Unit 1: Diarrheagenic Protozoans Flashcards
(36 cards)
Disease representing a zoonosis with cross infectivity between animals and humans
Giardiasis
G.lamblia found in beavers, dogs, cats, and primates
Factoids on Giardiasis
Major diarrheal disease found throughout the world.
May be asymptomatic colonization or acute/chronic diarrheal illness
Infections more common in children than adults
More problematic in the immunocompromised
Typically doesn’t cause a lot of tissue damage though
Caused by Giardiasis lamblia - flagellate protozoan
The two morphological stages of Giardia lamblia
1) Trophozoite - exists freely in the small intestine
TEARDROP shape with a BI-LOBED ventral adhesive disc, flagella, and TWO NUCLEI
Does not invade tissue or destroy RBCs, feeds on mucus secretions
2) Cyst - form passed into the environment
OVAL in shape, HYALINE wall, FOUR NUCLEI when mature
(1 cyst —> produces 2 trophozoites)
Giardia life cycle
Ingestion of cyst (infectious stage) from contaminated food/water
Excystation occurs in the stomach (acid and pancreatic enzymes)
Trophozoites (pathogenic) pass into the small bowel where they divide quickly (9-12 hour doubling time)
Trophozoites in large bowel envy start in neutral pH and bile salts
Cysts passed into the environment
Giardiasis epidemiology
High contagious (esp in travelers to endemic areas)
Contracted from drinking water contaminated by feces (ingestion of cysts)
WHO estimates that 1 billion people are currently infected
Infections highest among children in developing countries
Thought to contribute to 2.5 million deaths as a result of diarrhea
In US, high incidence in western states
Persons at high risk for giardiasis
Day care children, workers, close contacts
Backpackers/campers
Travelers to disease endemic areas
Persons who drink from shallow wells/surface water
Persons engaging in oral sexual practices
Pathophysiology/Clinical Presentation of Giardiasis
Can be communicable disease - infective dose = 10-25 cysts (>25 cysts = 100% infection rate)
~2 week incubation
Can be an STI
Intermittent episodes of watery diarrhea (NO BLOOD), abdominal cramps, distinction of abdomen
Can also have intestinal pain, anorexia, and VITAMIN B12 DEFICIENCY (malabsorption)
Virulence not well understood - ventral disc imprints found on intestinal mucosa, thought to contribute to mucosal damage (flattening of villi) if untreated
Lead to MALABSORPTION OF INTESTINAL TISSUE
Identification of giardiasis
Diagnosed via visualization of cysts and/or trophozoites in stool samples or O&P exam (ovuum/parasite)
Multiple stool samples may be necessary (difficult to detect due to shedding of cysts)
Serological test (ELISA) to detect Giardia-specific antigen 65 (GSA65) - used mainly in veterinary practices (can’t use in humans b/c antibodies can be carried for >2 years —> false positives)
Prognosis for giardiasis
Generally excellent
Most patients are asymptomatic and most infections are self-limiting (problematic in children and immunocomprised)
Can see weight loss, growth retardation
Re-infections are possible
Rarely associated with mortality (except in extreme dehydration cases)
Treatment and control of giardiasis
DOC = Metronidazole
Alternatives: tinidazole or albendazole (tolerated better in children than metro)
Drink purified water on camping trips (boil, iodine, or bottled)
Avoid fecal contamination
Educate patients on good personal hygiene, possibility of contracting disease through venereal transmission
Protozoan illness than can result in colitis and liver abscess
Amoebiasis
Why is diagnostic testing for Entamoeba histolytica nearly impossible?
Many species of Entamoeba but only E.histolytica is associated with disease in humans. Others are considered nonpathogenic but exist as part of microbiome
Exception - E.dispar is commensal (esp in HIV+ patients)
Morphological features of E.histolytica
1) Trophozoite - Amoeboid with ONE NUCLEUS Non-flagellated Feeds Pseudopod-forming Invasive and pathogenic
2) Cyst - round to oval in shape
FOUR NUCLEI (—> 1 cyst=4 amoeboids)
Cyst is the infectious stage
Life cycle of Entamoeba histolytica
Ingestion of cysts from the environment
Excystation in the colon
Forms highly motile trophozoites (pathogenic)
Colonizes the mucosa of the colon
- May excystation and be passed in feces
- OR invades intestinal mucosal barrier and gain access to the bloodstream (dissemination)
Amoebiasis epidemiology
Worldwide but more prevalent in tropical/subtropical areas
Fecal contamination of water and food
Causes more deaths than any parasite other than malaria and schistosomiasis
Reportable disease
50 million people infected worldwide, with 100K mortalities annually.
High risk populations for amoebiasis
Children Pregnant women Persons on long term corticosteroids Malnourished Generally immunocompromised Institutionalized persons Persons engaging in oral-anal sexual practices
Pathophysiology/clinical presentation of amoebiasis
(Asymptomatic colonization possible)
Disease can be initiated by small number of cysts
Diverse manifestations - dysentery to extra-intestinal
Incubation period of ~10 days
Signs/symptoms of acute amoebic colitis: • Abdominal cramps/tenderness • BLOODY STOOLS • Fever • Vomiting • Unintentional weight loss
Complications of Ameobiasis
Amoeba can hydrolyze the intestinal lining, resulting in ULCERS
Typically right upper quadrant pain, can be several inches in diameter
Organism can then invade the submucosa and underlying blood vessels
Death can occur from peritonitis, cardiac failure, and exhaustion
Can also experience anemia (due to hemolysis)
Virulence factors associated with entamoeba histolytica
Lectin - assists in adhesion to host cells (non-specific)
Phospholipases - disrupts host cell membranes (large scale tissue destruction)
Amoebapore - active peptide released to insert ion channels into host cell lipid structure —> lysis of host cells (specific to amoebas)
Cysteine proteases - highly active, act to degrade mucus (no mucus, no IgA), antibody, and complement, and to digest cellular matrix
Diagnosis of amoebiasis
1) Trophozoites or cysts in stool sample (difficult due to other commensal entamoeba species ie E.dispar)
2) Amoebic dysentery must be differentiated from bacterial colitis
3) Radiology is useful for extra-intestinal disease (CT and/or MRI - may reveal large cyst like structures/abscesses)
4) ELISA to identify E.histolytica (differentiates it from E.dispar) but $$$
5) PCR based test
Treatment and control of amoebiasis
DOC = Metronidazole
Alternative = Tinidazole
Both used in combo with iodoquinol
Large or unresponsive abscesses may be repaired surgically
Drink purified water on camping trips,
Purify water (note - CYSTS RESISTANT TO CHLORINE)
Avoid fecal contamination
Educate patients on good personal hygiene, possibility of contracting disease from venereal transmission
What’s so special about Cryptosporidiosis?
Caused by at least 15 different species
• Cryptosporidium hominis - humans the only host
•C. parvum - bovine and human hosts
Mainly affects CHILDREN
SELF LIMITING diarrheal illness in HEALTHY individuals
Serious disease in immunocompromised persons (severe, prolonged diarrhea in AIDS)
Morphological forms of cryptosporidium
Oocysts - contain FOUR sporozoites
Sporozoites - motile, bind to receptors on the surface of intestinal epithelial cells
Oocysts are the infectious stage
Does not multiply outside of the host
Has both asexual and sexual reproductive cycles in the host (can evolve b/c exchange of genetic info via sexual repro)
Life cycle of cryptosporidium
Ingestion of oocysts
Activated to release 4 infective sporozoites
Bind to receptors on small intestinal epithelial cells
Ingested into PARASITOPHOROUS VACUOLE
Once inside epithelial cells, undergoes sexual and asexual reproduction to form more oocysts
• THIN walled oocysts (asexual) lead to reinfection of host
• THICK walled oocysts (sexual) are shed into the environment
Oocysts shedding can continue for weeks after patient improves clinically
