12 - Parasitology: Ingested Protozoans

Question 1

What are the three phylums of ingested protozoan parasites in humans? Where are they located and what people are at risk?

Answer 1

1. Amoebozoa (Entamoeba histolytica): intestinal lumen, invasive into intestine and liver. Everyone, esp. people in crowded setting.
2. Metamonada (Giardia duodenalis): intestinal lumen. Everyone, esp people in crowded setting.
3. Apicomplexa(cryptosporidium parvum and homnis): intracellular bursh border of intest. epithelium. Everyone esp. immunocompromised (AIDS)
   - (Toxoplasma gondii): blood, tissue cysts in muscle brain and eyes. Everyone. Esp. immunocomp (AIDS); developing fetus.

Question 2

What is the life cycle of Entamoeba histolytica?

Answer 2

Lives in intestines and pts will release infective cysts and trophozoites in diarrhea(these people are asymptomatic).

Those cysts will be passed and become infective in the stool.

Question 3

What are two characteristics of entamoeba histolytica?How would you identify this species?

Answer 3

1. Diameter of infective cysts is VERY small

2. Trophozoites are often filled with RBCs when the disease is invasive and this is characteristic for this species.

Question 4

How is entamoeba histolytica transmitted?

Answer 4

Fecal/oral route for cysts; anal sex causes direct trans of trophozoites.

Flies and cockroaches can be vectors.

It’s INVASIVE.

Question 5

What is the epidemiology of entamoeba histolytica? What is it caused by?

Answer 5

Due to poor sanitation and human waste as fertilizer.

Endemic in the US, mainly in institutions with poor hygeine such as prisons or day cares.

Spread through anal sex.

Question 6

What are the three pathologies of entamoeba histolytica?

Answer 6

Carriers: asymptomatic,; chronic infection for months or yrs. Massive shedding of cysts.

Intestinal amebiasis (dysentery): invasive colonic epithelium, ulceration; abd. pain, cramps, diarrhea.

Extraintestinal amoebiasis: rare dissemination throughout body (mostly liver), fever, abscess formation.

Question 7

What is the immunity response associated with entamoeba histolytica? How is it diagnosed?

Answer 7

Humoral response in invasive disease; some acquired immunity in endemic areas.

Cysts in stool, cysts and trophozoites in bloody diarrhea. Trophozoites contain RBCs.

Question 8

What is the treatment of entamoeba histolytica?

Answer 8

Paromomycin for luminal phase; carriers should be treated.

Metronidazole or tinidazole, immediately followed by paromycin for invasive phas.e

Question 9

What is the life cycle of giardia duodenalis? What is the infective form?

Answer 9

Similar to entamoeba histolytica.

Trophozoites from the gut released with cysts into environ. (cysts are infective form that get back into humans, trophs do not survive in environment)

Cysts can get onto vegetation or into water and be ingested.

Question 10

What is the structure of giardia duodenaliscysts and trophozoites?

Answer 10

Cysts: small oval shaped

Trophozoite: pear shaped with tail like things. Suction cup to the intestine wall but do NOT penetrate.

Question 11

How is giardia duodenalis transmitted?

Answer 11

Fecal/oral (infectious dose is 10-100 cysts)

Direct person to person, oral/anal sex.

Shedding of cysts may occr in showers.

Question 12

What is the epidemiology of giardia duodenalis?

Answer 12

Endemic in many developing countries.

Epidemic in day-cares, nurseries.

Large wildlife reservoir causes contamination of streams and lakes.

Question 13

What immunity is associated with giardia duodenalis?

Answer 13

Role unclear; reinfection is possible.

Humoral responses are seen, as well as some resistance in endemic areas.

Question 14

How is giardia duodenalis diagnosed and treated? What should pregnant women be treated with?

Answer 14

Stool exam for cysts and trophozoites. Testing for giardia antigens in stool.

Treat asymptomatic carried and disased with metronidazole, tinidazole, nitazoxanide. (paromomycin for pregnant)

Question 15

What are aplicomplexan parasites?

Answer 15

Obligate intracellular; apical organelle for host cell invasion.

Life cycle alternates between asexual (schizogony) and sexual (sporulation) reproduction.

Question 16

What is the definitive hot for the sexual cycle of ingested and vector-borne apicomplexan parasites?

Answer 16

Ingested: crytosporidium hominis/parvum - humans; toxoplasma gondii - felines

Vector-borne: Plasmodium spp-mosquitoes; Babesia microti - ticks.

Question 17

What is the general life cycle of apicomplexan parasites?

Answer 17

In gut cells, sexually reproduction causes zygotes that releases sporazoites.

These can go and infect other cells.

Non-sexual reproduction phase causes amplification in tissue.

Question 18

What is the life cycle that applies to both Cryptosporidium hominis and parvum? Where are these taken up in the body?

Answer 18

Cysts from intestines and contaminate water/food. Oocytes are taken up by people.

Taken up in brush border of intestines and trophozoites develop. Asexual repro causes amplification.

Sexual repro also occurs to get more oocytes that can get into the enrivonment or thin-walled oocytes can autoinfect in the gut.

Question 19

What is the appearance of cryptosporidium oocytes?

Answer 19

They are very small; the size of yeast cells.

Question 20

How are C. hominis and C. parvum transmitted? What is the epidemiology?

Answer 20

Fecal/oral; oral/anal.

High infection in developing countries. Common secondary in AIDS patients. Epidemic outbreaks associated with faulty water purify. Commonly outbreaks involve swimming pools and water parks (parasite resistant to Cl).

Reservoir mainly in cattle.

Question 21

What is the pathology of C. hominis and C. parvum? When are the oocytes shed?

Answer 21

Symptoms like Giardia but shorter with breater fluid loss.

1-2 wk incubation; 3x or more diarrhea with NO blood.

Acute symp. for 1-2 wks (this is when ooctyes are shed); mild persist for a month.

Self-limiting with a healthy immune response.

Question 22

How are C. hominis and C. parvum diagnosed and treated?

Answer 22

Ooctyes in stool (acid fast staining)

No broadly effective therapy; oral rehydration, esp. for pts who are immunocompromised.

Short course of nitazoxanide for immu nocomp.

Question 23

What is the life cycle of Toxoplasma gondii? What is the definitive host?

Answer 23

Fecal oocytes can be ingested by cats (definitive hosts to get oocytes) mice, pigs, birds, and farm animals. In them cysts develop.

Cat litter, fruit, water can have oocytes. Can eat animals that have the cysts.

Vertical transmission from mom to baby can occur.

Question 24

Toxoplasma gondii: What form of this is released from cats intestines first? What happens next? What is the initial infectious form?

Answer 24

Unsporulated version.

Gets sporulated within 48-72 hours after leaving cats body.

Tachyzoites are initial infective form that are mobile and can be in the bloodstream. These are the cysts that can get into muscle and the brain.

Question 25

What is the transmission of

Toxoplasma gondii?

Answer 25

Undercooked meat with tissue cysts.

Fecal/oral: oocytes from contam soil, plants, cat litter.

Transplacental from mom.

Blood transfusion.

Question 26

What is the epidemiology of Toxoplasma gondii? What can serve as an intermediate host?

Answer 26

Worldwide; undercooked meat and house cats.

Any warm-blooded animal can serve as intermediate host.

Question 27

What is the pathology and immunity of Toxoplasma gondii?

Answer 27

Toxoplasmosis (CDC top 5)

Acute infection symptomatic: maybe chills/fever. Rapid control by cell-mediated immunity.

Life-long latent infection. Immunocomp people cannot control primary infection and can have reactivated infection. In utero infection possible and can cause birth defects.

Question 28

How do you diagnose Toxoplasma gondii?

Answer 28

Can look at antibodies to determine if there’s an acute or chronic infection.

Chronic isn’t a problem because it leads to immunity.

Question 29

What is the treatment for Toxoplasma gondii in immunocomp pts or for those with active chorioretinitis by ocular toxoplasmosis?

Answer 29

Pyrimethamine/sulonamide; pyrinmethamin/clindamycin.

Prophylactic trimethoprim (TMP)/sulfa if CD4 count <100.