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
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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
microfilariae L1
Vector
L2 larva
L3 larva
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
Procercoid larva
Plerocercoid larva
Coracidium
Copepod primary IH
Fish secondary IH
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