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

• 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 long-

term/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 Cyst

Cytostome Macronucleus

Macronucleus

Cilia

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/ Leishmanias/

trypomastigote forms 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

Trypomastigote/

Trypanosome

Triatomid Vector

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/long-

term (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