Protozoa I Flashcards
Sources of parasitic infections: insect or tick bite
Trypanosomiasis
Babesiosis
Malaria
Leishmaniasis
Sources of parasitic infections: Blood
Trypanosomiasis Babesiosis Malaria Leishmaniasis Toxoplasmosis
Sources of parasitic infections: water
Guinea worms Cryptosporidiosis Ascariasis and whipworm Giardiasis Amoebiasis Schistosomiasis (washing, swimming, wading)
Sources of parasitic infections: food
cryptosporidiosis Giardiasis Amoebiasis Toxoplasmosis Tapeworms (Taenia spp and Diphyllobothrium)
Factors influencing the geography of parasitic infections
-Local ecology:
local habitats
vectors
reservoirs (Animal; human)
Local socioeconomic conditions: sanitation water quality exposure to vectors Local habits and customs Untreated carriers
Protozoa definition
unicellular eukaryotes
Entamoeba histolytica: infectious cycle
Entamoeba histolytica (an intestinal protoza)
- Cysts and trophozoites passed in feces.
- Cysts found in formed stool, trophozoites found in diarrhea
- Infection via ingestion of mature cysts (fecally contaminated water, food, hands)
- Excystation in SI and trophozoites released, migrate to large intestine
- Attaches to colonic mucosa via Gal/GalNAc lectin and produces cysteine proteases that damage tissue
- Multiply by binary fission and produce cysts
- Both stages passed in feces
- Walls of cysts allow protection to survive in external environment for days to weeks
- Trophozoites are rapidly destroyed outside the body
- Often, trophozoites remain in intestinal lumen (asymptomatic carriers passing cysts in stool)
- Sometimes trophozoites invade intestinal mucosa (intestinal disease) or through the bloodstream (infect liver, brain lungs)
Consequences of amoebiasis
(E. histolytica)
- can lead to death
- amebic dysentery
- amebic liver abscess or other organs
- Most often: present in asymptomatic carriers
Diagnostic criteria for E. histolytica
- trophozoites in tissues or liquid feces
- cysts in colon or formed feces (spherical w/ 1-4 nuclei; glycogen granules; chromatid bodies)
- Antibodies in 95% with intestinal amebiasis
- Antigen can be detected in stool w/ specific immunoassay
How does E. histolytica lyse host cells?
- Can lyse neutrophils, monocytes, lymphocytes, and colonic cells and hepatocytes by a cell contact dependent mech involving phospholipase A and pore forming peptides
- Causes flask shaped colonic ulcers with raised edges
General overview of E. histolytica infection
- large bowel infection causing diarrhea/dysentery
- extracellular parasite
- can become invasive w/ intestinal, liver, other amebic abscesses
- Prevalence: 50 million worldwide, higher in developing countries; industrialized countries: risk higher in male homosexuals, travelers, immigrants, institutionalized pops
- 1-5% of US pop infected
- Fecal oral transmission
- less than 10% of infected show disease
Most common form of disease = colitis
-If invades mucosa and erodes through lamina propria see flask shaped ulcers contained by muscularis
Dx:
- trichrome stool analysis
- Immunodiagnosis for stool antigen or serology using enzyme immunoassay
- EIA and PCR for different species
Note: E. dispar is nonpathogenic but morphologically identical to E. histolytica
Giardia lamblia: infectious cycle
(another intestinal protozoa)
- Cysts are responsible for transmission (can survive in cold water for months)
- Both cysts and trophozoites can be found in feces
- Transmission: contaminated food, water, or fecal oral route
- Excystation in SI after exposure to stomach acid, releasing trophozoites which multiply by binary fission remaining in lumen of duodenum or jejunum where they can be free or attach to mucosa by ventral sucking disc
- Encystation as they travel toward colon
What is special about Giardia intestinalis?
- It is a flagellate
- it is the only common pathogenic protozoan found in the duodenum or jejunum
Diagnosis of Giardia
- cysts in formed stools or cysts/trophozoites in liquid stools (better still is duodenal aspiration)
- Trophozoites: heart shaped w/ 2 nuclei, 4 pairs of flagella, concave anteroventral sucking disc (usually in duodenum or jejunum)
- Cysts: ellipsoid, thick walled, 2 (immature) or 4 nuclei
- Other: Immunofluorescence or ELISA for antigens in stool
Consequences of infection with Giardia
- Most infections are asymptomatic
- Some cause low-grade inflammation, crypt hypertrophy and villous flattening to villous atrophy and severe malabsorption (severe diarrhea)
- Can cause watery, semisolid, greasy, bulky, foul-smelling stools
- Mucosal invasion = rare
- No enterotoxin
- May be life threatening in pts with hypogammaglobulinemia
General overview of Giardia infection
- extracellular parasite of large intestine
- Prevalence 2-5% in industrialized and 20-30% in developing countries
- Fecal oral
- More in warm climates, more prevalent in kids
- most frequent cause of non-bacterial diarrhea in US
- incubation period: 1-14 days (avg 7), lasts 1-3 weeks
- Abdominal pain, bloating, gas, foul smelling stools, greasy stools that tend to float, n/v
- US risk groups: travelers, kids in daycare, homosexual men
- Peak: late summer in US, UK, Mexico
- travelers, hikers, campers at risk
- Chlorination is NOT effective; boil or filter water if camping
- swimming pools vulnerable
Cyptosporidium parvum: infectious cycle
(Cryptosporidiosis)
- an intestinal protozoa
- sporulated oocysts, containing 4 sporozoites, excreted by infected host (human or animal) thru feces and possibly other routes like respiratory secretions
- transmission via contaminated water, occasionally food sources (chicken salad)
- Ingestion followed by excystation
- Sporozoites parasitize epithelial cells of GI tract or other tissues like respiratory tract
- Asexual multiplication (produce merozoites that can infect other intestinal epithelial cells), then sexual multiplication, producing microgamonts (male) and macrogamonts (female)
- Oocysts develop that sporulate in the infected host (thick walled= excreted, thin walled= autoinfection of host
- Oocysts are infective upon excretion
C. parvum is predominantly assoc with brush border of epithelial cells of the lower small bowel
-widespread in animals
Consequences of Cryptosporidium infection
- asymptomatic to severe life-threatening illness
- watery diarrhea is most common
- can see dehydration, wt loss, abdominal pain, fever, n/v
- can be chronic or mores severe in immunocompromised pts with CD4 less than 200
- most common site: small intestine (also see other digestive tract organs, the lungs, and possibly conjunctiva)
Diagnosis of Cryptosporidiosis
- oocysts containing 4 sporozoites in stool using modified acid fast staining
- enzyme immunoassay for C. parvum antigen in stool
General overview of Cyptosporidiosis
- infection of small intestine causing diarrhea/dysentery
- 750,000 cases in US/yr
- INTRACELLULAR parasite
- incubation period 7 days (2-10 d range)
- watery diarrhea
- immunocompetent: sx 1-2 weeks; chronic and more severe in immunocomp w/ CD4 less than 200
Dx:
clinical signs
direct flourescent antibody and enzyme immunoassay
fecal analysis
Oocysts survive chlorination
There are many reservoir hosts
Trichomonas vaginalis infection cycle
It is a flagellate that causes urogenital infections
-EXTRACELLULAR parasite
- resides in female lower genital tract and male urethra and prostate where it replicates by binary fission
- no cyst form, and does not survive well in the external environment
- only known host= humans
- transmitted via sexual intercourse
- trophozoite =infective and diagnostic stage
- incubation period: 5-28d
Consequences of infection with T. vaginalis
- damage to genital mucosa (microulcerations)
- frothy yellow or cream colored vaginal discharge
- inflammation or erosion of infected mucosal surfaces
- local tenderness, burning, itching
- “strawberry cervix”
In males the urethra, seminal vesicles and prostate may be infected
-may be asymptomatic, but a thin, white urethral discharge occurs in 10% of males
- Reinfection can occur, but partial immunity decreases severity
- common cause of infection to vulva, vagina, and cervix in 40% of women
Treatment of T. vaginalis
-metronidazole or tinidazole
Dx of T. vaginalis
- visualization of motile parasites in vaginal secretions
- culture in special media (takes 3-7d)
- Antigen detection test from Genzyme Corp
- DNA based tests and PCR
High risk groups: African americans, prison inmates, drug users and sex workers
-prevalence increases with age
Opportunistic protozoa (rare)
Acanthamoeba (amoeba; brain, eye)
Naeglaria fowleri (amoeba; nose to brain)
- commonly in lakes, swimming pools, tap water, and heating and air conditioning units
- transmission: water nasal access and contact lenses and saline solutions
- warm bodies of water
- diving or impact of water in nasal passages enables amoebic access (Naegleria)
- contaminated solutions for contacts or nasal washes (Acanthamoeba)
Naeglaria fowleri
-cause of primary amebic meningoencephalitis (PAM)= brain eating ameba (typically lethal)
PAM presentation:
- severe headache
- meningeal signs, fever, vomiting, and focal neurologic deficits, and progresses in less than 10d to coma and death
Dx: microscopic exam of CSF
- wet mount may detect motile trophozoites
- Giemsa stain
Acanthamoeba spp
Granulomatous meningoencephalitis, particularly in immunosuppressed patients
-headaches, altered mental status, focal neurologic deficit, progressing to death in several weeks
Keratitis, particularly associated with corneal injuries and with wearing contact lenses
- skin lesions
- corneal ulcers
Dx: microscopic exam of stained smears of biopsy specimens or corneal scrapings
-PCR
