Title: MEDICAL PARASITOLOGY
1MEDICAL PARASITOLOGY
2INFORMATION EMPHASIS
- Agent and Group ID general importance
- Epidemiology (distribution, transmission, etc)
- Pathogenic capability
- Diagnosis
- Control
3BASIC TERMINOLOGY PRINCIPLES
- Symbiosis Living together
- Commensalism One symbiont benefits, other
unaffected - Mutualism Both symbionts benefit
- Parasitism One symbiont benefits, other is
damaged
4COMMON 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
5PARASITE 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
6CONDITIONS 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, 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.
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
15Toxocara 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)
18Hookworm Life Cycle
19- 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
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
23Trichuris 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
28Enterobius 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/eliminat
ed, 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
31Strongyloides 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
34Trichinella 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
37Dracunculus 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
41Wuchereria 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
44Loa 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
48Onchocerca 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
51- 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
52- 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
53- 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
54Fasciolopsis buski life cycle
55- 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
56- 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
57- 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
58Heterophyidae life cycle
59- 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
60- 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
61Paragonimus westermani life cycle
62- 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
63- 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
64Fasciola hepatica life cycle
65- 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
66- 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
67Clonorchis/Opisthorchis life cycle
68- 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
69- Flatworm helminths, continued
- Schistosomes/Bloodflukes
- Generalized schistosomal life cycle
- Male Female Adults in DH
- Egg Miracidium
embryo Snail IH -
- Sporocyst larvae
- Cercaria
70- Flatworm helminths, continued
- Schistosoma mansoni, S. japonicum, S. haematobium
(blood flukes) - Transmission direct penetration of skin by
fork-tailed 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
71- 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
72Schistosoma species life cycle
73- 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
74- Flatworm helminths, continued
- Generalized Pseudophyllidean Life Cycle
- Adults in DH SI
- Egg Coracidium
- Procercoid larva Copepod primary IH
- Plerocercoid larva Fish secondary IH
- Adults in DH SI
75- 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
fish-eating mammals dogs, cats, bears, seals,
other - Damage potential low strong affinity for B12
76- 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
77Pseudophyllidean (Diphyllobothrium latum) life
cycle
78- 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
79- 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
80- 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
81- 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
82Taenia species life cycle
83- 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
84- 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
85Hymenolepis nana life cycle
86Hymenolepis diminuta life cycle
87Dipyllidium caninum life cycle
88- 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
89- 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
90Echinococcus species life cycle
91- 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
92- 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
effective-seldom/never 100 curative
93Cysticercosis-causing tapeworm life cycle