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helminths topics Flashcards

1
Q

IV. 24 Taenia saginata characteristics

A

Aka. Beef tapeworm
Cestode (tapeworm)

Intermediate host: cattle

Definite host: human

Transmitted via undercooked beef – cysterici are ingested 12m, 1-2mm in diameter with 4 suckers

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2
Q

IV. 24 Taenia saginata life cycle

A

Mature proglottidis give off eggs → cyst formation (cysticercosis) in intermediate host (i.e. cows) → Humans infected by eating meat → SI maturation → enteral taeniasis

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3
Q

IV. 24 Taenia saginata ddx

A

Proglottis or eggs in stool – eggs (thick double wall) only detect taenia genus, proglottis can differentiate spp

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4
Q

IV. 24 Taenia saginata treatment

A

Niclosamide and mebendazole

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5
Q

IV. 25 Taenia solium characteristics

A

Aka. Pork tapeworm

Intermediate host: Pigs

Definite host: Humans

Accidental intermediate host: Human (cysticercosis) ONLY SOLIUM

Transmitted via undercooked pork – cysticerci are ingested (eggs are transmitted via contaminated water) 6m, has rostellum with hooklets

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6
Q

IV. 25 Taenia solium life cycle

A

Mature proglottids give off eggs → cyst formation (cysticercosis) in intermediate host (i.e. cows) → Humans infected by eating meat → SI maturation → enteral taeniasis

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7
Q

IV. 25 Taenia solium clinical

A

~ Subcutaneous cysticerosis
~ Cerebral cysticerosis
~ Enteral taeniasis

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8
Q

IV. 25 Taenia solium ddx

A

Proglottids in stool
Cysts in tissue on CT scan
Serology – Ag detection of CSF by ELISA

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9
Q

IV. 25 Taenia solium treatment

A

Praziquantel
Niclosamide
+ corticosteroids and surgery

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10
Q

IV. 26 Diphyllobothrium latum characteristics

A

Aka. Fish tapeworm → largest tapeworm Definite host: humans

Reservoir: bears, other mammals Intermediate host: Fish

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11
Q

IV. 26 Diphyllobothrium latum pathogenesis

A

Humans infected by eating fish containing larvae, small intestinal maturation

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12
Q

IV. 26 Diphyllobothrium latum clinical

A

Abdominal pain with nausea and diarrhea, pernicious anemia due to B12 requirement of the parasite

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13
Q

IV. 26 Diphyllobothrium latum ddx

A

Finding eggs in stool

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14
Q

IV. 26 Diphyllobothrium latum treatment

A

Praziquantel

Niclosamide

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15
Q

IV. 26 Hymenolepis nana charcteristics

A

Dwarf tapeworm, 1-3 cm

Most prevalent in conditions of poor sanitation, and is endemic in tropical regions = hymenolepiasis

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16
Q

IV. 26 Hymenolepis nana pathogenesis

A

Swallowed eggs → SI maturation → developing helminths * some eggs pass out with feces

Asymptomatic infection – diagnosis based on finding eggs in stool

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17
Q

IV. 26 Hymenolepis nana treatment

A

Praziquantel

Niclosamide

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18
Q

IV. 27 Echinococcus species characteristics

A

E. granulosus: Carnivores, domestic animals ~ dog tapeworm

E. multilocularis: Wolf, fox ~ small fox tapeworm I

ntermediate host: Herbivores (sheep, cattle)

Definite host: Dogs

Accidental, dead-end host: humans

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19
Q

IV. 27 Echinococcus granulosus life cycle

A

After ingestion of eggs, the onchospheres penetrate the intestinal wall and reach host organs ~ liver/lung

They form cyst within a week, consisting of an external acellular part, and an internal/germinal.

The larvae develop from the germinal layer

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20
Q

IV. 27 Echinococcus granulosus hydatidosis

A

Hydatid cysts in lung, liver, brain

Fluid inside cyst is toxic → anaphylactic shock, death

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21
Q

IV. 27 Echinococcus granulosus ddx

A

Presence of isolated hooklets

CT or echography

ELISA, western blot

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22
Q

IV. 27 Echinococcus granulosus treatment

A

Sugery

Albendazole

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23
Q

IV. 27 Echinococcus multilocularis life cycle

A

Adult worm in small intestine of animal (reservoir), embryonated eggs in feces of that animal → orally into human OR from cyts in intermediate host until it reaches human → The activated onchosphere penetrates the small intestine, enters blood vessels and reaches liver via portal vein.

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24
Q

IV. 27 Echinococcus multilocularis pathogenesis

A 
Alveolar echinococcosis (AE)
The liver is the organ primarily affected, but could metastasize to any organ (brain, lungs etc). 
Causes infiltatrive growth – hepatomegaly, jaundice, abdominal pain
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25
Q

IV. 27 Echinococcus multilocularis ddx

A

CT/MRI

ELISA

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26
Q

IV. 27 Echinococcus multilocularis treatment

A

Surgery, chemotherapy

Benzimidazole

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27
Q

IV. 28 Fasciola Hepatica characteristics

A

Sheep liver fluke, high prevalence in Europe and south America

Definitive host: sheep, cattle, humans

Intermediate host: snails

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28
Q

IV. 28 Fasciola Hepatica organs affected

A

Biliary ducts

liver

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29
Q

IV. 28 Fasciola Hepatica pathogenesis

A

Consumption of larvae → Encystation in duodenum → Liver (maturation, necrosis of liver) → egg in bile duct → pass out with feces

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30
Q

IV. 28 Fasciola Hepatica clinical

A

Fever, severe eosinophilia, hepatosplenomegaly, bile duct obstruction

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31
Q

IV. 28 Fasciola Hepatica ddx

A

Eggs in feces

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32
Q

IV. 28 Fasciola Hepatica treatment

A

Triclabendazole

Bithionol

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33
Q

IV. 29 Paragonimus westermani characteristics

A

Lung fluke, high prevalence in Asia

Source of infection: eating undercooked freshwater crabs or crayfish (larvae)

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34
Q

IV. 29 Paragonimus westermani pathogenesis

A

Fluke develops in stomach → migration via intestinal wall → through diaphragm → pleural cavity where the adults lay eggs in lungs

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35
Q

IV. 29 Paragonimus westermani clincal

A

Pneumonia – can be fatal due to penetration of brain, heart, spinal cord

Fever, eosinophilia, chest pain, bloody sputum, lung tissue fibrosis (night sweats, pleuritis, bronchopneumonia)

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36
Q

IV. 29 Paragonimus westermani ddx

A

Eggs in feces/sputum

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37
Q

IV. 29 Paragonimus westermani treatment

A

Praziquantel + bithionol

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38
Q

IV. 30 Schistosomes characteristics

A

Only fluke with separate sexes

S. hematobium → IM hosts are snails (Bulinus) – urinary tract

S. mansoni → IM hosts are snails (biomphalaria) – GI

S. japonicum → IM hosts are snails (onchomelania) – GI

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39
Q

IV. 30 Schistosomes life cycle

A

1) Eggs hatch in water, releasing miracidia
2) Miracidia penetrate snail tissue and form sporocysts

3) Cercariae (infective form larvae) released
by snails, these are free-swimming

4) Cercariae penetrate human skin, loose tails and becomes schistosomulae
5) Blood stream → Liver: maturation
6) Migration to large intestine or venous plexus of urinary bladder

40
Q

IV. 30 Schistosomes clinical

A

Hepatosplenic schistosomiasis

~ Results from eggs embolization in hepatic venules

~ Formation of granulomas and portal fibrosis

~ Hepatosplenomegaly and hepatic insufficiency

41
Q

IV. 30 Schistosomes ddx

A

serology

42
Q

IV. 30 Schistosomes treatment

A

Praziquantel

43
Q

IV. 30 Schistosomes manosoni

A

S. mansoni → female lays eggs ~ 300 eggs/day → Africa

Adult Schistosomes live in pairs in the portal system and in the mesenteric venules

44
Q

IV. 30 Schistosomes japonicum

A

S. japonicum → Female lays eggs ~ 2000 eggs/day → Southeast Asia

S. mansoni → female lays eggs ~ 300 eggs/day → Africa

45
Q

IV. 30 Schistosomes hematobium characteristics

A

Female lays ~ 150 eggs/day

Adult schistosomes lives in pairs in pelvic veins (especially in venous plexus around urinary bladder)

46
Q

IV. 30 Schistosomes hematobium clinical

A

Urinary schistosomiasis

~ Eggs induce granuloma formation, bladder wall enlargement, hematuria

~ Hyperplasia of mucosa, fibrosis and calcification with polyp formation in urinary bladder and urethral stenosis

~ Hydronephrosis and cancer are late complications

~ Damage to seminal vesicles

47
Q

IV. 30 Schistosomes hematobium ddx

A

Eggs in urinary sediment ~ motility
Eggs in feces
ELISA, IF, RIA

48
Q

IV. 30 Schistosomes hematobium treatment

A

Praziquantel

49
Q

IV. 31 Ancylostoma dudenale and Necator americanus charcteristics

A

Intestinal nematodes
Hookworm

A. duodenale ~ old world hookworm
A. braziliense
N. americanus ~ new world hookworm

50
Q

IV. 31 Ancylostoma dudenale and Necator americanus pathogenesis

A

Bare foot in environment → larvae infect through skin → enter blood stream → infection of lung, pharynx, SI (cough/swallow) → sucking blood (0,3-0,9 ml/day) (A. duodenale → 0,15 ml, N. americanus → 0,03 ml)

51
Q

IV. 31 Ancylostoma dudenale and Necator americanus clinical

A

Hookworm infection
~ Live attached to mucosa of small intestine, where they feed on villous tissue

~ Hypochromic microcytic anemia (IDA)

~ Epigastric pain, hypoproteinemia, eosinophilia

Cutaneous larva migrans
~ A. braziliense

~ Intense skin scratching from dog/cat hookworm

52
Q

IV. 31 Ancylostoma dudenale and Necator americanus ddx

A

Larvae in feces

53
Q

IV. 31 Ancylostoma dudenale and Necator americanus treatment

A

Mebendazole/albendazole

Iron supplement

54
Q

IV. 32 Toxocara canis Toxocara cait characteristics

A

Geohelminths = Toxocara (cati, canis) ~ nematode

55
Q

IV. 32 Toxocara canis Toxocara cait pathogenesis

A
  1. Entry through mouth (eggs excreted by dog or cat)
  2. Larvae hatch in small intestine and penetrate mucosa
  3. Larvae enter portal system (some are trapped in liver)
  4. Larvae enter systemic circulation → dissemination (dead-end infection)
  5. Diseases depends on number of larvae ingested and the degree of the allergic response
56
Q

IV. 32 Toxocara canis Toxocara cait ddx

A

Larvae in tissue (~10cm)
ELISA – serology
No adult worms in human

57
Q

IV. 32 Toxocara canis Toxocara cait treatment

A

Albendazole

58
Q

IV. 32 Toxocara canis Toxocara cait clinical

A

Visceral larva migrans:
fever, cough, malaise, leukocytosis with hypereosinophilia, hepatomegaly, high titers of isohemagglutinins * myocarditis, encephalitis, pneumonia

Ocular larva migrans:
retinal granulomas and uveitis → blindness

59
Q

IV. 33 Trichinella spiralis characteristics

A

Nematode

Adult form lives in SI of flesh-eating mammals, i.e. pigs

Viable, encysted larvae is found in the meat (muscles of animals)

60
Q

IV. 33 Trichinella spiralis pathogenesis

A

Cycle
1) Entry by ingestion of cyst: contaminated meat

2) Excystation and maturation in SI
3) Larvae enter systemic circulation → dissemination ~ dead-end infection

61
Q

IV. 33 Trichinella spiralis clinical

A

Trichinellosis

Larvae encyst in striated muscle, causing inflammation, pain, myalgia, acute enteritis, fever, periorbital edema

62
Q

IV. 33 Trichinella spiralis ddx

A

Larvae in muscle biopsy

Serology – ELISA

63
Q

IV. 33 Trichinella spiralis treatment

A

Mebendazole

albendazole

64
Q

IV. 34 Enterobius vermicularis characteristics

A

Nematode

Pinworm – male: 2-5mm, female: 10-13mm

65
Q

IV. 34 Enterobius vermicularis pathogenesis

A

1) Entry through mouth – eggs (form environment) contain larvae
2) Eggs hatch in small intestine – migrate to large intestine and mature
3) Migrate to perianal area → lay eggs (1000/day) → perianal itch → scratch → autoinfection

66
Q

IV. 34 Enterobius vermicularis clinical

A

Perianal prurutis

67
Q

IV. 34 Enterobius vermicularis ddx

A

Eggs in perianal region – scotch tape smear used to see larva in eggs. *made in the morning before defecation/bathing

68
Q

IV. 34 Enterobius vermicularis treatment

A

Mebendazole

69
Q

IV. 35 Acaris lumbricoides characteristics

A

nematodes
Geohelminth
Most common and largest roundworm: males: 15-20 cm, female: 20-35cm

70
Q

IV. 35 Acaris lumbricoides pathogenesis

A

1) Entry through mouth, eggs containing infective larvae from soil
2) Hatch in small intestine, enter blood stream
3) Infection of lung, trachea, esophagus, small intestine

71
Q

IV. 35 Acaris lumbricoides clinical

A

Ascariasis
Larvae migrates through lung → pneumonitis
Migration into bile duct, gall bladder and liver → tissue damage

Peritonitis, abdominal pain, intestinal obstruction
* Protein deficiency (Kwashiorkor syndrome)

72
Q

IV. 35 Acaris lumbricoides ddx

A

Eggs in feces

73
Q

IV. 35 Acaris lumbricoides treatment

A

Mebendazole

74
Q

IV. 35 Trichuris trichuria characteristics

A

Geohelminth

Whipworm: males: 30-45mm, female: 35-50mm

75
Q

IV. 35 Trichuris trichuria pathogenesis

A

1) Entry through mouth: eggs contain larvae

2) Hatch in small intestine, migrate and mature in cecum, appendix, colon

76
Q

IV. 35 Trichuris trichuria clinical

A

Mucosal damage, abdominal pain, bloody stool (anemia), appendicitis, rectal prolapse

77
Q

IV. 35 Trichuris trichuria ddx

A

Eggs in feces (lemon-shaped)

78
Q

IV. 35 Trichuris trichuria treatment

A

Mebendazole

79
Q

IV 36. Strongyloides stercoralis characteristics

A

Geohelminth
Rhabditiform larvae = non-infective
Filariform larvae = infective

80
Q

IV 36. Strongyloides stercoralis clinical

A

Abdominal pain, nausea, vomiting, diarrhea, paralytic ileus, hepatitis

81
Q

IV 36. Strongyloides stercoralis ddx

A

Rhabditiform larvae in stool Hypereosinophilia
Antibody detection
Immunologic diagnosis by IF

82
Q

IV 36. Strongyloides stercoralis treatment

A

Thiabendazole and ivermectine

83
Q

IV. 36 Dirofilaria repens characteristics

A

Intermediate host: mosquito
Final host: Dogs, humans (rarely)

Larvae migrate to
~ Subcutaneous tissue → painless nodule

~ Very rarely to lungs lungs (coin-like lesion on X-ray)

~ Sometimes tissue under conjunctiva

  • Adults die before fully matured – cannot spread further
84
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis characteristics

A

Wucheria bancrofti: mosquitos of genus culex, anopheles, aedes

Brugia malayi: mosquitos of genus mansonia, anopheles, aedes

85
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis pathogenesis

A

1) Larvae enter via mosquito bite
2) Larvae mature to filaria (adult) in lymphatics and produce microfilariae which enter blood and spread
3) Disease → Adenolymphangitis, eosinophilia, Elephantiasis (LL, scrotum) *Brufia never genitals
4) Microfilariae ingested back into mosquitos

86
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis ddx

A

Detection of microfilaria in blood smear (at night) ~ mosquito activity

87
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis treatment

A

Diethylcarbamazine (DEC) and Ivermectin

Spraying for mosquitos, nets etc.

88
Q

IV. 37 Worms causing filariasis - Loaisis - Loa Loa characteristics

A

Transmitted by chrysops fly/Mango fly

After bite, the larvae travel subcutaneously where it produces microfilaria which travels through blood (most frequently to conjunctiva)

89
Q

IV. 37 Worms causing filariasis - Loaisis - Loa Loa ddx

A

Detection of microfilaria in blood smear ~ 3-7cm

90
Q

IV. 37 Worms causing filariasis - Loaisis - Loa Loa treatment

A

Diethylcarbamazine ~ for 10 years

Corticosteroids for allergic reaction
Surgery of the eye

91
Q

IV. 37 Worms causing filariasis - Onchocera volvulus pathogenesis

A

Transmitted by black fly/simulium

  1. Larvae enter via bite
  2. Larvae mature to filaria in subcutaneous nodules and produce microfilaria
  3. Microfliaria cause
  4. Microfilaria ingested back by black fly
92
Q

IV. 37 Worms causing filariasis - Onchocera volvulus ddx

A

Examination of blood free skin nips

93
Q

IV. 37 Worms causing filariasis - Onchocera volvulus treatment

A

Ivermectin, surgical removal of skin nodule

94
Q

IV. 37 Worms causing filariasis - Onchocera volvulus clinical

A

River blindness: due to hyperpigmentation and scarring of cornea

Skin lesions: pruritic dermatitis (elephant skin), depigmentation, loss of elasticity, subcutaneous nodules

95
Q

IV. 37 Worms causing filariasis - Dracunculus medinensis pathogenesis

A

Transmitted through water (copepods with larvae; intermediate host)

Copepods ingested and die in stomach

They release the larvae which penetrates the abdominal wall and mature.

Once the female matured in the abdominal cavity, it migrates to the surface of the skin (usually in lower limb) and making painful ulcers

96
Q

IV. 37 Worms causing filariasis - Dracunculus medinensis ddx

A

Female emerges from ulcer

97
Q

IV. 37 Worms causing filariasis - Dracunculus medinensis treatment

A

Slowly wrapping the worm on a stick

mrts (19 decks)

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