MEDICAL PARASITOLOGY
Protozoa and Helminths
INFORMATION EMPHASIS
• Agent ID and general importance
• Epidemiology (transmission, distribution, etc)
• Agent damage capability
• Diagnostics
• Control
BASIC TERMINOLOGY AND 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/Facultative Parasites
Endo/Ecto Parasites
Pseudo/Spurious Parasites
Zoonotic Parasites
Host-specific/Non-specific Parasites
Definitive/Intermediate Hosts
Paratenic/Transfer Hosts
Vector Hosts
SURVIVAL FACTS AND FUNCTIONS
• Parasites adapt to every niche in a host
• Best adapted are least pathogenic
• Parasite-host relationship is typically longterm/chronic/ “intimate”
CONDITIONS REQUIRED FOR ENDEMIC
PARASITISM
• Reservoir of Infection
• Means of Transmission to Susceptible Hosts
• Ability to Invade and Establish in New Hosts
• Ability to Reproduce
PROTOZOAN TERMINOLOGY
• Trophozoite: Active, vegetative LC stage
• Cysts: Protective LC stage
-Common cyst
-Oocyst, sporocyst, sarcocyst, pseudocyst, etc
• Cilia: Ciliate motility organelles
• Flagella: Flagellate motility organelles
• Pseudopod: Amoeba motility organelles
• Macronucleus: Ciliate body function control
• Axostyle: Flagellate “skeletal” rod
• Peristome: Funnel leading to cytostome/mouth
CILIATE PARASITE
Balantidium coli
Trophozoite
Cytostome
Macronucleus
Cilia
Cyst
Macronucleus
Ciliate parasite, continued
• Balantidium coli
Cyst transmission (fecal oral)
Pathogenic in humans, mucosal erosion
Frank blood in feces, sloughed mucosa
Reservoir hosts swine, probably other
Potential for serious damage high
Prevalence overall, low
Diagnosis: fecal analysis for cysts, trophs,
proctoscopy for lesions/biopsy
Treatment: oxytet; metronidazole; natural,
spontaneous clearance occasionally
Balantidium coli Life Cycle
FLAGELLATE PARASITES AND COMMENSALS
Trichomonads and Dientamoeba fragilis
Trophozoites only
Flagella
Nucleus/nuclei
Body shape & size
Flagellates, continued
Trichomonas tenax
Trophozoite transmission-direct oral
Mouth inhabitant, oral hygiene factor
Nonpathogenic, thrives in bad conditions
Reservoir unknown, probably wide
Considered classically commensalistic
Prevalence data spotty
Diagnosis by culture, microscopic exam of
oral fluids/scrapings
Eliminated by good oral hygiene
Pentatrichomonas hominis,
Dientamoeba fragilis
Transmission direct-oral, no cysts (you tell me)
Colon/caecum inhabitants
Non-pathogenic
Reservoir unknown, probably wide
Considered commensalistic (D. fragilis ???)
Prevalence unknown
Diagnosis usually incidental-fecal smear-stain,
wet mounts + microscopy
Treatment: incidental elimination-Flagyl, et.al.
Dientamoeba fragilis Life Cycle
Flagellate, continued
Trichomonas vaginalis
Transmitted by sexual intercourse
Induces vaginal pH change, erosion of
normal mucosa in women
Vaginal itching, burning, yellow discharge in
women, occasional urethritis, prostate
swelling in men
Human reservoir, zoonotic potential ??
Prevalence varies with population & culture
Diagnosis by visual features, microscopy
Treatment usually Flagyl
Trichomonas vaginalis Life Cycle
Flagellate Parasites and Commensals
Chilomastix mesnili Enteromonas hominis,
Retortamonas intestinalis, Giardia lamblia, et.al.
Trophozoites
Cysts
Nuclei
Nuclei
Flagella
Size & shape
Size & shape
Flagellates, continued
Chilomastix mesnili, Enteromonas sp.,
Retortamonas sp.,, others
Caecum/colon inhabitants
Transmission by cyst or trophozoite
Nonpathogenic, commensalistic
Thrive in most diarrheic conditions
Reservoir pool (probably) wide, unknown
Widespread, sanitation dependent
Diagnosis: microscopic fecal exam
Treatment: unnecessary in most cases,
Flagyl will work
Flagellates, continued
Giardia lamblia, etc
Cyst transmission
Pathogenic potential individually inconsistent
Clinical signs variable
Diarrhea/dysentery, periodic or steady
Gas production
Borborygmus
Anorexia
Skin rash
Fibromyalgia
Spontaneous lactose intolerance
Fatigue, mild/severe
Other
Flagellates, continued
Giardia, continued
Reservoir hosts: almost any mammal
Damage potential: individual factors
Immunocompetence of host
Natural, undefined host tolerance level
Other (fuzzy factors)
Worldwide distribution, sanitation dependent
Diagnosis: fecal ELISA, direct microscopic
exam for cysts/trophs
Treatment: Atabrine, Flagyl, other
Giardia Life Cycle
Flagellates, continued
HAEMOFLAGELLATES
Trypanosomes/
trypomastigote forms
Leishmanias/
amastigote forms
Haemoflagellates, continued
Trypanosoma brucei complex, T.b. gambiense,
T.b. rhodesiense, others
Vector transmission, Tse tse flies
Pathogenic, terminal ‘sleeping sickness’,
East African SS less acute than West
African SS
Signs: swollen cervical lymph nodes, fever,
rashes, headache, malaise, nausea,
eventually coma
Various wild/domestic animal reservoirs
West African much more acute and severe
than East African SS.
Haemoflagellates, continued
Trypanosoma brucei complex, continued
T.b. gambiense in West Africa, overlaps with
endemic East African T.b. rhodesiense
in center of continent
Microscopy of concentrated or cultured
blood or fluid aspirates, RES biopsy
normal diagnostic methods
Treatment: melarsoprol complex, suramin
Trypanosoma brucei complex, LC
Haemoflagellates, continued
Trypanosoma cruzi
American trypanosomiasis, Chaga’s disease
Vector/direct contact transmission; triatomids,
several species
Highly pathogenic late-term/chronic
Symptoms vary: fever; edema; swelling of
thyroid, spleen, liver, various lymph
nodes; CNS re mental impairment,
coma; tachycardia, weakness, chest
pain, anemia, megacolon,
megaesophagus, other, depending on
organism strain, length of infection,
condition of host, etc.
Haemoflagellates, continue
T. cruzi, continued
Reservoir large, many carnivore, omnivore &
herbivore species
Damage severe, early (fulminating) or late
(chronic), depends on various factors
Prevalence < 3% to > 50% in endemic areas
from southcentral USA to southern SA
Diagnosis: cell/fluid culture, xenodiagnosis,
direct microscopy
Treatment: no reliable/curative; nifurtimox,
primaquine & related drugs reduce but
do not eliminate blood stage, nothing
effective X cellular stage
T.cruzi, continued
Triatomid Vector
Trypomastigote/
Trypanosome
Haemoflagellates, continued
T. Cruzi life cycle
Haemoflagellates, continued
Leishmania topica complex, L.t. mexicana complex, L.t.
braziliense complex, et.al.
Vector trans. by sand flies
Superficial to extensive, shallow to deep
Cutaneous lesions, vary by strain/species
Oriental sore: limited, wet ulcer
Chiclero ulcer: ear ‘notches’
Diffuse cutaneous: dry, diffuse
Mucocutaneous: cartilage erosion
Reservoir: large; many native carnivore, omnivore,
herbivore vertebrates
Haemolagellates, continued
Leishmania tropica complex, continued
Lesion severity varies with species/strain,
simple limited wet/dry to severe erosion
Widespread in tropical, subtropical & warm
temperate regions worldwide
Lesion appearance is diagnostic, agents can
be cultured or viewed microscopically
Pentavalent antimony compound treatment,
with/without amphotericin B
Haemoflagellates, continued
Leishmania donovoni complex
Vector transmission, sandflies
Visceral, reticulo-endothelial system
inhabitation, often lethal
Fevers (variable), anemia, hepatomegaly
splenomegaly, ascites, Kala-azar
(blackening of facial skin), et.al.
Reservoir: domestic & wild vetebrates
Damage potential varies with species/strains
Distributed widely, tropics, subtropics, warm
temperate and cool temperate regions
Diagnosis by serology, culture of blood or biopsy
Antimony, amphotericin-B, allopurinol treatments
Leishmania sp. life cycle
Sarcodina
AMOEBIC PARASITES AND COMMENSALS
Entamoeba gingivalis
Trophozoite only, inhabits oral cavity Transmitted
directly (no cyst)
Commensalistic, considered nonpathogenic
Host reservoir: dogs, cats, monkeys, other?
Patho potential considered 0/low
Distribution undefined, prevalence 70-90% of
“unhealthy”, 7-35% of “healthy” mouths surveyed
Diagnosis: microscopy of tissue/scraping/fluid
Treatment: improve oral hygiene; probably Flagyl
Sarcodines, continued
Amebic parasites and commensals, continued
Entamoeba histolytica
Trophozoite in caecum/colon, if invasive
may inhabit liver, lungs, other tissues;
Cysts (infective stage) form in normal stools
Pathology variable: noninvasive; if invasive,
ulcerates colonic mucosa, spreads to
liver, lung, et.al., produces abcesses;
path potential indicated by colony site
Reservoir includes monkeys, dogs, pigs, et.al.
Distribution worldwide: tropical, subtropical,
warm temperate areas; sanitation dependent
Sarcondines, continued
E. histolytica, continued
Prevalence rated second to Giardia worldly
Diagnosis by microscopic ID of trophs, cysts
in feces, trophs in tissue-based
abcesses
Treated with Flagyl (metronidazol), various
Emetine formulations,
Diiodohydroxyquin, et.al.
Entamoeba histolytica
Cyst
Trophozoite
Amoeba sp. life cycle
Sarcodines, continued
Entamoeba coli, E. hartmanni, E. dispar, E.
sp.(unnamed), Endolimax nana, Iodamoeba
butschlii, a few others
Caecum/colon inhabitants, transmitted by
cysts,
All commensals (with rare exceptions)
Diarrhea enhances production of trophs
Reservoir: various vertebrate animals
Damage potential 0/low (some exceptions?)
Prevalence high, world-wide warm areas
Diagnosis: microscopic ID in feces
Treatment considered unnecessary
Entamoeba coli
Cyst
Trophozoite
Sporozoa/apicomplexa
SPOROZOA/APICOMPLEXA TERMINOLOGY
Sporogony: basic life cycle stage; sporozoite
generation
Schizogony/merogony: basic life cycle stage;
(asexual repro) merozoite generation
Gametogony/gamogony: basic life cycle stage;
(sexual repro) gametocyte generation
Oocyst: cyst produced in sporogony
Sporocyst: cyst within oocyst, produced in
sporogony
Sporozoite: basic infective unit in
oocysts/sporocysts
Sporozoa, continued
Sporozoan terminology, continued
Trophozoite: transitional zoite, between
sporozoite and schizont/merozoite
Merozoite: basic zoite product of schizogony
Tachyzoite: rapidly replicating merozoite
Bradyzoite: slowly replicating merozoite
Sarcocyst: end-stage schizont in intermediate
host with Sarcocystis sp. infection
Pseudocyst: end-stage schizont in intermediate
host with Toxoplasma gondii infection
Sporozoa, continued
Sporozoa, continued
Basic Life Cycle Stages
Sporogony: formation of sporocysts and
sporozoites
Schizogony/merogony: formation of
merozoites/tachyzoites/bradyzoites
Gamogony/gametogony: formation of
gametocytes and gametes
Sporozoa, continued
Isospora belli
Transmission direct, fecal oral, via oocysts
Pathogenic potential low, non-bloody diarrhea
common in immunodeficient hosts,
uncommon in others
Clinical signs absent, except in rare cases
Reservoir limited to humans, other anthropoids,
strongly host-specific
Damage low, destroys superficial mucosal cells
Prevalence world-wide, sanitation dependent
Diagnosis by microscopic ID of oocysts in fecal
flotation
Treatment usually unnecessary, pyrimethamine + a
sulfa, trimethoprim, when needed
Isospora sp. life cycle
Sporozoa, continued
Cyclospora cayetanensis
Transmission direct fecal-oral, via oocysts
Pathogenic potential low/moderate, non-bloody
diarrhea in sporadic cases, most severe in
immunodeficient individuals
Diarrhea ~3 weeks in “healthy” hosts,
longer/much longer in immonodeficient; can
be cyclic, recurrent; long-term may +
anorexia, fatigue, weight loss, fever
Reservoir hosts: reptiles, rodents, insectivores,
probably other domestic & wild animals;
species ID is incomplete in host animals
Sporzoa, continued
C. cayetanensis, continued
Damage: jujunal villous atrophy, crypt
hyperplasia, inflammation
Prevalence spotty, outbreaks in New Guinea,
Nepal, Peru, Chicago, Canada, other
Diagnosis: microscopic ID of oocysts from fresh
feces, acid-fast-stained smears, fluorescent
Ab-stain preps
Treatment: trimethoprim + sulfamethoxazole
Cyclospora sp. life cycle
Sporozoa, continued
Cryptosporidium parvum
Transmission direct, fecal-oral, via oocysts
Pathogenic potential variable: low in “healthy”,
moderate/high in “deficient” hosts,
depending on immunocompetence level
Clinical signs: non-bloody diarrhea/dysentery,
mild/short-term (~2 weeks) to severe/longterm (steady or recurrent)
Reservoir: complete spectrum unknown, but
many domestic animals are known
Damage potential and mechanisms vary with
hosts & species, poorly understood
Sporozoa, continued
C. parvum, continued
Prevalence world-wide, sanitation dependent,
Diagnosis: microscopic ID of oocysts in feces
by flotation, acid-fast or immunofluorescent
staining; histologic or immunohistologic
exam of biopsy of intestinal mucosa
Treatment: paramomycin may be suppressive
in specific cases, not curative (no curative
medication known)
Cryptosporidium sp. life cycle
Sporozoa, continued
Sarcocystis bovihominis, S. suihominis, probably
others
Transmission: ingestion of beef or pork (or
other), uncooked/undercooked, containing
sarcocysts in muscle fibers
Pathogenic potential low in human DH
Clinical signs absent except in rare cases
Reservoir limited to human DH (+ possibly
other anthropoids), and bovine/porcine IHs
Damage low in human DH, inconsequential
erosion of intestinal mucosa
Sporozoa, continued
S. bovihominis, S. suihominis, etc. continued
Prevalence world-wide, determined by cultural
food prep and consumption factors
Diagnosis: microscopic ID of oocysts and/or
sporocysts in feces
No treatment identified: trimethoprim +
sulfamethoxazol probably suppressive
Sporozoa, continued
Sarcocystis lindemanni
Transmission by ingestion of sporocysts from
unknown DHs in fecal contamination
Pathogenic potential unknown
Clinical signs unknown
Reservoir unknown
Damage potential unknown
Prevalence unknown, probably sanitation
dependent
Diagnosis: histologic examination of muscle
Treatment unknown
Sarcocystis species Life Cycle
Sporozoa, continued
Toxoplasma gondii
Transmission direct via oocysts (fecal-oral),
ingestion of infected meat, transplacental,
nursing, organ transplantation, et.al.
Pathogenicity moderate to high, depending on
strain, host “health” factors
Clinical signs: Acute infection; range from
unnoticeable to severe flu-like (chills, fever,
headache, fatigue, lymphoid pain & swelling)
Transplacental; death & abortion, various
encephalomyelitis, megacephaly,
microcephaly, blindness, deafness
Sporozoa, continued
T. gondii, continued
Reservoir enormous: nearly all warm-blooded
vertebrates including birds, suitability varied
Damage potential dependent on strain, host
susceptibility, host “health” condition
Prevalence variable, depending on association
with feline DHs, and food (meat) preference
& preparation
Diagnosis: Indirect; fluorescent Ab, latex aggl.,
serum ELISA, other serotests. Direct;
culture of body fluids & tissue samples,
immunohistochemistry, histopathology
Treatment: Pyrimethamine + a pyrimidine
Toxoplasma gondii life cycle
Sporozoa, continued
Plasmodium vivax
Transmission: female Anopheles mosquito vector,
blood transfusion
Pathogenicity high, especially in 1st infections,
moderate/high in subsequent infections and
relapses, depending on host condition
Symptomatics: ~12-20 day prepatency (no signs);
prodroma (influenza-like; headache, nausea,
vomiting, anorexia, muscle aches); sudden,severe
shock-like chill (paroxysm), fever cycle quickly
stabilizing at ~48 hr, continuous for 3-10 weeks;
recrudescences/relapses for 5-8 years
Reservoir: humans, monkeys, apes, Anopheles vector
Sporozoa,continued
P. vivax, continued
Damage: extensive hemolysis, production of
toxic parasite metabolites
Prevalence: world-wide tropical and sub-tropical
less common in warm temperate regions
Diagnosis: microscopic ID/differentiation of
species by microscopic exam of stained
smears of blood properly collected and
prepared
Treatment: Quinine & related alkaloids, at least
15 additional, used or in trial, singly or in
combination, efficacy variable
Plasmodium sp. life cycle
Sporozoa, continued
Plasmodium ovale
All factors involving this species are nearly
identical to those listed for P. vivax, except
for severity of damage, symptoms,
prevalence and duration of infection.
Damage potential: low/moderate, primary
erythrocytic cycle ~2-3 weeks, total duration
of infection ~1-2 years
Symptoms: similar to P. vivax but less severe,
same fever cycle periodicity
Prevalence: widespread tropical & subtropical
Treatment: same as for P. vivax, et.al.
Sporozoa, continued
Plasmodium malariae
Transmission as described for P. vivax
Pathogenic potential high re: hemolysis and
CNS involvement late in infection
Symptoms similar to P. vivax & P ovale, with
longer fever cycle periodicity (72 hr), 3-24
weeks primary duration, 20-50 years
duration of untreated infection with
probability of recrudescence
Reservoir as described for P. vivax, P. ovale
Damage high; anemia, CNS & kidney syndrome
Sporozoa, continued
P. malariae, continued
Prevalence more common in subtropical and
warm temperate regions than tropical, but
endemic where other species occur
Diagnosis as described for P. vivax & P. ovale
Treatment as described for P. vivax & P. ovale
Sporozoa, continued
Plasmodium falciparum
Transmission as described for P. vivax, et.al.
Pathogenic potential highest of all Plasmodium
species, most likely of all to kill IH (human)
Clinical signs similar to those described: shorter
(8-11 days) incubation period, prodroma
similar but mild, cycle periodicity ~ 48hr,
initial paroxysm severe & long (16-36hr), 2-3
week duration of primary attack, 6-17
months duration of untreated infection
Reservoir: humans, monkeys, apes, Anopheles
mosquito vector
Sporozoa, continued
P. falciparum, continued
Damage as described: hemolysis, etc., but also
causes cytoadherence to endothelium of
damaged and intact parasitized cells and
cellular debris; all organs (brain, kidneys,
liver, etc.) are affected
Prevalence world-wide, but confined to tropics
and subtropics
Treatment as described for other species
Spoorozoa, continued
Babesia spp. (B. microti, B. divergens, B. gibsoni)
Transmission by vector ixodid tick DHs
Pathogenic potential high in splenectomized and other
immunocompromised humans, may be mild or
serious in intact hosts, species/strain differences
are known
Clinical signs: malaise, headache, fever, chills,
swetting, fatigue, weakness, anemia, jaundice,
renal failure
Reservoir: rodents, livestock, other “natural”
hosts, humans appear to be accidentals
Damage high in immunodeficient, moderate in most
others; much depends on species/strain of agent
involved
Sporozoa,continued
Babesia spp., continued
Prevalence widespread in “natural” reservoir
hosts, spotty in humans: Europe, NE USA,
Texas, Mexico, NC USA, et.al.
Diagnosis: microscopic ID and differentiation
from malarial (Plasmodium sp.) agents
Treatment: oral quinine + IV clindamycin, a few
others, less efficacious
Babesia sp. life cycle