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MEDICAL PARASITOLOGY

MEDICAL PARASITOLOGY. Protozoa and Helminths. INFORMATION EMPHASIS Agent ID and general importance Epidemiology (transmission, distribution, etc) Agent damage capability Diagnostics Control. BASIC TERMINOLOGY AND PRINCIPLES Symbiosis: Living together

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MEDICAL PARASITOLOGY

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  1. MEDICAL PARASITOLOGY Protozoa and Helminths

  2. INFORMATION EMPHASIS Agent ID and general importance Epidemiology (transmission, distribution, etc) Agent damage capability Diagnostics Control

  3. BASIC TERMINOLOGY AND PRINCIPLES Symbiosis: Living together Commensalism: One symbiont benefits, other unaffected Mutualism: Both symbionts benefit Parasitism: One symbiont benefits, other is damaged

  4. COMMON TERMS • Obligate/Facultative Parasites • Endo/Ecto Parasites • Pseudo/Spurious Parasites • Zoonotic Parasites • Host-specific/Non-specific Parasites • Definitive/Intermediate Hosts • Paratenic/Transfer Hosts • Vector Hosts

  5. SURVIVAL FACTS AND FUNCTIONS • Parasites adapt to every niche in a host • Best adapted are least pathogenic • Parasite-host relationship is typically long-term/chronic/ “intimate”

  6. CONDITIONS REQUIRED FOR ENDEMIC PARASITISM • Reservoir of Infection • Means of Transmission to Susceptible Hosts • Ability to Invade and Establish in New Hosts • Ability to Reproduce

  7. PROTOZOAN TERMINOLOGY • Trophozoite: Active, vegetative LC stage • Cysts: Protective LC stage -Common cyst -Oocyst, sporocyst, sarcocyst, pseudocyst, etc • Cilia: Ciliate motility organelles • Flagella: Flagellate motility organelles • Pseudopod: Amoeba motility organelles • Macronucleus: Ciliate body function control • Axostyle: Flagellate “skeletal” rod • Peristome: Funnel leading to cytostome/mouth

  8. CILIATE PARASITE Balantidium coli Trophozoite Cyst Cytostome Macronucleus Macronucleus Cilia

  9. Ciliate parasite, continued • Balantidium coli Cyst transmission (fecal oral) Pathogenic in humans, mucosal erosion Frank blood in feces, sloughed mucosa Reservoir hosts swine, probably other Potential for serious damage high Prevalence overall, low Diagnosis: fecal analysis for cysts, trophs, proctoscopy for lesions/biopsy Treatment: oxytet; metronidazole; natural, spontaneous clearance occasionally

  10. Balantidium coli Life Cycle

  11. FLAGELLATE PARASITES AND COMMENSALS Trichomonads and Dientamoeba fragilis Trophozoites only Flagella Nucleus/nuclei Body shape & size

  12. Flagellates, continued Trichomonas tenax Trophozoite transmission-direct oral Mouth inhabitant, oral hygiene factor Nonpathogenic, thrives in bad conditions Reservoir unknown, probably wide Considered classically commensalistic Prevalence data spotty Diagnosis by culture, microscopic exam of oral fluids/scrapings Eliminated by good oral hygiene

  13. Pentatrichomonas hominis, Dientamoeba fragilis Transmission direct-oral, no cysts (you tell me) Colon/caecum inhabitants Non-pathogenic Reservoir unknown, probably wide Considered commensalistic (D. fragilis ???) Prevalence unknown Diagnosis usually incidental-fecal smear-stain, wet mounts + microscopy Treatment: incidental elimination-Flagyl, et.al.

  14. Dientamoeba fragilis Life Cycle

  15. Flagellate, continued Trichomonas vaginalis Transmitted by sexual intercourse Induces vaginal pH change, erosion of normal mucosa in women Vaginal itching, burning, yellow discharge in women, occasional urethritis, prostate swelling in men Human reservoir, zoonotic potential ?? Prevalence varies with population & culture Diagnosis by visual features, microscopy Treatment usually Flagyl

  16. Trichomonas vaginalis Life Cycle

  17. Flagellate Parasites and Commensals Chilomastix mesnili Enteromonas hominis, Retortamonas intestinalis, Giardia lamblia, et.al. Trophozoites Cysts Nuclei Nuclei Flagella Size & shape Size & shape

  18. Flagellates, continued Chilomastix mesnili, Enteromonas sp., Retortamonas sp.,, others Caecum/colon inhabitants Transmission by cyst or trophozoite Nonpathogenic, commensalistic Thrive in most diarrheic conditions Reservoir pool (probably) wide, unknown Widespread, sanitation dependent Diagnosis: microscopic fecal exam Treatment: unnecessary in most cases, Flagyl will work

  19. Flagellates, continued Giardia lamblia, etc Cyst transmission Pathogenic potential individually inconsistent Clinical signs variable Diarrhea/dysentery, periodic or steady Gas production Borborygmus Anorexia Skin rash Fibromyalgia Spontaneous lactose intolerance Fatigue, mild/severe Other

  20. Flagellates, continued Giardia, continued Reservoir hosts: almost any mammal Damage potential: individual factors Immunocompetence of host Natural, undefined host tolerance level Other (fuzzy factors) Worldwide distribution, sanitation dependent Diagnosis: fecal ELISA, direct microscopic exam for cysts/trophs Treatment: Atabrine, Flagyl, other

  21. Giardia Life Cycle

  22. Flagellates, continued HAEMOFLAGELLATES Trypanosomes/ Leishmanias/ trypomastigote forms amastigote forms

  23. Haemoflagellates, continued Trypanosoma brucei complex, T.b. gambiense, T.b. rhodesiense, others Vector transmission, Tse tse flies Pathogenic, terminal ‘sleeping sickness’, East African SS less acute than West African SS Signs: swollen cervical lymph nodes, fever, rashes, headache, malaise, nausea, eventually coma Various wild/domestic animal reservoirs West African much more acute and severe than East African SS.

  24. Haemoflagellates, continued Trypanosoma brucei complex, continued T.b. gambiense in West Africa, overlaps with endemic East African T.b. rhodesiense in center of continent Microscopy of concentrated or cultured blood or fluid aspirates, RES biopsy normal diagnostic methods Treatment: melarsoprol complex, suramin

  25. Trypanosoma brucei complex, LC

  26. Haemoflagellates, continued Trypanosoma cruzi American trypanosomiasis, Chaga’s disease Vector/direct contact transmission; triatomids, several species Highly pathogenic late-term/chronic Symptoms vary: fever; edema; swelling of thyroid, spleen, liver, various lymph nodes; CNS re mental impairment, coma; tachycardia, weakness, chest pain, anemia, megacolon, megaesophagus, other, depending on organism strain, length of infection, condition of host, etc.

  27. Haemoflagellates, continue T. cruzi, continued Reservoir large, many carnivore, omnivore & herbivore species Damage severe, early (fulminating) or late (chronic), depends on various factors Prevalence < 3% to > 50% in endemic areas from southcentral USA to southern SA Diagnosis: cell/fluid culture, xenodiagnosis, direct microscopy Treatment: no reliable/curative; nifurtimox, primaquine & related drugs reduce but do not eliminate blood stage, nothing effective X cellular stage

  28. T.cruzi, continued Triatomid Vector Trypomastigote/ Trypanosome

  29. Haemoflagellates, continued T. Cruzi life cycle

  30. Haemoflagellates, continued Leishmania topica complex, L.t. mexicana complex, L.t. braziliense complex, et.al. Vector trans. by sand flies Superficial to extensive, shallow to deep Cutaneous lesions, vary by strain/species Oriental sore: limited, wet ulcer Chiclero ulcer: ear ‘notches’ Diffuse cutaneous: dry, diffuse Mucocutaneous: cartilage erosion Reservoir: large; many native carnivore, omnivore, herbivore vertebrates

  31. Haemolagellates, continued Leishmania tropica complex, continued Lesion severity varies with species/strain, simple limited wet/dry to severe erosion Widespread in tropical, subtropical & warm temperate regions worldwide Lesion appearance is diagnostic, agents can be cultured or viewed microscopically Pentavalent antimony compound treatment, with/without amphotericin B

  32. Haemoflagellates, continued Leishmania donovoni complex Vector transmission, sandflies Visceral, reticulo-endothelial system inhabitation, often lethal Fevers (variable), anemia, hepatomegaly splenomegaly, ascites, Kala-azar (blackening of facial skin), et.al. Reservoir: domestic & wild vetebrates Damage potential varies with species/strains Distributed widely, tropics, subtropics, warm temperate and cool temperate regions Diagnosis by serology, culture of blood or biopsy Antimony, amphotericin-B, allopurinol treatments

  33. Leishmania sp. life cycle

  34. Sarcodina AMOEBIC PARASITES AND COMMENSALS Entamoeba gingivalis Trophozoite only, inhabits oral cavity Transmitted directly (no cyst) Commensalistic, considered nonpathogenic Host reservoir: dogs, cats, monkeys, other? Patho potential considered 0/low Distribution undefined, prevalence 70-90% of “unhealthy”, 7-35% of “healthy” mouths surveyed Diagnosis: microscopy of tissue/scraping/fluid Treatment: improve oral hygiene; probably Flagyl

  35. Sarcodines, continued Amebic parasites and commensals, continued Entamoeba histolytica Trophozoite in caecum/colon, if invasive may inhabit liver, lungs, other tissues; Cysts (infective stage) form in normal stools Pathology variable: noninvasive; if invasive, ulcerates colonic mucosa, spreads to liver, lung, et.al., produces abcesses; path potential indicated by colony site Reservoir includes monkeys, dogs, pigs, et.al. Distribution worldwide: tropical, subtropical, warm temperate areas; sanitation dependent

  36. Sarcondines, continued E. histolytica, continued Prevalence rated second to Giardia worldly Diagnosis by microscopic ID of trophs, cysts in feces, trophs in tissue-based abcesses Treated with Flagyl (metronidazol), various Emetine formulations, Diiodohydroxyquin, et.al.

  37. Entamoeba histolytica Cyst Trophozoite

  38. Amoeba sp. life cycle

  39. Sarcodines, continued Entamoeba coli, E. hartmanni, E. dispar, E. sp.(unnamed), Endolimax nana, Iodamoebabutschlii, a few others Caecum/colon inhabitants, transmitted by cysts, All commensals (with rare exceptions) Diarrhea enhances production of trophs Reservoir: various vertebrate animals Damage potential 0/low (some exceptions?) Prevalence high, world-wide warm areas Diagnosis: microscopic ID in feces Treatment considered unnecessary

  40. Entamoeba coli Trophozoite Cyst

  41. Sporozoa/apicomplexa SPOROZOA/APICOMPLEXA TERMINOLOGY Sporogony: basic life cycle stage; sporozoite generation Schizogony/merogony: basic life cycle stage; (asexual repro) merozoite generation Gametogony/gamogony: basic life cycle stage; (sexual repro) gametocyte generation Oocyst: cyst produced in sporogony Sporocyst: cyst within oocyst, produced in sporogony Sporozoite: basic infective unit in oocysts/sporocysts

  42. Sporozoa, continued Sporozoan terminology, continued Trophozoite: transitional zoite, between sporozoite and schizont/merozoite Merozoite: basic zoite product of schizogony Tachyzoite: rapidly replicating merozoite Bradyzoite: slowly replicating merozoite Sarcocyst: end-stage schizont in intermediate host with Sarcocystis sp. infection Pseudocyst: end-stage schizont in intermediate host with Toxoplasma gondii infection

  43. Sporozoa, continued Sporozoa, continued Basic Life Cycle Stages Sporogony: formation of sporocysts and sporozoites Schizogony/merogony: formation of merozoites/tachyzoites/bradyzoites Gamogony/gametogony: formation of gametocytes and gametes

  44. Sporozoa, continued Isospora belli Transmission direct, fecal oral, via oocysts Pathogenic potential low, non-bloody diarrhea common in immunodeficient hosts, uncommon in others Clinical signs absent, except in rare cases Reservoir limited to humans, other anthropoids, strongly host-specific Damage low, destroys superficial mucosal cells Prevalence world-wide, sanitation dependent Diagnosis by microscopic ID of oocysts in fecal flotation Treatment usually unnecessary, pyrimethamine + a sulfa, trimethoprim, when needed

  45. Isospora sp. life cycle

  46. Sporozoa, continued Cyclospora cayetanensis Transmission direct fecal-oral, via oocysts Pathogenic potential low/moderate, non-bloody diarrhea in sporadic cases, most severe in immunodeficient individuals Diarrhea ~3 weeks in “healthy” hosts, longer/much longer in immonodeficient; can be cyclic, recurrent; long-term may + anorexia, fatigue, weight loss, fever Reservoir hosts: reptiles, rodents, insectivores, probably other domestic & wild animals; species ID is incomplete in host animals

  47. Sporzoa, continued C. cayetanensis, continued Damage: jujunal villous atrophy, crypt hyperplasia, inflammation Prevalence spotty, outbreaks in New Guinea, Nepal, Peru, Chicago, Canada, other Diagnosis: microscopic ID of oocysts from fresh feces, acid-fast-stained smears, fluorescent Ab-stain preps Treatment: trimethoprim + sulfamethoxazole

  48. Cyclospora sp. life cycle

  49. Sporozoa, continued Cryptosporidium parvum Transmission direct, fecal-oral, via oocysts Pathogenic potential variable: low in “healthy”, moderate/high in “deficient” hosts, depending on immunocompetence level Clinical signs: non-bloody diarrhea/dysentery, mild/short-term (~2 weeks) to severe/long- term (steady or recurrent) Reservoir: complete spectrum unknown, but many domestic animals are known Damage potential and mechanisms vary with hosts & species, poorly understood

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