboratory: 1) Macroscopic stool examination: Stool is bulky, offensive with blood & mucus, scanty exudate and is acidic. 2) Microscopic stool examination: For detection of trophozoites in diarrhoeic stool and or cystsin formed stool by: a- Direct stool examination: b- Concentration methods:

30. 3- Sigmoidoscopy to visualize lesions & take biopsy from ulcer: [may show trophozoites]. Sigmoidoscopy Sigmoidoscope 4- Other Methods of diagnosis: a- Serologic tests: are useful in chronic amoebiasis & with tissue invasion e.g. IHA & ELISA. b- Radiological examination using barium enema. c- Detection of coproantigen. d- Molecular techniques.

31. Diagnosis of extra intestinal amoebiasis 1- Clinical: According to the affected organs. 2- Laboratory: -Examination of aspirate from abscess. The specimen must be taken from its border for detection of trophozoite stage. - Leucocytosis: due to 2nd bacterial infection. 3- Radiology: Ultrasonography, CT & MRI. 4- Serologic tests: For detection of antibodies.

32. Radiological diagnosis of amoebic liver abscess Ultrasound of amoebic liver abscess CT of amoebic liver abscess

33. Treatment Treatment of intestinal amoebiasis 1- Asymptomatic cases or carriers: (luminal) Diloxanide furoate (Furamide): 500 mg t.d.s. for 10 days. 2- Acute intestinal cases: (tissue + luminal) Metronidazole: 750 mg t.d.s. for 10 days followed by Diloxanide furoate: 500 mg t.d.s. for 10 days plus antibioticsas Tetracycline [250 mg 4 times daily; for 5 days] In severe cases: above ttt + bed rest + adequate Fluid +electrolyte replacement. 3- Chronic intestinal cases: Metronidazole followed by Diloxanide furoate as before.

34. Treatment of extra intestinal amoebiasis -Metronidazole followed by Diloxanide furoate as before plus Chloroquine phosphate (Resochin) for small abscesses. Large abscesses require medical treatment and closed aspiration or surgical drainage. ==== Surgical drainage of abscess Thick chocolate- colored or anchovy-sauce pus Closed aspiration of abscess

35. Epidemiology 1- The main source of infection is cyst passers. 3-Cysts are killed by dryness, heat (↑ 55ºC) and by chlorine. 2-Cysts remain viable in faeces for few days & in water for a long periods.

36. . Prevention & Control 1-Health education. 2- Safe water supply. 3- Proper sewage disposal. 4- Treatment of cases & 5- Repeated examinations of food handlers. 6- Insect control.

37. Differences between amoebic & bacillary dysentery

38. Parasites causing dysentery Phylum Ciliophora 2- Balantidium coli Disease: Balantidiasis, Balantidial dysentery. Distribution: Cosmopolitan. Definitive host: Man. Reservoir host: Pig. Habitat: Large intestine, especially the caecum.

39. Morphology 1- Trophozoite [vegetative form] Size:75x50 umShape: oval covered with cilia (locomotion) has 2 nuclei [micronucleus & macronucleus]. 2- Cyst [infective stage] Size: 40-60 µm in diameter, Shape: round surrounded by a thick cyst wall. Cyst has 2 nuclei [micronucleus & macronucleus]. Trophozoite & Cyst are diagnostic stages

40. Life cycle • Infection occurs after ingestion of cysts (IS) in contaminated food or water. • Excystation occurs in the small intestine. • Trophozoites colonize the large intestine & reproduced either by asexual transverse binary fission or sexual conjugation. • Some trophozoites invade the wall of the colon using cytolytic enzymes & multiply. • Encystation occurs upon passing through the colon and being excreted in feces.

41. Life Cycle of Balantidium coli Pass out in stool In the lumen Trophozoites multiply by both Transverse binary fission & Conjugation Cyst enters with food Attached to mucosa trophozoite Mucosa of large intestine

42. Mode of infection Heteroinfection Autoinfection Ingestion of cysts in 1- Contaminated food or water. 2- Flies and food handlers 3- Faeco-oral. Source of infection: Infected man (person to person) or from infected pigs (pigs to man) as in farms or slaughter houses.

43. Pathogenesis & Clinical picture of Balantidiasis Similar to amoebiasis  flask-shaped ulcers, But no Extra-intestinal lesions. Invasion of the mucosa is facilitated by a- The mechanical action of cilia. b- The cytolytic enzyme hyaluronidase.

44. Clinical picture 1- Asymptomatic carrier (cyst passer). 2- Acute infection: The patient suffers from diarrhea or dysentery. 3- Chronic infection: Itis characterized by diarrhea alternating with constipation, tender colon & loss of weight. Complications 1- Intestinal perforation & peritonitis, 2- haemorrhage. 3- secondary bacterial infection.

45. Diagnosis of Balantidiasis 1- Clinical: Clinical picture & History of close contact with pig. 2- Laboratory: Stool examination for detection of: Trophozoites & Cysts 3-Sigmoidscopy: to visualize the lesion & take a biopsy. trophozoite cyst

46. Metronidazole: 750 mg/ 3 times/day for 5 daysOR Treatment of Balantidiasis Prevention & Control 1- Sanitary disposal of human and pig faeces. 2- Treatment of the patients. 3- Treatment of infected pigs. Tetracycline: 500 mg/4 times/ day for 10 days

47. How Entamoeba & Balantidium cause Dysentery Entamoeba trophozoite Balantidium trophozoite Boring action of cilia Histolytic enzyme Flask-shaped ulcer Flask-shaped ulcer

48. Parasites causing dysentery3-Τrichuristrichiura[Trich: hair, uris: tail] [Trichocephalus trichiurus] (Whip worm)

49. Disease:Trichuriasis or Trichocephaliasis. Geographical distribution: Warm moist regions with poor sanitation. D.H. : Man. NoR.H. orI.H. Habitat: Large intestine of man [in the caecum]. [the thin anterior narrow part is deeply embedded in the submucosa].

50. Morphology 1- Adultworms are whip-like Anterior narrow part (3/5) contains a cellular esophagus. Posterior broad part (2/5) contains rest of the organs. Male: 3 - 4.5 cm, with coiled posterior end with one spicule. Female: 3.5 - 5 cm with straight posterior end. The vulva opens at the junction of the thin & thick portions.