MEDICAL PARASITOLOGY

HELMINTHS & PROTOZOA

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

BASIC TERMINOLOGY & PRINCIPLES

Symbiosis: Living together

Commensalism: One symbiont benefits, other unaffected

Mutualism: Both symbionts benefit

Parasitism: One symbiont benefits, other is damaged

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

PARASITE SURVIVAL FACTORS Parasites have successfully adapted to (all?) environmental niches in hosts Parasites best adapted are least pathogenic Parasite-host relationships are typically longterm/chronic/intimate

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

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

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

Enteric helminths, continued

GENERALIZED NEMATODE LIFE CYCLE Adults Eggs Embryos L1 L2 larva

L3 larva
L4 larva L5 juvenile

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

Enteric helminths, continued

A. lumbricoides, continued Prevalence: world-wide, temperate and tropical regions, possibly 1 billion infected Diagnosis: eggs in feces, observation of dropout adult worms Treatment: piperazine, albendazole, mebendazole, pyrantel pamoate

Enteric helminths, continued

Ascaris lumbricoides life cycle

Extra-enteric helminths, continued

Toxocara canis, Toxocara cati, Balisascaris columnaris, 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.

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

Toxocara canis life cycle

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

Enteric helminths, continued

A. 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)

Hookworm Life Cycle

Extra-enteric helminths, continued

Ancylostoma caninum, A. braziliense, Uncinaria stenocephala, 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

Extra-enteric helminths, continued

A. 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

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

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

Trichuris trichiura life cycle

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

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

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

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

Enterobius vermicularis life cycle

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)

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

Strongyloides stercoralis life cycle

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

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

Trichinella spiralis life cycle

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

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

Dracunculus medinensis life cycle

Filarid helminths

Filarid Helminth Life Cycle DH Adults L4 larva L5 larva Vector L2 larva L3 larva

microfilariae L1

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

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

Wuchereria bancrofti life cycle

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

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

Loa loa life cycle

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

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

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

Onchocerca volvulus life cycle

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

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

Flatworm helminths, continued

Flatworm terms, continued Procercoid, plerocercoid: larvae of pseudophyllidean tapeworms Scolex: organ of attachment, adult tapeworms Proglottids: tapeworm body segments Strobila: tapeworm body (all segments) Sporocyst, redia: larvae of fluke species Cercaria: end stage of asexual reproduction of flukes Metacercaria: encysted cercaria infective to DH

Flatworm helminths, continued

Trematodes/Flukes Generalized Fluke Life Cycle

Adults in DH
Egg Miracidium (embryo)

Snail primary IH
Sporocyst &/or Redia larva
Cercaria

Vegetation/secondary IH
Metacercaria

Flatworm helminths, continued

Fasciolopsis buski (intestinal fluke) Transmission: ingestion of metacercaria on aquatic vegetation Pathogenic potential 0/low Clinical signs: none, rash, intestinal discomfort Reservoir hosts: numerous, herbivores Damage potential: low, minor SI mucosal damage Prevalence: high, ~ 10 m infections annually in oriental and asian, tropical/subtropical areas Diagnosis: ID of eggs in fecal sedimentation Treatment: prazyquantel, niclosamide

Fasciolopsis buski life cycle

Flatworm parasites, continued

Echinostoma spp. (spiny-mouthed flukes) Transmission: ingestion of metacercaria in snail secondary IH Pathogenic potential low/moderate Clinical signs: # dependent, none/mild irritation Reservoir: many snail-eating mammal DHs Damage potential low: some SI abrasion Prevalence: oriental, asian tropical/subtropical countries Diagnosis: microscopic ID of ova in fecal sed Treatment: praziquantel, niclosamide

Flatworm helminths, continued

Heterophyes spp., Metagonimus spp. Transmission: ingestion of metacercaria in fish secondary IH Pathogenic potential: low early, rising to high over time, re: worm #s, infection longevity Clinical signs: none early, myocarditis, seizures, neurologic defecits, other, in chronic infections Reservoir hosts: most piscivorous mammals Damage potential: dependent on tissue-infested ova lodged in various organs, emitting toxins produced by embryos; egg #s determine level of damage

Flatworm helminths, continued

Heterophyes, Metagonimus, continued Prevalence: high in oriental, asian and other countries where endemic, and cultural consumption of raw fish is common Diagnosis: microscopic ID of ova in feces via sedimentation concentration Treatment: nothing effective against systemically lodged ova; prazyquantel, tetrachloroethylene X adults

Heterophyidae life cycle

Flatworm helminths, continued

Paragonimus westermani (lung fluke) Transmission: ingestion of metacercaria in crustacean secondary IH Pathogenic potential: moderate to high dependent on worm #s, species toxicity, level of tissue damage Clinical signs: none, fever, cough, bloody sputum, chest pain, bronchitis, dyspnea Reservoir: huge, almost any crustacean-eating mammal Damage potential: early migration through tissues minor; encapsulation in lungs major

Flatworm helminths, continued

P. westermani, continued Prevalence: worldwide, dependent on human consumption of raw crustaceans Diagnosis: microscopic ID of ova in sputum or sedimentation-concentrated feces; ID of ova in needle biopsy of encapsulations in lungs Treatment: praziquantel, bithionol

Paragonimus westermani life cycle

Flatworm helminths, continued

Fasciola hepatica (sheep, et.al., liver fluke) Transmission: ingestion of metacercaria on vegetation Pathogenic potential moderate/high dependent on worm #s & length of infection period Clinical signs: none early, fever, chills, pain, jaundice, eosinophilia, liver enlargement, other Reservoir: huge, almost any herbivorous or omnivorous animal is suitable host Damage potential: moderate to high depending on worm #s; migration through tissues & liver parenchyma, mechanical & toxic effects, hyperplasia of biliary epithelium, cirrhosis

Flatworm helminths, continued

F. hepatica, continued Prevalence: millions of human infections probable, worldwide distribution dependent on aquatic vegetation production and consumption Diagnosis: microscopic ID of ova in fecal sedimentation Treatment: bithionol, praziquantel

Fasciola hepatica life cycle

Flatworm helminths, continued

Clonorchis sinensis, Opisthorchis spp. (oriental liver flukes) Transmission: ingestion of metacercaria in fish secondary IH Pathogenic potential: 0 early, low/moderate late infection, depending on worm #s Clinical signs: similar to those described for F. hepatica, but usually less intense until worms reach very large population levels Reservoir: huge, nearly all piscivorous mammals in endemic areas Damage potential: moderate, similar but usually smaller magnitude than F. hepatica

Flatworm helminths, continued

C. sinensis, O. spp., continued Prevalence: high in oriental & other countries where fish are eaten raw; sporadic in many countries, dependent on local cultural factors; some outbreaks tied to transport of fresh fish in non-endemic areas Diagnosis: microscopic ID of ova in feces processed by sedimentation concentration Treatment: praziquantel, albendazole

Clonorchis/Opisthorchis life cycle

Flatworm helminths, continued

Dicrocoelium dendriticum (terrestrial liver fluke) Transmission: ingestion of metacercaria in ant secondary IH; primary IH is a terrestrial snail/slug This agent is mentioned only to provide an example of adaptability, and is confined to warm, moist areas of the world where gastropod secondary IHs mingle with scavenging, arthropod-ingesting DHs; most of the internal factors described for other liver flukes are applicable to D. dendriticum

Flatworm helminths, continued

Schistosomes/Bloodflukes Generalized schistosomal life cycle

Male & Female Adults in DH Egg Miracidium embryo Snail IH

Sporocyst larvae
Cercaria

Flatworm helminths, continued

Schistosoma mansoni, S. japonicum, S. haematobium (blood flukes) Transmission: direct penetration of skin by forktailed cercaria in water Pathogenic potential: high, based on worm populations and location in veins, capability of eggs to erode tissue, other Clinical signs: none early or if worm #s low, transient skin reaction at entry, malaise, fever, skin rashes, cough, acute hepatitis, abcesses, hepatomegaly, cardiomyopathy, haematuria Reservoir: limited?, monkeys, rodents, humans

Flatworm helminths, continued

S. mansoni, S. japonicum, S. haematobium, continued Damage potential high, dependent on location of adults, excretions of adults and miracidia in ova, population #s, egg locations & #s, damage is accumulative over time Prevalence: distribution worldwide in tropical, subtropical, temperate regions; human infections nearly equal to prevalence of malaria, Diagnosis: microscopic ID of ova in feces, urine or biopsy specimen Treatment: praziquantel, oxamniquin, bilarcil

Schistosoma species life cycle

Flatworm helminths, continued

Shistosoma spp. Transmission: cercarial penetration of skin in water This group of schistosomes do not develop to adulthood in humans. They are parasites of birds and other animals, but will infect humans when in contact in water. They cause a cutaneous larval migrans referred to as swimmers itch, which is transitory and usually eliminated by the immune response

Flatworm helminths, continued

Generalized Pseudophyllidean Life Cycle Adults in DH SI

Egg Coracidium

Procercoid larva

Copepod primary IH
Fish secondary IH

Plerocercoid larva

Adults in DH SI

Flatworm helminths, continued

Pseudophyllidean tapeworms Diphyllobothrium latum (broad fish tapeworm) Transmission: ingestion of plerocercoid larva in uncooked fish Pathogenic potential: low, dependent on host sensitivity, location of worm in SI Clinical signs: usually none, pernicious anemia if worm is anchored near pyloric sphincter Reservoir hosts: various wild & domestic fisheating mammals; dogs, cats, bears, seals, other Damage potential low: strong affinity for B12

Flatworm helminths, continued

D. latum, continued Prevalence worldwide, where freshwater or brackish water fish are consumed raw Diagnosis: observation of proglottid chains in stools; microscopic ID of ova in feces Treatment: prazyquantel, niclosamide

Pseudophyllidean (Diphyllobothrium latum) life cycle

Flatworm helminths, continued

Generalized Cyclophyllidean Life Cycle Adults in DH SI

Egg with Onchosphere/Hexacanth Embryo Larva (Cysticercoid, cysticercus, coenurus, hydatid) in IH

Adults in DH SI

Flatworm helminths, continued

Cyclophyllidian tapeworms Taenia solium (pork tapeworm) Transmitted by ingestion of cysticercus larvae in uncooked pork (adult worm in SI); ingestion of TW eggs in human fecal contamination (cysticercus/larval development in tissues) Pathogenic potential: low as adult in SI; low/moderate as larvae in tissues Clinical signs: usually none with adult infection, dependent on location with larval infection Reservoir hosts: humans and pigs Damage potential 0 to low with adults, low/moderate with larvae, location dependent

Flatworm helminths, continued

T. solium, continued Prevalence: worldwide, where humans and pigs interact, and pork is eaten raw Diagnosis: observation of proglottid chains in stool for adult worms; biopsy removal of larva from tissue site, microscopic ID of hooklets in a crush mount Treatment: prazyquantel, niclosamide X adults; albendazole somewhat effective X cysticerci, untreated larval infections often subside (symptom-wise) within 2 to 5 years

Flatworm helminths, continued

Taenia saginata (beef tapeworm) Transmission by ingestion of cysticercus larva in fresh, raw beef Pathogenic potential 0/low Clinical signs: none, usually Reservoir hosts: bovine IHs, human DHs Damage potential 0/low Prevalence worldwide, wherever beef is eaten raw and cattle are exposed to human feces Diagnosis: sight of proglottid chains in stool Treatment: prazyquantel, niclosamide

Taenia species life cycle

Flatworm helminths, continued

Hymenolepis nana, H. diminuta, Dipyllidium caninum, others Transmission: ingestion of arthropod IH host containing cysticercoid larva Pathogenic potential 0/very low Clinical signs: usually none, sensitive DH may show diarrhea, headache, abdominal pain, dizziness, anorexia, other nonspecific signs Reservoir hosts: rodents, dogs, normal DHs Damage potential 0/very low Prevalence world-wide, dependent on distribution of normal DHs

Flatworm helminths, continued

H. nana, H. diminuta, D. caninum, continued Diagnosis complicated by small size of worms, making their observation in stools difficult; eggs may sometimes be observed in fecal flotation examinations Treatment: prazyquantel, niclosamide

Hymenolepis nana life cycle

Hymenolepis diminuta life cycle

Dipyllidium caninum life cycle

Flatworm helminths, continued

Larval Tapeworm Infections Echinococcus granulosus, E. multilocularis (unilocular/multilocular hydatidosis respectively) Transmission: ingestion of ova in feces of DH Pathogenic potential high, dependent on larval type and organ involved Clinical signs dependent on size of cyst, organ location: related to pressure, abrasion, other Reservoir hosts: DH carnivores/omnivores, IH prey species primarily herd animals (sheep, etc) Damage potential dependent on organ location, size of cyst; moderate to high

Flatworm helminths, continued

E. granulosus, E. multilocularis, continued Prevalence in humans spotty, dependent on human interaction with canine DH and herbivore IH; distribution world-wide from equator to arctic, wherever predator-prey activity occurs (everywhere?) Diagnosis: microscopic ID of protoscoleces from needle biopsy of cyst, X-ray/other image detection of cyst in organ (liver, lung, brain, other); skin test, serotest Treatment: Surgical removal of cyst (unilocular), albendazole somewhat (variably) effective

Echinococcus species life cycle

Flatworm helminths, continued

Taenia spp. of carnivores Transmission: ingestion of eggs in DH feces Pathogenic potential low to moderate, dependent on host sensitivity, #s & location of cysticerci in IH (human) Clinical signs: none, CNS-related abnormalities, subcutaneous nodules, et.al., site dependent Reservoir hosts: DH carnivores, IH prey Damage potential: dependent on worm species, larva type (cysticercus or coenurus), larva location; host sensitivity, number of larvae

Flatworm helminths, continued

Taenia spp., continued Prevalence; worldwide, equator to arctic in normal carnivore DHs, prey IHs, spotty, somewhat infrequent/rare in humans Diagnosis: microscopic ID of larval biopsy Treatment: albendazole somewhat effectiveseldom/never 100% curative

Cysticercosis-causing tapeworm life cycle