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Microbiology > Parasites/helminths > Flashcards

Parasites/helminths Flashcards

1
Q

Giardias Etiology

A

G.lamblia

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2
Q

Giardias reservoir

A

beavers, dogs, cats, primates.

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3
Q

Giardias epidemiology

A

Common in children. Highly contagious. June-october. Common in the rocky mountains. Communicable as an STI.

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4
Q

Giardias Life cycle

A

Ingestion of cyst. Excystation in stomach. trophozoites pass to small bowel. Trophozoites encyst in the large bowel and then the cysts are excreted.

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5
Q

Giardias Symptoms

A

Intermittent episodes of watery diarrhea (no blood), cramps, abdominal distension, anorexia (malabsorption), vitamin B12 deficiency.

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6
Q

Giardias Diagnosis

A

O/P examination of multiple stool samples. ELISA for GSA65.

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7
Q

Giardias treatment

A

metronidazole.

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8
Q

Amebiasis etiology

A

Entamoeba Histolytica

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9
Q

Giardias trophozoites

A

exist freely in the intestine. bilobed adhesive disc with flagella and 2 nuclei. Feeds on the mucous and flattens the villi.

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10
Q

Giardias Cysts

A

Passed into the environment. Hyaline wall with 4 nuclei.

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11
Q

Amebiasis trophozoite

A

1 nucleus, non-flagellated, pseudopod, invasive and pathogenic.

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12
Q

Amebiasis Cysts

A

round with 4 nuclei. infectious.

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13
Q

Amebiasis Life cycle

A

ingestion of cysts. excystation in the colon. Highly motile. colonizes colon mucosa. encyst and are passed into the environment or invade the mucose to enter the blood stream and disseminate.

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14
Q

Amebiasis Epidemiology

A

Common in tropical/subtropical areas.

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15
Q

Amebiasis symptoms

A

Can range from asymptomatic to dysentery to extraintestinal manifestions. Acute amoebic colitis: cramps, tenderness, bloody stools, fever, vomiting, weight loss. Ulcers and right upper quadrant pain.

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16
Q

Amebiasis Mortality causes

A

peritonitis, cardiac failure and exhaustion

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17
Q

Amebiasis Lectin

A

adhesion

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18
Q

Amebiasis Phospholipases

A

Disrupt the cell membrane.

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19
Q

Amebiasis amebapore

A

peptide released that inserts ion channels into the host lipid structure causing lysis.

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20
Q

Amebiasis cyestein proteases

A

degrade mucus, antibodies, complement and cellular matrix.

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21
Q

Amebiasis Diagnosis

A

ELISA; differentiates between E. hystolitica and E. dispar (Commensal). Radiology will detect ascesses extraintestinal.

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22
Q

Amebiasis Treatment

A

Metronidazole and surgery for large abcesses.

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23
Q

Cryptosproridiosis etiology

A

Cryptosporidium hominis (humans) and C. parvum (bovine and human).

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24
Q

Cryptosproridiosis Oocyst

A

Infectious. Contains 4 sporozoites.

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25
Q

Cryptosproridiosis Sporozoites

A

motile. bind receptors on the surface of intestinal epithelium. Ingested into parasitophorous vacuole (near surface but still separated from the cytoplasm).

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26
Q

Cryptosproridiosis life cycle

A

Asexual and sexual reproduction inside the host

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27
Q

Cryptosproridiosis thin oocyst

A

Asexual. reinfect the host.

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28
Q

Cryptosproridiosis thick oocyst

A

Sexual. Shed into the environment. Highly infectious immediately after being released. Shedding can continue for weeks after the patient improves.

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29
Q

Cryptosproridiosis epidemiology

A

Person-to-person. Resistant to chlorine. Commonly associated with AIDS.

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30
Q

Cryptosproridiosis symptoms

A

watery (not bloody) diarrhea, dehydration, weight loss, fever, abdominal pain. Lasts for 2 weeks.

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31
Q

Cryptosproridiosis Diagnosis

A

Isolate oocysts from the stool (zinc sulfate centrifugal flotation) then use immunoflourescence or ELISA.

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32
Q

Cryptosproridiosis treatment

A

nitazoxanide or paroromycin.

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33
Q

Cyclosporiasis etiology

A

cyclospora cayetanensis

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34
Q

Cyclosporiasis epidemiology

A

common in latin america. contaminated water and imported food. Resistant to chlorine.

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35
Q

Cyclosporiasis description

A

Large oocyst that is autofluorescent. Acid-fast.

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36
Q

Cyclosporiasis life cycle

A

oocysts are shed in the feces and must sporulate in the environment which can take days to become infectious.

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37
Q

Cyclosporiasis symptoms

A

Low grade fever, chills, cramps, nausea, vomiting, explosive (not bloody) diarrhea, rapid weight loss, profound fatigue.

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38
Q

Cyclosporiasis treatment

A

bactrim.

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39
Q

Blastocystis hominis description

A

polymorphic. large central vacuole with multiple nuclei around the rin.

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40
Q

Blastocystis hominis epidemiology

A

comes from animal feces.

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41
Q

Blastocystis hominis treatment

A

metronidazole

42
Q

balantidium coli description

A

Large microbe with a macronucleus and cilia.

43
Q

balantidium coli epidemiology

A

zoonotic. Pigs.

44
Q

balantidium coli complications

A

Gut perforation.

45
Q

balantidium coli treatment

A

metronidazole or tetracycline.

46
Q

Nematodes (roundworms) Morphology

A

elongated cylindrical body that tapers at the ends. covered with multi-layered cuticle. Presence of seperate sexes.

47
Q

Enterobius vermicularis classification

A

“pinworm.” Nematode (roundworm). Causes enterobiasis. Most common helminth infection.

48
Q

Enterobius vermicularis description

A

small (8-12mm) white worms.

49
Q

Enterobius vermicularis epidemiology

A

person-to-person transmission or through the environment. Common in cosmopolitan and temperate regions. common in children.

50
Q

Enterobius vermicularis life cycle

A

eggs are deposited in the perianal region. ingested (self-infection or transmission). larvae hatch in the small intestine. adults mature in the colon (2 months). gravid females migrate to the perianal region at night and deposit the eggs. eggs become infectious in 4-6 hours.

51
Q

Enterobius vermicularis symptoms

A

perianal itching. secondary infections, sleep distrubance, abdominal pain.

52
Q

Enterobius vermicularis Diagnosis

A

cellophane tape method. Take sample first thing in the morning or at night for three consecutive days. Also sample under the fingernails. Microscopic analysis.

53
Q

Enterobius vermicularis Treatment

A

mebendazole or albendazole for all members of the household.

54
Q

Ascaris lumbricoides classification

A

Largest intestinal nematode.

55
Q

Ascaris lumbricoides epidemiology

A

transmission via contaminated soil. common in children. world wide distribution especially in warm climates.

56
Q

Ascaris lumbricoides life cycle

A

eggs are ingested. larvae are released in the duodenum. larvae penetrate the mucosa. travel to the lungs. oropharynx. swallowed. mature in the duodenum. Can live for 2 years. Release 200,000 eggs/day.

57
Q

Ascaris lumbricoides presentation

A

asymptomatic. high worm load: blockages, loeffler’s syndrome (eosinophil accumulation in the lungs), abdominal pain.

58
Q

Ascaris lumbricoides diagnosis

A

detection of eggs in a stool sample.

59
Q

Ascaris lumbricoides treatment

A

mebendazole or albendazole.

60
Q

Trichus trichiura classification

A

Nematode (roundworm). “whipworm”

61
Q

Trichus trichiura description

A

small (40mm) with whiplike morphology. Have eggs with capsules tapered at the ends.

62
Q

Trichus trichiura epidemiology

A

contaminated soil. common in children. world wide distribution.

63
Q

Trichus trichiura life cycle

A

eggs are ingested. larvae are released in the duodenum. mature in the colon. release the eggs in feces.

64
Q

Trichus trichiura presentation.

A

asymptomatic. high worm load: frequent, painful passoage of stool with mucus, blood and water. rectal prolapse. growth retardation and anemia.

65
Q

Trichus trichiura diagnosis

A

presence of eggs in stool sample.

66
Q

Trichus trichiura treatment

A

albendazole or mebendazole.

67
Q

Hookworm classification

A

nematode (roundworm)

68
Q

Hookworm etiology

A

Necator americanus and ancylostoma duoddenale.

69
Q

Hookworm description

A

small (12mm) feed on blood from the intestinal mucosa.

70
Q

Hookworm epidemiology

A

inadequate disposal of feces leads to contaminated soil. Larvae can penetrate the skin.

71
Q

Hookworm life cycle

A

eggs hatch in soil. Larvae (filiform) penetrate the skin. travel to the lungs. oropharynx. swallowed. mature in the duodenum. eggs are excreted into the soil.

72
Q

Hookworm presentation

A

blood-filled pruritic lesion at the site of penetration (ground itch). Anemia due to continual blood loss.

73
Q

Hookworm diagnosis

A

presence of eggs in the stool

74
Q

Hookworm treatment

A

mebendazole.

75
Q

Strongyloides stercoralis classification

A

nematode (roundworm) “threadworms” small (12mm).

76
Q

Strongyloides stercoralis epidemiology

A

tropical/subtropical areas. related to poor sanitation.

77
Q

Strongyloides stercoralis life cycle

A

larvae penetrate the skin. travel to lungs. oropharynx. swallowed. mature in the mucosa of the duodenum. larvae are released in the feces. free living multiplication cycle in the soil.

78
Q

Strongyloides stercoralis presentations

A

diarrhea, abdominal pain, constipation, malabsorption, signs of larval migration. Autoinfection can result in chronic infections. Life threatening in patients with defect in cell mediated immunity.

79
Q

Strongyloides stercoralis diagnosis

A

presence of larvae in the stool, duodenal aspirate or sputum in hyperinfected person.

80
Q

Strongyloides stercoralis treatment

A

thiabendazole.

81
Q

Trematodes (flukes) morphology

A

flattened, leaf-like, suckers, hermaphroditic. 2 intermediate hosts and 1 definitive.

82
Q

Clonorchis sinensis classification

A

Trematode (fluke). “chinese liver fluke” small (20mm).

83
Q

Clonorchis sinensis epidemiology

A

far east. transmission occurs via ingestion of larvae in raw fish.

84
Q

Clonorchis sinensis life cycle

A

fish containing encysted larvae is ingested. excytation occurs in the duodenum. larvae go into the biliary duct. mature. eggs are released. eaten by aquatic snails. larvae (cercariae) are released. cercariae encyst under the scales or flesh of a fish.

85
Q

Clonorchis sinensis presentation

A

usually asymptomatic unless it becomes chronic.

86
Q

Clonorchis sinensis diagnosis

A

presence of eggs in stool sample with a geographic history

87
Q

Clonorchis sinensis treatment

A

praziquantel

88
Q

Tapeworm classification

A

trematode (fluke). Taeniasis.

89
Q

Tapeworm etiology

A

taenia solium (pork) and taenia saginata (beef)

90
Q

Tapeworm description

A

large (3-9m). with scolex head structure. eggs are released in proglottids and are immediately contagious.

91
Q

Tapeworm epidemiology

A

humans. world wide distribution.

92
Q

Tapeworm life cycle

A

eggs are ingested by pigs or cows. hatch in the duodenum. larvae penetrate the cell wall. larvae (cysticerci) develop in the muscle. Human ingests poorly cooked meat. matures into a tapeworm in the jejunum. proglottids are released in the feces

93
Q

cysticercosis

A

T. solium can develop cysticercosis in humans if infective eggs are ingested.

94
Q

Tapeworm presentation

A

usually asymptomatic with one worm. may have mild GI symptoms. Cysticercosis can cause blindness or seizures depending on where the worm goes.

95
Q

Tapeworm diagnosis

A

eggs/proglorrids in the stool sample. Cysticrosis shows lesions on CT scan with histological demonstration to confirm.

96
Q

Tapeworm treatment

A

praziquantel

97
Q

Diphyllobothrium latum classification

A

trematode (fluke). “fish tapeworm”. eggs are released singly not in proglottids.

98
Q

Diphyllobothrium latum epidemiology

A

widespread from alaska to the great lakes.

99
Q

Diphyllobothrium latum life cycle

A

larvae in the muscle of fish. ingested. larvae are released in the duodenum. mature in the jejunum. eggs are released in the feces. hatch in fresh water. work the way up the food chain.

100
Q

Diphyllobothrium latum presentation

A

asymptomatic. Worm competes for B12 so anemia.

101
Q

Diphyllobothrium latum diagnosis

A

presence of eggs in the stool ID of the adult worm.

102
Q

Diphyllobothrium latum treatment

A

praziquantel

Microbiology (4 decks)

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