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Microbiology > Unit 1: Diarrheagenic Protozoans > Flashcards

Unit 1: Diarrheagenic Protozoans Flashcards

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Biology 101 flashcards
1
Q

Disease representing a zoonosis with cross infectivity between animals and humans

A

Giardiasis

G.lamblia found in beavers, dogs, cats, and primates

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2
Q

Factoids on Giardiasis

A

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

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3
Q

The two morphological stages of Giardia lamblia

A

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)

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4
Q

Giardia life cycle

A

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

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5
Q

Giardiasis epidemiology

A

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

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6
Q

Persons at high risk for giardiasis

A

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

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7
Q

Pathophysiology/Clinical Presentation of Giardiasis

A

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

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8
Q

Identification of giardiasis

A

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)

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9
Q

Prognosis for giardiasis

A

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)

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10
Q

Treatment and control of giardiasis

A

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

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11
Q

Protozoan illness than can result in colitis and liver abscess

A

Amoebiasis

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12
Q

Why is diagnostic testing for Entamoeba histolytica nearly impossible?

A

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)

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13
Q

Morphological features of E.histolytica

A 
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

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14
Q

Life cycle of Entamoeba histolytica

A

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)
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15
Q

Amoebiasis epidemiology

A

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.

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16
Q

High risk populations for amoebiasis

A 
Children
Pregnant women
Persons on long term corticosteroids
Malnourished
Generally immunocompromised 
Institutionalized persons
Persons engaging in oral-anal sexual practices
17
Q

Pathophysiology/clinical presentation of amoebiasis

A

(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
18
Q

Complications of Ameobiasis

A

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)

19
Q

Virulence factors associated with entamoeba histolytica

A

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

20
Q

Diagnosis of amoebiasis

A

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

21
Q

Treatment and control of amoebiasis

A

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

22
Q

What’s so special about Cryptosporidiosis?

A

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)

23
Q

Morphological forms of cryptosporidium

A

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)

24
Q

Life cycle of cryptosporidium

A

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

25
Q

What are parasitophorous vacuoles?

A

Deposits on outer surface of intestinal wall, releases mature cryptosporidium sporozoites

26
Q

Epidemiology of cryptosporidosis

A

Not well defined in the US

Endemic cases are transmitted person to person (fecal-oral)

Sporadic cases usually from contaminated water and food
• Animal to human contamination (cows)
• Frequently found in recreational water (RESISTANT TO CHLORINE)

Recommended decontamination of pools with HIGH SALT

Associated with AIDS

Prevalent in developing countries

27
Q

Pathophysiology and Clinical Presentation of Cryptosporidosis

A

Highly infectious - can cause infection with 10 oocysts (oocysts immediately infectious after excretion)

5-10 day incubation period

Infections difficult to treat b/c of the vacuole (protective membrane)

Infection thought to result from increased intestinal permeability, chloride secretion, and malabsorption

Diarrhea (WATERY) is the cardinal symptom (NO BLOOD)

Other Sx: dehydration, weight loss, fever, abdominal pain
Pt several wasted, lasted for ~2 weeks

Bad prognosis if CD4 cell counts are low

28
Q

Dx and Tx of Cryptosporidosis

A

Isolate OOCYSTS in stool sample (via ZINC SULFATE CENTRIFUGAL FLOTATION)

Immunofluorescence (b/c often coinfection with Giardia)

ACID FAST OOCYSTS are round

ELISA - highly specific and sensitive

DOC: Nitazoxanide or paroromycin

29
Q

Acid-fast oocysts

A

Cryptosporidium

30
Q

Autofluorescent oocyst

A

Key ID feature for Cyclospora cayetanensis

Much larger than the oocysts of cryptosporidium

31
Q

What is Cyclosporiasis?

A

Diarrheagic protozoan disease linked to patients in LATIN AMERICA

Causative agent: Cyclospora cayetanensis (larger, autofluorescent oocyst)

Disease has been associated with ingestion of oocyst contaminated water and IMPORTED FOODS (fresh fruits/veggies)

32
Q

Life cycle of cyclosporiasis

A

Ingestion of oocysts
Similar progression as other pathogens discussed in this lecture
Oocysts RESISTANT TO CHLORINE
Oocysts shed in feces MUST sporulate in the environment (requires days, certain temp — so not a lot of autoinfection/reinfection)

33
Q

Clinical presentation of cyclosporiasis

A 
Low grade fever
Chills
Abdominal cramps
Nausea
Vomiting
Explosive, non-bloody, watery diarrhea
Rapid weight loss
Profound fatigue
34
Q

Dx and Tx of cyclosporiasis

A

LARGE oocyst identified in stool samples (may be difficult due to low numbers)

ACID FAST, AUTOFLUORESCENT oocyte

PCR based test now available

DOC: Trimethoprim-sulfamethoxazole

35
Q

Blastocystis hominis

A

Polymorphic protozoan

Disease results from ingestion of cysts from contaminated food/water (animal feces)

KEY FEATURES: Large central vacuole, multiple nuclei (10-12) distributed around rim of cytoplasm —> easy to ID on stain

Tx: Metronidazole

36
Q

Balantidium coli

A

Extremely large intestinal microbe

Zoonotic (pigs)

Can result in gut perforation (large scale damage)

Has both trophozoite and cyst forms

KEY FEATURES: MACROnucleus, cilia evident on trophozoite

Tx: Tetracycline or Metronidazole

Microbiology (6 decks)

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