MEDICAL PARASITOLOGY

1. MEDICAL PARASITOLOGY HELMINTHS & PROTOZOA

2. INFORMATION EMPHASIS • Agent and Group ID; general importance • Epidemiology (distribution, transmission, etc) • Pathogenic capability • Diagnosis • Control

3. BASIC TERMINOLOGY & 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 vs Facultative Parasites • Endo- vs Ecto-parasites • Pseudo- vs Spurious Parasites • Zoonotic Parasites • Host-specific vs Non-host-specific Parasites • Definitive vs Intermediate Hosts • Paratenic/Transfer Hosts • Vectors

5. PARASITE SURVIVAL FACTORS • Parasites have successfully adapted to (all?) environmental “niches” in hosts • Parasites best adapted are least pathogenic • Parasite-host relationships are typically long-term/chronic/”intimate”

6. CONDITIONS NECESSARY FOR SUCCESSFUL ENDEMIC PARASITISM • Reservoir of infection • Means of transmission from infected to susceptible, “new” hosts • Ability to invade and successfully reside in “new” hosts • Ability to reproduce

7. HELMINTH/WORM TERMINOLOGY • Adults: sexually reproductive life cycle stage • Larvae: developmental or asexually reproductive life cycle stage • Eggs: stage protective of zygote &/or embryo • Cysts: usually a larval stage encapsulated in tissues of an intermediate host • Hypobiosis: worms in temporary developmental arrest • Monoecious/hermaphroditic: both sexes 1 body • Dioecious: sexes separate; males & females • Parthenogenesis: ability to produce offspring without fertilization of eggs

8. Helminths, continued Worm-terms, continued • Oviparous: production of eggs, discharged from uterus of female • Ovoviviparous: production of eggs which hatch prior to discharge from uterus of female • Viviparous: production of embryos/L1 larvae, no rigid encapsulation of embryo

9. Enteric helminths, continued GENERALIZED NEMATODE LIFE CYCLE Adults Eggs Embryos L1 L2 larva L3 larva L4 larva L5 juvenile

10. Enteric Helminths Ascaris lumbricoides • SI roundworm transmitted fecal-oral via eggs • Pathogenic potential low to high, depending on host species and condition, number of eggs ingested, secondary bacterial agents carried • Clinical signs: larval migration; none, pneumonitis, asthmatic reaction. Adults; SI blockage, plugging of bile duct, perforation of SI, appendix or other site, malnourishment • Reservoir: human DH • Damage potential: dependent on worm #s, host susceptibility to larval and adult action

11. Enteric helminths, continued • lumbricoides, continued • Prevalence: world-wide, temperate and tropical regions, possibly 1 billion infected • Diagnosis: eggs in feces, observation of ‘drop-out’ adult worms • Treatment: piperazine, albendazole, mebendazole, pyrantel pamoate

12. Enteric helminths, continued Ascaris lumbricoides life cycle

13. Extra-enteric helminths, continued Toxocara canis, Toxocara cati, Balisascariscolumnaris, others (Visceral Larval Migrans) • Transmission: fecal-oral, ingestion of infective ova • Pathogenic potential high, dependent on #s of larvae, migrational destination(s) • Clinical signs determined by #s of larvae, sites infected; cough, fever, hypereosinophilia, retinochoroiditis, epilepsy, myocarditis, other • Reservoir hosts: canines, felines, mustelids, raccoons, badgers, oppossums, other • Damage potential high: carriers of bacterial contaminants, direct toxicity & tissue destruct.

14. Extra-enteric helminths, continued T. canis, T. cati, B. columnaris, et.al. • Prevalence worldwide, sanitation dependent, cold/cool temperate regions to equator • Diagnosis: serology, lesion/abcess pathological examination (gross & histo), high eosinophil count is strongly suggestive • Treatment: systemic anthelmintics have been used with varying degrees of success, depending on diagnostic timing; fenbendazole & other benzimidazoles, probably avermectins

15. Toxocara canis life cycle

16. Enteric helminths, continued Ancylostoma duodenale & Necator americanus (hookworms) • Transmission via contact of skin with L3 larva • Pathogenic potential: population dependent, each worm sucks blood from mucosa in SI, larval migration usually insignificant • Clinical signs: minor reaction (ground itch), # dependent, at larval entry; pneumonitis via migrating larvae, if large #s; eosinophilia, occult blood in stools, diarrhea, anemia, edema, et.al. • Reservoir: humans, possibly other anthropoids • Damage potential depends on condition & sensitivity of host, and #s of worms

17. Enteric helminths, continued • Duodenale & N. americanus, continued • Prevalence world-wide, in tropics, subtropics, and warm temperate regions; some zonal variation by species • Diagnosis by ID of ova in feces • Treatment: albendazole, mebendazole, pyrantel pamoate, piperazine (probably)

18. Hookworm Life Cycle

19. Extra-enteric helminths, continued Ancylostoma caninum, A. braziliense, Uncinariastenocephala, et.al. (cutaneous larval migrans) • Transmission: penetration of skin by direct contact with infective L3 larvae • Pathogenic potential: low, transient • Clinical signs: “serpiginous tracks”/”creeping eruption” on skin near invasion sites • Reservoir hosts: canines, felines, other animals with host-specific species of hookworms • Damage potential: limited to numbers of worms involved, host sensitivity to cutaneous trauma

20. Extra-enteric helminths, continued • caninum, A. braziliense, U. stenocephala, et.al • Prevalence: worldwide distribution, tropical, subtropical, warm & cool temperate, sub-arctic (Uncinaria) • Diagnosis: visual observation of characteristic “tracks/burrows” on skin surface • Treatment: albenazole, other benzimidazoles

21. Enteric helminths, continued Trichuris trichiura (whipworm) • Transmission: fecal-oral via embryonated ova • Pathogenic potential: low to moderate, dependent on worm numbers & location in LI • Clinical signs: dependent on worm #s; none, bloody(frank)/mucoid diarrhea, abdominal pain & distention, rect. prolapse, anemia, weakness, eosinophilia • Reservoir: mainly human, others possible but host specificity not well documented • Damage hinges on results & numbers of worm mucosal perforations, bacterial/viral involvement, degrees of blood loss, worm location

22. Enteric helminths, continued T. trichiura, continued • Prevalence: worldwide tropical, subtropical, warm temperate sanitation dependent; SE USA, spotty in other states with large populations of infected immigrants • Diagnosis: microscopic ID of ova in feces • Treatment: albendazole is drug of choice

23. Trichuris trichiura life cycle

24. Enteric helminths, continued Capillaria phillipinensis • Transmission: ingestion of larvae in fresh and brackish-water fish • Pathogenic potential high due to worm site and autoinfection factors • Symptoms: abdominal pain, borborygmus, diarrhea early; anorexia, nausea, vomiting, et.al • Reservoir unknown: probably many fish-eating mammals • Damage potential high: populations build via autoinfection; adults and larvae migrate through mucosal tissue in (mainly) jujunal SI

25. Enteric helminths, continued C. phillipinensis, continued • Prevalence high/moderate in Phillipine areas where eating raw fish is a cultural event • Diagnosis: microscopic ID of ova in feces, differentiation from whipworm eggs (Trichuris) • Treatment: mebendazole drug of choice, other benzimidazoles also efficacious

26. Enteric helminths, continued Enterobius vermicularis (pinworm) • Transmission by ingestion of embryonated ova • Pathogenic potential 0/low • Clinical signs: occasional anal itching from night-time exit migration of female worm for oviposition; occasional host skin pruritis to egg ‘glue’; rare migration & disintegration of female worms into urogenital tract of female, with lesions in abdominal cavity via oviducts • Reservoir hosts human (family & friends) • Damage potential 0; no tissue invasion/insult, no apparently toxic by-product production

27. Enteric helminths, continued E. vermicularis, continued • Prevalence world-wide, arctic to equator • Diagnosis: microscopic ID of ova &/or worms on transparent cellophane tape swab of perineum • Treatment: albendazole, and others

28. Enterobius vermicularis life cycle

29. Extra-enteric Helminths Strongyloides stercoralis • Transmission: ingestion of, or skin contact with L3 larva, possibly congenital & transmammary • Pathogenic potential very high due to autoinfection, infection site, parasite-host incompatibility • Clinical signs: skin reaction at larval entry (ground itch), pneumonitis re primary larval migration, diarrhea/dysentery, malabsorption, mucosal ulceration, frank or occult bloody stool • Reservoir hosts: none necessary, free-living agent with invasion capability (facultative P)

30. Extra-enteric helminths, continued S. stercoralis, continued • Damage potential high/extreme: direct damage to SI villar epithelium extensive; worm population buildup intensifies, eventually colonizes colonic mucosa, nutritional absorption restricted/eliminated, dehydration intense • Prevalence: free-living colonies numerous, distribution similar to hookworms, human infections rare, sporadic, but significant • Diagnosis; isolation, microscopic ID of ova, larvae in feces or intestinal biopsies • Treatment: albendazole, ivermectin, others

31. Strongyloides stercoralis life cycle

32. Extra-enteric helminths, continued Trichinella spiralis • Transmission: ingestion of encysted larvae in meat • Pathogenic potential: moderate in majority of infected hosts; # of infective larvae, host tolerance are major factors • Clinical signs: occasional diarrhea during early stages; fever, eosinophilia, muscle pain/stiffness during larval invasion of muscle • Damage potential: low/moderate in ‘healthy’ hosts, high in those in which myocarditis, encephalitis or chronic pneumonitis occur

33. Extra-enteric helminths, continued T. spiralis, continued • Prevalence: low to high, dependent on cultural preferences regarding meat selection & preparation; no climatic factors are involved • Diagnosis: serologic testing, histologic ID of larvae in muscle biopsy • Treatment: corticosteroids, mebendazole, albendazole

34. Trichinella spiralis life cycle

35. Extraenteric helminths, continued Dracunculus medinensis • Transmitted by ingestion of copepod IH • Clinical signs: skin “blister” followed by ulcer with anterior end of female worm visible, cutaneous bulge of skin over body of worm, various immune responses (rashes, asthma) • Reservoir hosts: canines, many other mammals • Damage potential: low to moderate, depending on sensitivity of host to worm excretions and other worm-related antigens • Prevalence worldwide, from equator into cool temperate climatic areas

36. Extraenteric helminths, continued D. medinensis, continued • Diagnosis: observation of skin ulcer, at bottom of which end of female worm is visible • Treatment: removal of worm by gentle extraction from burrow by winding on a stick, with concomitant use of metronidazole or thiabendazole

37. Dracunculus medinensis life cycle

38. Filarid helminths Filarid Helminth Life Cycle DH Vector Adults microfilariae L1 L2 larva L4 larva L3 larva L5 larva

39. Filarid helminths Wuchereria bancrofti (filariasis/elephantiasis) • Transmission by mosquito vectors • Pathogenic potential moderate - high, long term • Clinical signs: variable re host factors and worm species/strains; none, renal disease, hematuria, proteinuria, hyperimmune reactivity, eosinophilia, lymphangitis (soft edematous swelling of extremeties, followed by eventual hardening) • Reservoir hosts: humans, some monkeys • Damage potential variable: immune reactions to worms & worm products varies with individuals, long-term, plugging of lymph vessels

40. Filarid helminths, continued W. bancrofti, continued • Prevalence: throughout tropical and subtropical countries, into some warm temperate areas • Diagnosis: recovery and microscopic ID of microfilaria from blood samples • Treatment: diethylcarbamazine, followed by ivermectin for prevention of reinfection

41. Wuchereria bancrofti life cycle

42. Filarid helminths, continued Brugia malayi, et.al. • Transmission by mosquito species different from those involved with W. bancrofti • Pathogenic potential essentially similar to that described for W. bancrofti • Clinical signs similar to those of W. bancrofti • Damage potential similar to that of W. bancrofti • Prevalence similar to W. bancrofti, regional differences dependent on vector habitat preferences • Diagnosis: microscopic diff of microfilariae from other species • Treatment: diethylcarbamazine + Ivermectin

43. Filarid helminths, continued Loa loa (african eyeworm) • Transmission via chrysops/mango fly vectors • Pathogenic potential moderate, dependent on host sensitivity factors • Clinical signs: eosinophilia, few obvious signs except when adults are migrating across eye; occasional swellings, edema in local sites • Reservoir hosts: monkeys known, possibly et.al • Damage potential low, minor host response normally • Prevalence: tropical, rain forest vector habitat • Diagnosis: ID of microfilaria, extraction of adult • Treatment: Diethylcarbamazine + ivermectin

44. Loa loa life cycle

45. Filarid helminths, continued Mansonella spp., Dipetalonema spp., et.al. • Transmission by midges & blackflies • Pathogenic potential low to zero • Clinical signs usually non-existent • Reservoir hosts: humans, monkeys • Damage potental low, dependent on host sensitivity to specific worms • Prevalence: tropical, subtropical, warm temperate regions where vectors exist • Diagnosis: ID of microfilariae in blood • Treatment: Diethylcarbamazine + ivermectin, when warranted

46. Filarid helminths, continued Onchocerca volvulus (river blindness) • Transmitted by blackfly vectors • Pathogenic potential moderate, dependent on death & decomposition of microfilariae • Clinical signs: adult clusters cause subcutaneous nodules, microfilariae cause blindness • Reservoir hosts: large domestic animals, probably others • Damage potential low/moderate, depending on host sensitivity, toxicity of worm ‘strain’, number and death/decomposition rate of larvae in eye

47. Filarid helminths, continued O. volvulus, continued • Prevalence variable, 5 to 80% in endemic areas near streams needed by blackfly reproduction • Diagnosis; observation of adults in prominent subcutaneous nodules, skin biopsy and histologic examination for microfilariae • Treatment: surgical removal of adults, diethylcarbamazine, ivermectin for larvae

48. Onchocerca volvulus life cycle

49. Filarid helminths, continued Dirofilaria immitis (canine heartworm infection) • Transmission by mosquito vector • Pathogenic potential in human (unnatural host) low/moderate, dependent on host sensitivity • Clinical signs usually absent in humans, dependent on location of worm • Reservoir hosts; canines (dogs, coyotes, etc.) • Damage potential low in humans, dependent on host sensitivity, #s of worms, location of worms • Prevalence wide: tropical, subtropical, warm and cool temperate regions • Diagnosis: usually biopsy of dead, encysted worm • Treatment: surgical removal

50. Flatworms/Platyhelminths Flatworm-related Terminology • Cestodes/tapeworms: segmented flatworms • Trematodes/flukes: leaf-shaped (except for schistosomes), single-unit flatworms • Oncosphere/hexacanth: egg-encased embryo of cyclophyllidean tapeworms • Coracidium: egg-encased embryo of pseudophyllidean tapeworms • Miracidium: egg-encased embryo of flukes • Cysticercoid, cysticercus, coenurus, hydatid cysts: cyclophyllidean tapeworm larval types in IHs