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helminths topics Flashcards

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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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IV. 27 Echinococcus multilocularis ddx
CT/MRI | ELISA
26
IV. 27 Echinococcus multilocularis treatment
Surgery, chemotherapy | Benzimidazole
27
IV. 28 Fasciola Hepatica characteristics
Sheep liver fluke, high prevalence in Europe and south America Definitive host: sheep, cattle, humans Intermediate host: snails
28
IV. 28 Fasciola Hepatica organs affected
Biliary ducts | liver
29
IV. 28 Fasciola Hepatica pathogenesis
Consumption of larvae → Encystation in duodenum → Liver (maturation, necrosis of liver) → egg in bile duct → pass out with feces
30
IV. 28 Fasciola Hepatica clinical
Fever, severe eosinophilia, hepatosplenomegaly, bile duct obstruction
31
IV. 28 Fasciola Hepatica ddx
Eggs in feces
32
IV. 28 Fasciola Hepatica treatment
Triclabendazole | Bithionol
33
IV. 29 Paragonimus westermani characteristics
Lung fluke, high prevalence in Asia Source of infection: eating undercooked freshwater crabs or crayfish (larvae)
34
IV. 29 Paragonimus westermani pathogenesis
Fluke develops in stomach → migration via intestinal wall → through diaphragm → pleural cavity where the adults lay eggs in lungs
35
IV. 29 Paragonimus westermani clincal
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)
36
IV. 29 Paragonimus westermani ddx
Eggs in feces/sputum
37
IV. 29 Paragonimus westermani treatment
Praziquantel + bithionol
38
IV. 30 Schistosomes characteristics
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
39
IV. 30 Schistosomes life cycle
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
IV. 30 Schistosomes clinical
Hepatosplenic schistosomiasis ~ Results from eggs embolization in hepatic venules ~ Formation of granulomas and portal fibrosis ~ Hepatosplenomegaly and hepatic insufficiency
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IV. 30 Schistosomes ddx
serology
42
IV. 30 Schistosomes treatment
Praziquantel
43
IV. 30 Schistosomes manosoni
S. mansoni → female lays eggs ~ 300 eggs/day → Africa Adult Schistosomes live in pairs in the portal system and in the mesenteric venules
44
IV. 30 Schistosomes japonicum
S. japonicum → Female lays eggs ~ 2000 eggs/day → Southeast Asia S. mansoni → female lays eggs ~ 300 eggs/day → Africa
45
IV. 30 Schistosomes hematobium characteristics
Female lays ~ 150 eggs/day Adult schistosomes lives in pairs in pelvic veins (especially in venous plexus around urinary bladder)
46
IV. 30 Schistosomes hematobium clinical
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
IV. 30 Schistosomes hematobium ddx
Eggs in urinary sediment ~ motility Eggs in feces ELISA, IF, RIA
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IV. 30 Schistosomes hematobium treatment
Praziquantel
49
IV. 31 Ancylostoma dudenale and Necator americanus charcteristics
Intestinal nematodes Hookworm A. duodenale ~ old world hookworm A. braziliense N. americanus ~ new world hookworm
50
IV. 31 Ancylostoma dudenale and Necator americanus pathogenesis
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
IV. 31 Ancylostoma dudenale and Necator americanus clinical
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
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IV. 31 Ancylostoma dudenale and Necator americanus ddx
Larvae in feces
53
IV. 31 Ancylostoma dudenale and Necator americanus treatment
Mebendazole/albendazole | Iron supplement
54
IV. 32 Toxocara canis Toxocara cait characteristics
Geohelminths = Toxocara (cati, canis) ~ nematode
55
IV. 32 Toxocara canis Toxocara cait pathogenesis
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
IV. 32 Toxocara canis Toxocara cait ddx
Larvae in tissue (~10cm) ELISA – serology No adult worms in human
57
IV. 32 Toxocara canis Toxocara cait treatment
Albendazole
58
IV. 32 Toxocara canis Toxocara cait clinical
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
IV. 33 Trichinella spiralis characteristics
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
IV. 33 Trichinella spiralis pathogenesis
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
IV. 33 Trichinella spiralis clinical
Trichinellosis Larvae encyst in striated muscle, causing inflammation, pain, myalgia, acute enteritis, fever, periorbital edema
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IV. 33 Trichinella spiralis ddx
Larvae in muscle biopsy | Serology – ELISA
63
IV. 33 Trichinella spiralis treatment
Mebendazole | albendazole
64
IV. 34 Enterobius vermicularis characteristics
Nematode | Pinworm – male: 2-5mm, female: 10-13mm
65
IV. 34 Enterobius vermicularis pathogenesis
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
IV. 34 Enterobius vermicularis clinical
Perianal prurutis
67
IV. 34 Enterobius vermicularis ddx
Eggs in perianal region – scotch tape smear used to see larva in eggs. *made in the morning before defecation/bathing
68
IV. 34 Enterobius vermicularis treatment
Mebendazole
69
IV. 35 Acaris lumbricoides characteristics
nematodes Geohelminth Most common and largest roundworm: males: 15-20 cm, female: 20-35cm
70
IV. 35 Acaris lumbricoides pathogenesis
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
IV. 35 Acaris lumbricoides clinical
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)
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IV. 35 Acaris lumbricoides ddx
Eggs in feces
73
IV. 35 Acaris lumbricoides treatment
Mebendazole
74
IV. 35 Trichuris trichuria characteristics
Geohelminth | Whipworm: males: 30-45mm, female: 35-50mm
75
IV. 35 Trichuris trichuria pathogenesis
1) Entry through mouth: eggs contain larvae | 2) Hatch in small intestine, migrate and mature in cecum, appendix, colon
76
IV. 35 Trichuris trichuria clinical
Mucosal damage, abdominal pain, bloody stool (anemia), appendicitis, rectal prolapse
77
IV. 35 Trichuris trichuria ddx
Eggs in feces (lemon-shaped)
78
IV. 35 Trichuris trichuria treatment
Mebendazole
79
IV 36. Strongyloides stercoralis characteristics
Geohelminth Rhabditiform larvae = non-infective Filariform larvae = infective
80
IV 36. Strongyloides stercoralis clinical
Abdominal pain, nausea, vomiting, diarrhea, paralytic ileus, hepatitis
81
IV 36. Strongyloides stercoralis ddx
Rhabditiform larvae in stool Hypereosinophilia Antibody detection Immunologic diagnosis by IF
82
IV 36. Strongyloides stercoralis treatment
Thiabendazole and ivermectine
83
IV. 36 Dirofilaria repens characteristics
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
IV. 37 Worms causing filariasis - Lymphatic filariasis characteristics
Wucheria bancrofti: mosquitos of genus culex, anopheles, aedes Brugia malayi: mosquitos of genus mansonia, anopheles, aedes
85
IV. 37 Worms causing filariasis - Lymphatic filariasis pathogenesis
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
IV. 37 Worms causing filariasis - Lymphatic filariasis ddx
Detection of microfilaria in blood smear (at night) ~ mosquito activity
87
IV. 37 Worms causing filariasis - Lymphatic filariasis treatment
Diethylcarbamazine (DEC) and Ivermectin Spraying for mosquitos, nets etc.
88
IV. 37 Worms causing filariasis - Loaisis - Loa Loa characteristics
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
IV. 37 Worms causing filariasis - Loaisis - Loa Loa ddx
Detection of microfilaria in blood smear ~ 3-7cm
90
IV. 37 Worms causing filariasis - Loaisis - Loa Loa treatment
Diethylcarbamazine ~ for 10 years Corticosteroids for allergic reaction Surgery of the eye
91
IV. 37 Worms causing filariasis - Onchocera volvulus pathogenesis
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
IV. 37 Worms causing filariasis - Onchocera volvulus ddx
Examination of blood free skin nips
93
IV. 37 Worms causing filariasis - Onchocera volvulus treatment
Ivermectin, surgical removal of skin nodule
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IV. 37 Worms causing filariasis - Onchocera volvulus clinical
River blindness: due to hyperpigmentation and scarring of cornea Skin lesions: pruritic dermatitis (elephant skin), depigmentation, loss of elasticity, subcutaneous nodules
95
IV. 37 Worms causing filariasis - Dracunculus medinensis pathogenesis
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
IV. 37 Worms causing filariasis - Dracunculus medinensis ddx
Female emerges from ulcer
97
IV. 37 Worms causing filariasis - Dracunculus medinensis treatment
Slowly wrapping the worm on a stick

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