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Pathology: Infectious disease section > Parasites II: helminths and Vermin > Flashcards

Parasites II: helminths and Vermin Flashcards

1
Q

what is the tissue response

A

eosinophilia

  • IgE, mast cells
  • eosinophils chemotactic factors
  • IL-4 and IL-5
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2
Q

most important fatal helminth disease in humans

A

schistosomiasis

  • S. mansoni: latin america, Africa, Middle east
  • S. japonicum: Asia
  • S. haematobium: Africa
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3
Q

death usually results from what for schistosomiasis

A

hepatic granulomas and fibrosis

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4
Q

special difference with S. haematobium

A

hematuria and obstruction of bladder

-predisposes to squamous cell carcinoma of bladder

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5
Q

Life cycle of schistosomiasis

A
  • sporocytes in fresh water snails
  • ceraria infect humans by penetrating through skin
  • migrate in peripheral vasculature to portal and pelvic venous system where they develop into adult worms
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6
Q

what is reaction of body to egg formation?

A

granulomas and fibrosis

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7
Q

where do eggs shed for schistosomiasis?

A

shed in feces

-complete life cycle when hatch in water

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8
Q

pathogenesis of schistosomiasis

A

hepatic damage is due to toxic products and cell-mediated immunity

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9
Q

induction of what factors cause induction of IgE

A

IL-3, 4,5

  • induction of IgE synthesis, mastocytosis, and eosinophils
  • resistance to reinfection-> IgE levels
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10
Q

what do eggs from schistosomiasis induce?

A

lymphocytes to secrete fibrogenic factors with fibroblast proliferation and portal fibrosis

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11
Q

hallmark of schistosomiasis

A

hepatic fibrosis out of proportion to the parasite injury

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12
Q

schistosomiasis granuloma

A
  • calcified pinhead granulomas form around the egg

- include macrophages, lymphocytes, neutrophils and eosinophils

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13
Q

how do these granulomas cause portal hypertension?

A

pipestem portal fibrosis results in portal hypertension, splenomegaly, esophageal varices and ascites

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14
Q

which schistosomiasis associated with bladder cancer

A

S. Haematobium

-squamous cell carcinoma of bladder

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15
Q

Liver flukes

A

Clonorchis siensis

  • infected by eating improperly cooked fish
  • live in biliary ducts
  • usually asymptomatic
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16
Q

what can liver flukes result in

A

biliary hyperplasia, fibrosis, portal cirrhosis

-chronic infection-> cholangitis, cholelithiasis, pancreatitis, cholangiocarcinoma

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17
Q

tapeworms

A

Taenia saginata-> beef tape worm

taenia solium-> pork tapeworm

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18
Q

Taenia saginata

A

ingestion of undercooked beef

-NO cysticercosus (but does cause it in pig)

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19
Q

taenia solium

A

ingestion of undercooked pork with encysted cysticerci

-attach to intestinal wall with scolices, proglottids with eggs shed in feces

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20
Q

cysticercosus

A

T. solium eggs ingested-> larvae hatch-> penetrate gut wall

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21
Q

how to T. solium cysts get into CNS?

A

hematogenous dissemination

-convulsions, increased intracranial pressure, mental disturbances

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22
Q

what kind of cyst cause a host reaction in T. solium cysticercosus

A

degeneration cysts result in local inflammation and focal scarring, calcifications

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23
Q

Echinococcus

A

E. granulosus

E. multilocularis

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24
Q

E. granulosus

E. multilocularis

A

canine tapeworms

  • ingestion of eggs from infected animals
  • asymptomatic and chronic
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25
Q

E. granulosus

A

southwest US

  • hydatid cysts may result in an anaphylactic reaction if the cysts ruptures
  • DO NOT spill contents of cysts
26
Q

E. multilocularis

A

northern US and Canada

-liver disease, usually fatal

27
Q

where do Echinococcus cysts most commonly found?

A

hydatid cysts most commonly in liver and lungs

28
Q

Enterobius vermicularis

A

pinworms

  • most common in US
  • worm of intestine
  • spread by oral ingestion of eggs extruded from anus
  • anal puritis
  • lifespan: 2 months
29
Q

Trichuris trichiura

A

whipworms

  • common in tropics
  • warm, moist areas of southern US
  • symptoms depend on wormload, local hyperemia, lesions of colonic mucosa
  • NOT invasive
30
Q

Necator Americans/Ancylostoma duodenale

A

hookworms

  • attach to upper levels of small intestine
  • transmitted by infectious larvae, not eggs
  • larvae penetrate between toes
  • dissemination follows a route similar to ascaris
31
Q

dissemination of ascaris, hookworms, and stronglyoides

A

ingestions of eggs-> bloodstream-> lungs-> invasion by filariform larvae-> esophagus-> adult forms reside in intestines

32
Q

hookworm pathology

A

small, itchy papule where they penetrate the skin

  • mild pneumonitis may result from traveling thru the lungs
  • most significant symptoms and signs occur from ingestion of blood of host leading to blood loss (.2ml/worm/day)
33
Q

strongyloides stercoralis

A
  • distribution parallels hookworms, similar life cycle
  • entry of filaria through skin
  • Appalachia, SE US
  • cat/dogs as reservoirs
34
Q

manifestations of strongyloides stercoralis

A

usually mild

-in IC’s, hyperinfection may result with severe penumonitis and duodenitis

35
Q

most common parasite of humans after pinworms

A

Ascaris lumbricoides

36
Q

Ascaris lumbricoides

A

tropics and subtropics

  • large worms
  • live unattached in lumen of small intestine
37
Q

signs and symptoms of Ascaris lumbricoides

A

eosinophilic pneumonitis of lung including dyspnea, dry cough, fever, eosinophilia

  • colicky epigastric or periumbilical pain
  • malnutrition
38
Q

greatest danger related to Ascaris lumbricoides

A

results from abdominal migration in body including blockage of biliary ducts
-obstruction of small intestine may also occur

39
Q

small intestine parasites

A

giardia
hookworm
stryongyloides
ascaris

40
Q

Trichinella spiralis

A
  • ingestion of improperly cooked pork
  • larvae penetrate tissue-> disseminate hematogenously-> encyst in muscle cells
  • muscle cells involved: diaphragm, EOM, laryngeal, deltoid, gastrocnemius, intercostal muscles
  • eosinophilia, fever, myalgias, periorbital edema
41
Q

how does Trichinella spiralis cause eosinophilic infiltrate in lungs?

A

trapped larvae in lungs

42
Q

how can Trichinella spiralis cause heart failure

A

patchy interstitial myocarditis with eosinophilia and giant cells resulting in scarring, heart failure

43
Q

Larval Migrans syndromes (LMS)

A
  • zoonotic disease: nonhuman hookworms cannot complete life cycle in humans
  • LMS: intense eosinophilic inflammatory reaction by host
  • treatment: decrease inflammatory reaction: steroids and antihistamines
44
Q

cutaneous larval migrans

A

Ancylostoma

  • creeping eruption: associated with hookworms of dog, cat
  • causes intensely pruritis skin lesions
  • plumbers, construction workers, duck hunters, others exposed to infected soil
45
Q

visceral larval migrans

A

Toxocara canis, T. cati

  • dog/cats infected-> dissemination through body
  • usually S-L
  • puppies-> give to children
  • hepatomegaly, hypereosinophilia, hypergammaglobulinemia, history of geophagia
46
Q

neural larval migrans

A

Balisascaris

  • -wildlife
  • infections of raccoons
  • children of poor hygiene and geophagia
  • disease depends on # of organisms and re-infections
  • CNS disease: results in eosinophilic meningoencephalitis
  • larvae not lost in stools, diagnosis by tissue
47
Q

lymphatic filariasis

A

wuchereria bancrofti

  • subSaharan africa, L.A. and SE asia
  • mosquitos
  • larvae develop in lymphatic channels-> chronic damage to lymphatics (T cell mediated)-> granulomas around adult parasites
  • can result in lymphatic dilatation and lymphedema is terms elephantiasis when in lower limb
  • scrotum, penis, vulva, leg or arm
48
Q

Filariasis

A
  • infected larvae transmitted by infected biting arthropods during blood meal
  • larvae migrate to appropriate site of host’s body-> develop into micro-filariae producing adults
  • adults dwell in various human tissue-> can live there for several years
  • microfilariae infect biting arthropods
49
Q

river blindness

A

onchocerca volvulus

  • filarial nematode: transmitted by blackflies
  • MAJOR cause of blindness in Africa: punctate keraitis, damage to retinal (cross reaction between parasite antigen and retinal pigment epithelial cells)
  • chronic pruritic dermatitis, sub, cut. dermal nodules (onchocercoma)
50
Q

head lice

A

pediculus humanus capitis

51
Q

body lice

A

pediculus humanus humanus

52
Q

crab louse

A

Pthirus pubis

53
Q

scabies

A

sarcoptes scabei

54
Q

chiggers

A

larvae of prostigmata (mites)

55
Q

Fleas

A

human (Pulex irritans) or rat (xenopsylla cheopis)

56
Q

body lice and head lice vectors for

A

louse borne typhus: rickettsia prowazeki
trench fever: rochalimaea quintana
louse-borne relapsing fever: Borrellia recurrentis

57
Q

crab louse characteristics

A

STD
Blue spots
-.2-.3 cm in diameter, irregular outline, painless, do not disappear on pressure, deeper tissue
-appear after hours after crab lice has bitten and last for days
-poisonous saliva injected by crab louse (similar to melanoderma caused by body louse)

58
Q

scabies characteristics

A

close contact spread

  • burrow in skin but never beyond stratum corneum
  • intense pruritic lesions: mediated by IgE, mast cells, E
  • re-occur every 28 days after locally laid eggs hatch
  • other races cause in animals: just itchy in humans
59
Q

chigger bites

A

(mites)

  • take up residence in hair follicles
  • inject digestive enzymes that rupture cells, causing an intense local inflammatory response
60
Q

rhinosporidiosis

A

Mesomycetozoea

  • aquatic protistan
  • india, Sri. Lanka, Texas, SW US
  • traumatic inoculation of organism from water source
  • causes granulomatous of mucous membranes resulting in polyp formation
  • infections of nose, nasopharynx, conjunctiva

Pathology: Infectious disease section (11 decks)

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