Parasitology. Protozoans

Intro. Intestinal Parasitic Protozoans. Atrial and Intestinal Blood and Tissue Flagellates.

Direct Transmission

organism never leaves host - changes/transfers between hosts

intimate body contact - kissing, sexual intercourse

Fecal/Oral Transmission

in environment via fecal contamination

environmentally resistant cysts - in food, water, fomites

Vector borne Transmission

blood sucking arthropods pass organism during blood meal

intermediate host = vector → life cycles

Predator/Prey Transmission

parasite in prey tissues are eaten by predators

predators shed spored or infective stages for prey

General Life Cycle Stages

trophozoite form - multiplication by binary fission

cyst form - protective cover secreted for survival

Characteristics of Trophozoite Form

feeding stage

nuclear division, cytoplasmic division

moves

What triggers cyst formation?

excess/reduced food

temperature

desiccation

excess waste

oxygen level

Reproductive Cyst

cyst protects parasite → nuclei divide

increase in number of trophozoites

Protective Cyst

cyst wall protects organism

no morphological changes

Intermediate Hosts

some have none, others have hematophagous invertebrates

perfect vectors → mosquitos, mites, bugs, flies

can have complex (sexual/asexual) life cycles

Amebiasis

Entamoeba histolytica

Entamoeba histolytica Morphology

trophozoite - feeding stage, active stage, growing stage

cyst - reproductive, resistant stage, 1-4 nuclei, diagnosti stage

Entamoeba histolytica Life Cycle

ingestion of mature cysts

exyst in small intestine → trophozoites

move to large intestine

trophozoites in large intestine → intestinal phase ( if in circulation → extra-intestinal)

multiply by binary fission and produce cysts

cysts and trophozoites in feces

trophozoites cannot survive environment → only cysts in feces

Entamoeba histolytica Epidemiology

higher incidence in developing countries

mostly asymptomatic

10-20% symptomatic

Entamoeba histolytica Pathology - Intestinal

tear drop/flask shaped ulcer (acute)

break submucosa and spread laterally (acute)

diarrhea, constipation, lower back pain, fatigue, pain in lower quadrant (chronic)

damage depends on pathogenicity of strain (chronic)

Entamoeba histolytica Pathology - Extra-Intestinal

liver - via blood vessels or erosion of gut (most common)

skin - via erosion of gut and abdominal wall

lungs - via erosion of gut

brain - via circulation (leads to death)

Entamoeba histolytica Diagnosis

loose stools, dysentery (intestinal)

proctoscopic exam (intestinal)

cyst in stool, trophozoites in fresh stools (intestinal)

imaging, aspirates, signs & symptoms (extra-intestinal)

Entamoeba histolytica Prevention

water treatment

treat carriers

cook vegetables/food

personal hygiene

Entamoeba gingivalis Morphology

no cyst stage

trophozoites in oral cavity → gums/gingivia

Entamoeba gingivalis Epidemiology

direct transmission → spread by droplet infection

kissing, sharing utensils or drinking vessels

Entamoeba gingivalis Pathology

non-pathogenic

often in conjunction with periodontal disease

Entamoeba gingivalis Diagnosis

trohpozoites in mouth

Entamoeba gingivalis Prevention

goof oral hygiene

not sharing utensils

Infective stage of Entamoeba histolytica

cyst

What do Ancanthomoeba spp. and Naeglaria fowleri have in common?

they are free-living amoeba that can infect a human host

Ancanthamoeba spp. Life Cycle

cyst ↔ trophozoite (in environment)

trophozoites multiply via mitosis

enter human body via eye, broken skin, or nasal passages

Infective stage of Acanthamoeba spp.

trophozoite

Acanthamoeba spp. Epidemiology

free living in soil and freshwater

common among contact lense users

in air, sewage, swimming pool tap water, A/C units, contact lense cases

Acanthamoeba spp. Pathology

granulomatous amoebic encephalitis (GAE) → infection of central nervous system

GAE → headache, seizures, mental abnormalities, death (through nasal passages/skin)

keratitis → corneal ulceration (through eyes)

Acanthamoeba spp. Diagnosis

cysts or trophozoites in tissue

Naegleria fowleri Life Cycle

cyst ↔ trophozoite ↔ flagellated form

trophozoites multiply via promitosis

trophozoites and flagellates in body

trophozoites penetrate nasal mucosa

enter brain through olfatory nerves

Difference between promitosis and mitosis

promitosis - nuclear membrane remains intact

mitosis - nuclear membrane does not remain intact

Infective stage of Naegleria fowleri

trophozoite

Naegleria fowleri Epidemiology

in warm fresh water in hot climates (ponds, lakes, rivers)

hot springs and warm water discharge sites (power plants)

unchlorinated or poorly chlorinated swimming pools

heat resistant

Naegleria fowleri Pathology

primary amoebic meningoencephalitis (PAM) → consume astrocytes and neurons

1-9 days for symptoms to appear → death 2 weeks after symptoms

headache, fever, nausea, stiff neck

confusion, lack of attention, hallucinations, seizures, loss of balance

Naegleria fowleri Diagnosis

trophozoites in CSF

tissue flagellated forms in CSF

Naegleria fowleri Morphology

cyst form

trophozoite form - infective stage, divides by promitosis

flagellated form - temporary non-feeding stage

Balantidium coli Morphology

large ciliated protozoan

cyst stage

trophozoite stage - divides by binary fission

Balantidium coli Life Cycle

ingestion of cysts

exystation in small intestine

trophozoites in large intestine (multiply by binary fission)

some trophozoites invade wall of large intestine, others turn into cysts

cysts are passed in stool

Infective stage of Balantidium coli

cyst

Balantidium coli Epidemiology

28% of pig farmers/slaughter workers infected

pigs = primary reservoir

Balantidium coli Pathology

potential tissue invader

burrows into mucosa

can cause diarrhea

humans have good natural resistance

Balantidium coli Diagnosis

cysts or ciliate stage in stool

Balantidium coli Prevention

water treatment

personal hygiene

treat carriers

Trichomonas vaginalis/hominis Life Cycle

trophozoites in vaginal/prostatic secretion and urine

multiply by longitudinal binary fission

trophozoites in vagina or orifice of urethra

direct transmission - sexual intercourse

Trichomonas vaginalis/hominis Epidemiology

mostly asymptomatic

more common in females → more symptomatic

less common in males → less symptomatic

Trichomonas vaginalis/hominis Pathology

vaginitis & urethritis - inflammation and WBC infiltration

female → pruritus, burning, vaginal discharge, irritation

male → urethritis with discharge, can be asymptomatic in prostate

erosion and necrosis of cervix → cervical cancer

Trichomonas vaginalis/hominis Prevention

as with any STD - use condoms, cover female genitals with latex or polyurethane square

Infective stage of Trichomonas vaginalis/hominis

trophozoite

Giardia lamblia (duodenalis) Life Cycle

ingestion of contaminated food or water

exyst in small intestine

trophozoites divide via longitudinal binary fission

cysts and trophozoites in stool

Giardia lamblia (duodenalis) Epidemiology

fecal/oral transmission by ingestion of cysts - contamination, hand to mouth, anal-oral sexual contact

more common in developing countries and warm climates

animals may act as reservoir - contact when hiking or camping

Giardia lamblia (duodenalis) Pathology

attach to villi/microvilli of duodenal and jejunum mucosa - erodes microvilli

does not invade tissue, feeds on secretions

malabsorption, inflammation, diarrhea

Giardia lamblia (duodenalis) Diagnosis

cyst in stools

liquid stools

history of exposure

Giardia lamblia (duodenalis) Prevention

good hygiene - frequent hand washing

avoid contaminated water

peel/wash fruits and vegetables

Infective stage of Giardia lamblia (duodenalis)

cyst

American Trypanosomiasis

Trypanosoma cruzi

Chagas Disease

Trypanosoma cruzi

Vector for Trypanosoma cruzi

triatomine bug

Trypanosoma cruzi Life Cycle

triatomine bug takes blood meal → metacyclic trypomastigotes in feces

metacyclic trypomastigotes penetrate bite wound

turn into amastigotes

multiply in cells by binary fission

amastigotes → trypomastigotes

trypomastigotes burst out of cell into bloodstream (can infect other cells and turn into amastigotes)

triatomine bug takes blood meal → ingests bloodstream trypomastigotes

epimastigotes in midgut → multiply

metacyclic trypomastigotes in hindgut → triatomine bug takes blood meal

Trypanosoma cruzi Life Cycle Stages

metacyclic trypomastigotes - in triatomine hindgut → feces, infective stage, invades cells

amastigotes - divide by binary fission, intracellular

bloodstream trypomastigotes - in blood, do not replicate, can infect other sites, vector intake

epimastigotes - in triatomine midgut, multiplies by binary fission

Trypanosoma cruzi Epidemiology

vector - reduviidae bugs (blood feeders)

Central & South America - endemic and enzootic areas

United States - animal infection (feral dogs, ground squirrels, rodents), blood transfusion, congenital transfer

Trypanosoma cruzi Pathology - Acute

chagoma

Romana’s sign

fever, hepatomegaly, splenomegaly, electrophysiology changes in heart (arrythmia)

organism move from blood → tissue

Chagoma

inflamed swelling at site of triatomine bug bite

Romana’s sign

occurs when bite is associated with eye, swelling of the eyelid

Trypanosoma cruzi Pathology - Intermediate

clinically asymptomatic

few or no parasites in bloodstream → in intracellular positions in tissue (amastigotes)

in heart, esophageal nerve cells, colon associated nerve

Trypanosoma cruzi Pathology - Chronic

10-20 years after infection

megaesophagus, megacolon - damaged nerve cells that control peristaltic action

cardiomegaly - amastagotes in heart muscle, apical aneurysm, weak heart muscle wall

Trypanosoma cruzi Diagnosis

blood sample - trypomastigotes, chagoma, Romana’s sign (early)

antibodies - serology, DNA - PCR, xenodiagnoses, electrocardiogram/echodiagram (intermediate)

signs and symptoms (chronic)

Trypanosoma cruzi Prevention

vector control

netting when sleeping

screen blood used for transfusion

education

Infective stage for Trypanosoma cruzi

metacyclic trypomastigotes