Helminthic infections are caused by parasitic worms. Successful parasites live in and obtain nutrients from the host without killing it. The severity of disease depends on the parasite burden and host immune response. Parasites enter through ingestion, arthropod bites, or skin/mucous membrane penetration. Some parasites must migrate within the host to complete their lifecycle, but non-human parasites in humans often become dead-end infections. Mechanisms of evading the immune response include antigenic variation, intracellular infection, encystation, and camouflage. Tissue damage results from direct destruction, hypersensitivity reactions, or eosinophilia during migration. Helminths are classified as nematodes, trematodes

1. Helminthic infectionsHelminthic infectionsHelminthic infectionsHelminthic infections

2. Infection vs. diseaseInfection vs. diseaseInfection vs. diseaseInfection vs. disease
•successful parasites live in, but do notsuccessful parasites live in, but do not
kill their hostskill their hosts
•protozoa multiply within hostsprotozoa multiply within hosts
expression of disease depends on hostexpression of disease depends on host
factorsfactors
•helminths do not multiply within hostshelminths do not multiply within hosts
severity of disease depends on parasiteseverity of disease depends on parasite
burden and immunologic response toburden and immunologic response to
parasitesparasites

3. Parasite modes of entryParasite modes of entryParasite modes of entryParasite modes of entry
•IngestionIngestion
•Arthropod bitesArthropod bites
•Penetration of intact skinPenetration of intact skin
or mucous membranesor mucous membranes

4. Spread and tropismsSpread and tropismsSpread and tropismsSpread and tropisms
•Some parasites must migrate toSome parasites must migrate to
certain locations within the hostcertain locations within the host
in order to complete their lifein order to complete their life
cyclecycle
•Non-human parasites, inNon-human parasites, in
humans, often fail to migratehumans, often fail to migrate
properly andproperly and becomebecome “dead-end“dead-end
infections”infections”

5. Mechanisms for evading the
host response
Mechanisms for evading the
host response
•antigenic variation - trypanosomes
•intracellular infection - plasmodia
•encystation* - amoebae, cestodes
•camouflage - schistosomes
* “cyst” has multiple meanings

6. Tissue damage and hostTissue damage and host
responseresponse
Tissue damage and hostTissue damage and host
responseresponse
•direct destruction of tissuedirect destruction of tissue
•hypersensitivity reactionshypersensitivity reactions
•eosinophiliaeosinophilia
–occurs with helminths, not protozoaoccurs with helminths, not protozoa
–results from tissue migrationresults from tissue migration

7. Classification of helminthsClassification of helminthsClassification of helminthsClassification of helminths
Nematodes (roundworms)Nematodes (roundworms)
Platyhelminthes (flatworms)Platyhelminthes (flatworms)
Trematodes (“flukes”)Trematodes (“flukes”)
Cestodes (“tapeworms”)Cestodes (“tapeworms”)

8. Helminthic diseasesHelminthic diseases
•Intestinal
–Others
–Strongyloides
•Invasive
–Trichinosis
–Filaria
–Schistosomiasis
–Cysticercosis
–Echinococcus
(autoinfection cycle)
(muscle pain, uncooked carnivores)
(worms in lymphatics or under skin)
(liver or urinary tract
granulomas and fibrosis)
(cysts in brain, seizures)
(massive cysts in liver or lung)
roundworms
flukes
tapeworms

9. Intestinal nematodesIntestinal nematodesIntestinal nematodesIntestinal nematodes
Larvae pass
through lungs
Larvae penetrate
through intact skin
strongyloides
hookworm
Eggs ingested
trichiuris
enterobius
Larvae enter
bloodstream
ascaris
Adult worms in the
the intestine
Eggs
Larvae hatch
from eggs

10. Strongyloides life cycleStrongyloides life cycle
Adult worms in the
the intestine
Eggs
1st stage
larvae hatch
from eggs
Larvae penetrate
through intact skin
Larvae enter
bloodstream
Larvae pass
through lungs
Larvae molt
twice to form
filariform larvae
(infectious)
Autoinfection

11. Strongyloides - clinical featuresStrongyloides - clinical features
•uncomplicated
–GI upset
•autoinfection
•hyperinfection
–rash
–bronchspasm, CXR infiltrates
–diarrhea
–profound eosinophilia
–recurrent Gram-negative
bacteremia

12. Trichinella spiralisTrichinella spiralis - life cycle- life cycleTrichinella spiralisTrichinella spiralis - life cycle- life cycle
• ““cycle of carnivorism” among hogs and ratscycle of carnivorism” among hogs and rats
• humans ingest encysted larvae in infected,humans ingest encysted larvae in infected,
undercooked porkundercooked pork
• larvae exist in stomach and burrow into smalllarvae exist in stomach and burrow into small
intestinal mucosaintestinal mucosa
• adult males and female reemerge and produceadult males and female reemerge and produce
larvae which penetrate intestine and circulatelarvae which penetrate intestine and circulate
in bloodstreamin bloodstream
• larvae enter skeletal muscle cells and encystlarvae enter skeletal muscle cells and encyst

14. Clinical features of trichinosisClinical features of trichinosisClinical features of trichinosisClinical features of trichinosis
•Most common sxs:Most common sxs:
–muscle pain and tendernessmuscle pain and tenderness
–fever +/- chillsfever +/- chills
–edema (often periorbital)edema (often periorbital)
•>10% eosinophilia (often ~50%)>10% eosinophilia (often ~50%)
•elevated CPKelevated CPK
•+/- chronic neurologic/myocardial sxs+/- chronic neurologic/myocardial sxs
•self-limited (2% mortality)self-limited (2% mortality)

15. Treatment of trichinosisTreatment of trichinosisTreatment of trichinosisTreatment of trichinosis
•antihelminthic (albendazole) toantihelminthic (albendazole) to
kill any intestinal adultskill any intestinal adults
•steroids to relieve inflammatorysteroids to relieve inflammatory
reactionsreactions
•antipyreticsantipyretics

16. Life cycles of two types of filariaLife cycles of two types of filariaLife cycles of two types of filariaLife cycles of two types of filaria
Arthropod
vector
Adult
worm pairs
Larvae
(microfilariae)
Lymph- mosquitoes peripheral circulate
dwelling lymphatics in bloodstream
(e.g, Wuchereria
bancroftii )
Skin- biting flies skin nodules migrate through
dwelling or migratory dermis

19. O. volvulus microfilaria in skin snip

20. O. volvulus nodule

21. DirofilariaDirofilaria in a human lungin a human lung

22. Role of endosymbiontRole of endosymbiont WohlbachiaWohlbachia
sp. in filiaria infectionsp. in filiaria infection
Role of endosymbiontRole of endosymbiont WohlbachiaWohlbachia
sp. in filiaria infectionsp. in filiaria infection
•Rickettsia-like organisms requiredRickettsia-like organisms required
for fecundity and viability of filariafor fecundity and viability of filaria
•Wohlbachia-free worms produceWohlbachia-free worms produce
less inflammation in tissue (? LPS)less inflammation in tissue (? LPS)
•Implications for rx:Implications for rx:
–ivermectin kills microfilaria onlyivermectin kills microfilaria only
–tetracycline may destroy adult wormstetracycline may destroy adult worms

23. Geographic distribution ofGeographic distribution of
schistosomiasisschistosomiasis
Geographic distribution ofGeographic distribution of
schistosomiasisschistosomiasis
S. mansoniS. mansoni
S. hematobiumS. hematobium
S. japonicumS. japonicum

24. Schistosomiasis - life cycleSchistosomiasis - life cycleSchistosomiasis - life cycleSchistosomiasis - life cycle
S.m. S.h. S.j.

26. “pipestem” fibrosis

27. Schistosomiasis - pathogenesisSchistosomiasis - pathogenesisSchistosomiasis - pathogenesisSchistosomiasis - pathogenesis
•egg granuloma (type IV reaction)-->egg granuloma (type IV reaction)-->
fibrosisfibrosis
•morbidity ~ worm (egg) burdenmorbidity ~ worm (egg) burden
•concomitant immunity to schistosomulaconcomitant immunity to schistosomula
•adult worms: invisible to the immuneadult worms: invisible to the immune
system (survive for years)system (survive for years)

28. Schistosomiasis- clinical featuresSchistosomiasis- clinical featuresSchistosomiasis- clinical featuresSchistosomiasis- clinical features
•Cercarial dermatitisCercarial dermatitis
•Intestinal schistosomiasisIntestinal schistosomiasis (granulomas -->(granulomas -->
polyps, protein loss, malabsorption, strictures)polyps, protein loss, malabsorption, strictures)
•Hepatosplenic schistosomiasisHepatosplenic schistosomiasis (portal(portal
hypertension --> ascites, varices, splenomegaly,hypertension --> ascites, varices, splenomegaly,
normal hepatic function)normal hepatic function)
•Urinary schistosomiasisUrinary schistosomiasis (hematuria, chronic(hematuria, chronic
infection, obstruction)infection, obstruction)
• Other (cardiopulmonary, CNS, etc.)Other (cardiopulmonary, CNS, etc.)

29. Drug treatment ofDrug treatment of
schistosomiasisschistosomiasis
Drug treatment ofDrug treatment of
schistosomiasisschistosomiasis
•Praziquantel increasesPraziquantel increases
permeability of adult parasite topermeability of adult parasite to
CaCa++++
..
•Tetanospasm --> deathTetanospasm --> death

30. Control of SchistosomiasisControl of Schistosomiasis
REDUCE CARRIERS mass rx program
ELIMINATE SNAILS molluscicides
destroy snail habitats
snail-eating fish
PREVENT WATER
CONTAMINATION latrines, toilets
public health education
PREVENT HUMAN
EXPOSURE water systems

31. TapewormsTapeworms
•Definitive hosts: harbor adult worms
•Intermediate hosts: harbor tissue cysts
(containing worm heads)
•Humans acquire infection two ways:
–ingestion of eggs from feces (to acquire
tissue cysts)
–ingestion of tissue cysts in undercooked
meat (to acquire a tapeworm)
= Intermediate host
= Definitive host

32. TaeniasisTaeniasis
Tapeworm Cysticercosis
poor
hygiene
poor
sanitation
ingestion of
undercooked pork

34. CysticerciCysticerci Hydatid CystHydatid Cyst

35. Isolated cysticerci Hydatid cyst

36. EchinococcosisEchinococcosis
Cystic Hydatid Disease
contact
with
dogs
ingestion of
entrails
ingestion of
eggs in
pastures

38. Treatment of cysticercosis andTreatment of cysticercosis and
echinococcosisechinococcosis
Treatment of cysticercosis andTreatment of cysticercosis and
echinococcosisechinococcosis
•Antihelminthic therapy (e.g.,Antihelminthic therapy (e.g.,
albendazole, praziquantel)albendazole, praziquantel)
•(Echinococcus only)(Echinococcus only)
–Surgical removalSurgical removal
–Irrigation-evacuation of cystsIrrigation-evacuation of cysts

39. ReferencesReferences
•Pictures – Derm atlas
•Oxford Handbook of
Dermatology for primary
care ,Saxe ,Jessop
•Topics in Paediatrics
,Basson& Ginsberg

40. THANK YOUTHANK YOU