34 Parasitic infections

Question 1

Cryptosporidium demographics

Answer 1

Most common cause of waterborne diseases

Seen in: recreational water facilities, exposure to cattle, infected people, contaminated food and water

Question 2

Cryptosporidium causative agent

Answer 2

Protozoans
C parvum (zoonotic)
C hominis (human-human)

Oocysts - double wall, environmentally resistant

Question 3

Cryptosporidium life cycle

Answer 3

Ingestion: contaminated food
Excystation: oocysts release sporozoites (1:4) in intestines -> affect apical enterocytes (reproduction site)
Parasitism: sporozoites -> trophozoites attach to brush borders -> destruction and atrophy -> malabsorption (osmotic diarrhea)
Reproduction: asexual reproduction -> merozoites; merozoites -> gametocytes -> sexual reproduction
Sporulation:
1 Thick walled cysts (infectious, resistant to chlorine)
2 Thin walled cysts (stay in intestine, cause autoinfection)

Question 4

Cryptosporidium symptoms in immunocompetent

Answer 4

Asymptomatic
Carrier state, sheds oocysts
Self- limiting diarrhea (2-3 wks)

Symptomatic
PWFS diarrhea (days-weeks)

Question 5

Cryptosporidium symptoms in immunocompromised

Answer 5

<200 CD4 count

pfws diarrhea

Question 6

Cryptosporidium diagnosis

Answer 6

Kinyoun’s modified acid fast stain (OIO)

ELISA: serum, can only see IgG

Question 7

Cryptosporidium treatment, prevention, control

Answer 7

Nitrazoxanide (tapeworms)
Paromomycin

safe sex, don’t touch farm animals and feces, don’t swallow water when swimming, drink safe water (water filters)

Question 8

Cyclospora demographics

Answer 8

All age groups

Pre-packaged salad mix, foods, and herbs (vegetable produce)

Question 9

Cyclospora causative agent

Answer 9

Protozoan

C cayetanensis

Question 10

Cyclospora life cycle

Answer 10

Ingestion: food/water with sporulated oocysts
Excystation: oocysts release sporozoites in SI epithelia (not infective, must live outside to become infective)
Reproduction: sexual and asexual
Release: unsporulated oocysts via feces
Sporulation: incubate in outside envi (3-5 d, 22-32C)

Question 11

Cyclospora symptoms

Answer 11

immunocompetent: diarrhea, fever, pain

Question 12

Cyclospora diagnosis

Answer 12

Microscopy: stools

formalin-ether concentration technique, wet mount (UV/DIC), modified acidfast/safranin (cheap)

Question 13

Cyclospora treatment, prevention, and control

Answer 13

self-limiting
cotrimoxazole

wash hands and food

Question 14

Cystoisospora demographics

Answer 14

tropical/subtropical
immunocompromised hosts
dense institutions

Question 15

Cystoisospora causative agent

Answer 15

Protozoan
C belli (elongated oocysts)

Question 16

Cystoisospora life cycle

Answer 16

Ingestion: food/water with sporulated oocysts
Excystation: infects cytoplasm of enterocyte–> rupture of enterocyte
Reproduction: sexual and asexual
Release: unsporulated oocysts (feces)
Sporulation: outside environment; sporoblast = 2 sporocysts + 4 sporozoites

Question 17

Cystoisospora symptoms

Answer 17

diarrhea, fever, malabsorption, abdominal pain, eosinophilia

Question 18

Cystoisospora diagnosis

Answer 18

Microscopy: fect, wet mount, modified acid-fast/safranin

Question 19

Cystoisospora treatment, prevention, control

Answer 19

sulfonamides

proper hygiene

Question 20

Toxoplasma demographics

Answer 20

common in hiv/aids pts
africa, france, low income
can resolve spontaneously in immunocompetent individuals

Question 21

Toxoplasma causative agent

Answer 21

Toxoplasma gondii

obligate intracellular parasite
tachyzoites (aggressive trophozoites)
round oocysts

Question 22

Toxoplasma life cycle

Answer 22

ENTERO-ENTERIC PHASE
oocytes with sporozoites enter host (cat) -> sporozoites infect enterocytes -> multiply and form oocysts -> poop out oocysts w/ sporo -> infect other host -> macrophages pick up oocysts -> multiply as tachyzoites -> tachyzoites infect nucleated cells (neural/muscular) -> tachyzoites become bradyzoites -> immune response -> bradyzoites form cysts -> ingestion of dead 2º host

HUMAN PHASE
human ingest oocysts from cat poop/blood transfusion -> infection of brain, muscle, eyes, heart

Question 23

Toxoplasma symptoms

Answer 23

Immunocompetent: self-limiting, lymphadenopathy, fever/flu

Immunocompromised: encephalitis, seizures, mental status change, CNS mass lesion, <100 CD4
pneumonitis jiroveci (dry cough, fever, dyspnea)

Question 24

Toxoplasma pathogenesis and immunology

Answer 24

virulence factors: rhoptry neck proteins (RONs) open cell membrane, rhoptry-derives serine-threonine kinases (ROPs) evades immune response

parasitophorous vacuole: envelops parasite

IL12 (from enterocytes): activates t cell mediated IFNy dependent macrophage activation
HIV patients have low T cell count = no response

Question 25

Congenital toxoplasmosis

Answer 25

transplacental infections increase risk of infection in later pregnancy higher fatality in early pregnancy infections Triad: chorioretinitis, hydrocephalus, intracerebral calcifications

Question 26

Toxoplasma diagnosis

Answer 26

biopsy (blood, bronchoalveolar lavage, lymph node, amniotic fluid) PCR, ELISA fundoscopy MRI/UTS

Question 27

Toxoplasma treatment and prevention

Answer 27

pyrimethamine + sulfadiazine + leucovorin pyrimethamine + clindamycin + leucovorin Leucovorin: counter effects of sulfadiazine (inhibits folic acid synthesis) and pyrimethamine (teratogen) Ocular toxoplasmosis: pyrimethamine + sulfadiazine, coritcosteroids Congenital toxoplasmosis: pyrimethamine + sulfadiazine, spiramycin

Question 28

Toxoplasma prevention and control

Answer 28

public health: regulation of cats, water filtration and purification, awareness pregnancy: avoid cats, raw meat, gardening/soil cats: keep cats indoors, no raw meat, clean litter boxes