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Parasitology > GIT Helminths > Flashcards

GIT Helminths Flashcards

Necator americanus, Strongyloides stercolaris, Trichuris trichiura, Ascaris lumbroides, Enterobius vermicularis

1
Q

Anatomy of GIT

A 
Mouth
Oesophagus 
Stomach 
Small intestines - duodenum, jejenum
Large inestines - ascending, transverse, descending 
Rectum, anus
Liver, gall bladder, pancreas
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2
Q

Trematodes

A

Flukes

  • Classify depending on location found
  • – Blood flukes, liver flukes, lung flukes, intestinal flukes
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3
Q

Intestinal cestodes

A 
Tapeworms 
-- Species: 
Taenia solium 
T. saginata 
Diphyllobothrium 
Hymenolepis 
Dipylidium caninum 
Echinococcus 
Spirometra 
Taenia multiceps
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4
Q

Nematodes

A

Ascaris lumbricoides - ascariasis
Trichuris trichuria - whipworm - trichuriasis
Necator americanus + Ancylostoma duodenale - hookworms
Enterobius vermicularis - pinworm - entrobiasis
Strongyloides stercoralis - strongyloidiasis

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5
Q

Ascariasis - life cycle

A

Begins with eggs maturing in soil
human ingests eggs via food/drink/contaminated hands
Larvae burrow out of GI lumen into venous blood -> right heart -> lungs
Mature and live in lungs until coughed up
Then goes back to GIT

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6
Q

Why do ascaris prefer the lungs to develop?

A

Maybe higher O2 conc’n in lungs compared to GIT

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7
Q

Definitive host of acaris

A

humans; they mate there reaching final form

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8
Q

Why do they prefer hatching in soil?

A

Body temp too high

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9
Q

Risk factors - Ascariasis

A

Poor sanitation

Warm weather

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10
Q

Early illness ascariasis - symptoms due to

A
  • lung migration
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11
Q

Late illness ascariasis - symptoms due to

A
  • worm burden
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12
Q

Early infection - Eosinophils levels

A

When the body recognizes larvae moving in the blood, Eosinophilic levels rise in blood and lung tissue.

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13
Q

IgE - mediator of immune response causes what symptoms

A

–immune response causes transient cough, wheezing, chest pain, hemoptysis

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14
Q

Sputum sample

A

–Eosinophils in areas they shouldn’t be in
or
–Charcot-Leyden Crystals (sign of high burden of Eosinophils)

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15
Q

Late infection of ascaris is often asymptomatic (T/F)

A

True

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16
Q

Diagnosis of Ascariasis

A

Colonoscopy findings, feces observation (OAP)

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17
Q

Symptoms - Ascariasis

A

nausea
Abd pain
Diarrhoea

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18
Q

Ascariasis fertilized eggs distinguished from unfertilized eggs, how?

A

They are round rather than elongated and have a thicker cell wall.

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19
Q

Ascaris - fertilile egg

A

Round/ovoidal with thick shell; mammilated coat

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20
Q

Ascaris - infertile egg

A

Elongated, triangular, kidney shaped; thin shell; mammilated covering missing

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21
Q

Complications

A

Bowel blockage - heavy infection
Worms crawling to biliary tree - blocks biliary flow = biliary sepsis
Worms moving to peritoneum carrying fecal content - peritonitis

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22
Q

Treatment- Ascariasis

A

Albendazole, mebendazole, pyrantel

Surgery for obstruction

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23
Q

Trichuriasis - pathogen and egg shape

A

Trichuris trichiura

Long void, two clear bulbs on each end, football shaped

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24
Q

Trichuriasis transmission and complication

A

Soil; fecal oral

Rectal prolapse - occurs when rectum loses attachment to internal body and protrudes from anus

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25
Q

Trichuriasis pathogenesis

A
  1. eggs are ingested and travel to the intestines
  2. the larvae emerge and take up residence
  3. They become either male or female adults
  4. Adult worm resembles a bull whip - one side thick and other thin - thin side burrows into gut - fat end remains out in gut
  5. Eggs passed into stool
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26
Q

Eggs sit in soil for 3-5 wks for maturation to become fertile (T/F)

A

True

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27
Q

Risk factors and treatment - Trichuriasis

A

Poor sanitation
Warm weather to nurture eggs
-Mebendazole + Albendazole

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28
Q

Clinical presentation - Trichuriasis -Illness severity correlates with worm burden (T/F)

A

True

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29
Q

Light infection symptoms - Trichuriasis

A

-Asymptomatic

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30
Q

Moderate infection symptoms - Trichuriasis

A
  • Nausea
  • Abd pain
  • Diarrhoea
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31
Q

Heavy infection - symptoms

A
  • anemia, growth stunting, rectal prolapse (due to tenesmus-irritation of worms)
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32
Q

Host may/may not respond to infection (T/F)

A

True

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33
Q

Host may not respond to infection due to?

A

Heads of worm buried in mucosa

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34
Q

Antigen presentation occurs where?

A

Antigen persentation to gut associated lymphatic tissue (GALT)

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35
Q

Eosinophilia usually mild so immunization is unclear in Trichuriasis (T/F)

A

True

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36
Q

Life cycle - hookworms

A

Burrow into epidermis until they penetrate dermis
Move to vascular supply -> heart -> lungs
Maturation in lungs (same as ascaris)
When coughed up -> stomach -> jejunum (SI) - reproduction
Eggs must exit body to complete life cycle

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37
Q

Virulence factors - hookworms

A

Mouthparts to hold on to intestines - keeps from swept away with feces and sucks blood

38
Q

Transmission - hookworms

A

Fecal, soil, skin; not oral

39
Q

Anthroponosis in dogs

A

Related to dog hookworm

40
Q

Unholy trinity - lung issues

A
  • Overlaps Trichuris, Ascaris, hookworm
41
Q

Human hookworm

A

Necator americanus

42
Q

Risk factors - Necator

A
  • poor sanitation
  • warm weather
  • bare skin
  • Impoverished persons affected
43
Q

When does high worm burden occur in hookworm infections?

A

Penetration to GIT in late infection

44
Q

Skin migration in hookworms referred to as?

A

Cutaneous Larva migrans

45
Q

Larva migrans

A

Worms moving through the skin for a few days

IgE comes to respond to invaders - histamine released to local tissues, causes itchiness = secondary infection

46
Q

IgE response in local tissues causes what symptoms in hookworm infection?

A

Transient cough, wheezing, chest pain, hemoptysis - increase in eosinophils

47
Q

Clinical manifestations - hookworm infection

A

CLM rash
Loeffler’s
GI upset
Iron deficiency anemia

48
Q

Dog hookworm species

A

Ancylostoma brazilliense

49
Q

Ancylostoma life cycle

A

Dog poops depositing eggs

Walking by and larvae burrow in skin

50
Q

Clinical manifestation - Ancylostoma

A

Creeping eruption - itchy response, IgE response

Won’t penetrate - will remain under skin until death

51
Q

Diagnosis of hookwoms

A

Ova and Parasite test - eggs are smooth, lobes of embryo inside

52
Q

Treatment - Necator americanus

A

Albendazole
Ivermectin
Both oral and well absorbed - to tissues

53
Q

Late infection treatment - hookworms

A

Antihistamines for itching

Iron repletion for growth restriction

54
Q

Prevention - hookworms

A

Shoes

55
Q

Are vaccines possible - hookworms?

A

Possible, since there is tissue migration can do humoral response

56
Q

Strongyloidiasis etiology

A

Strongyloides stercoralis

57
Q

Strongyloides stercolaris - life cycle

A
  1. Enters via skin - dermis penetration
  2. Moves to heart -> lungs -> respiratory tree -> oesophagus -> intestine
  3. Maturation in duodenum/bronchus
  4. Eggs hatch to larvae -> move to bowel lumen
  5. Larvae metamorphose in bowel - feces - to filiform larvae (infectious larvae)
58
Q

New host infection occurs via which route?

A

Larvae passed in feces

59
Q

Autoinfection

A

primary host infection in away that completes life cycle

60
Q

Autoinfection occurs in strongyloides how?

A

Stays on skin/rectal area when wiping

Infectious larvae in stool penetrates the rectal wall

61
Q

How are strongyloides different from other roundworms?

A

They have a free living cycle in soil and can also complete their cycle in humans

62
Q

Risk factors - strongyloides

A

Poor sanitation
Warm weather
Bare skin/ direct contact with feces
- fatal in immunocompromised + newborns

63
Q

Clinical features - early illness - Strongyloides

A

Skin and lung migration

64
Q

Clinical features - late illness - Strongyloides

A

Immunosuppression = high worm burden

65
Q

Skin migration

A

Rash (Larva currens) - pruritic, IgE mediated

Infection shorter than cutaneous migrans

66
Q

Lung migration pathogenesis

A

Larvae reaches lungs
IgE migration to lungs - causes immune response which leads to transient cough, wheezing, chest pain, hemoptysis
—Eosinophil in blood/ Charcot-Leyden

67
Q

Late infection symptoms - Strongyloides

A

Nausea
Abd pain
Diarrhea

68
Q

Hyperinfection - causation

A
  • if autoinfection causes strongyloides to persist; can occur for yrs/decades
  • Causes decrease in T lymphocytes

-depletion of T lymphocytes will cause lowered immunity which leads to hyperinfection

69
Q

Hyperinfection risk factors

A

-immunosuppresion heavy - chemo, organ transplant

70
Q

Hyperinfection - clinical features

A

(worms reproduce faster due to low immune response and migrate to ectopic sites carrying fecal bacteria from gut)

  • causes infection from bacteria in blood = sepsis
  • death
71
Q

Chronic auto-infection symptoms

A

Larva currens on exam - butt cheeks

- blood test +ve high eosinophils

72
Q

Diagnosis - Strongyloides early infection

A
  • biopsy of bowel wall = worms
  • OAP - false negatives, worms few in num hard to find
  • Serology - ELISA - good if patient has good immune system (cause worms go to blood)
73
Q

Hyperinfection - Diagnosis

A

GNR in blood, low eosinophils
Larvae in sputum - lung migration
Serology - too late to help - long waiting time

74
Q

Treatment - early infection

A

Ivermectin preferred over albendazole

Treat patient before immunosuppression

75
Q

Treatment - hyperinfection

A

Add ivermectin + albendazole
Reduce immunesuppression
Broad spectrum antibiotics for sepsis

76
Q

Prevention - Strongyloides

A

Wear shoes

77
Q

Good indicators of strongyloides hyperinfection - symptoms

A

Pneumonia + sepsis

78
Q

Enterobius vermicularis

A

Pinworm

79
Q

Transmission - Enterobius vermicularis

A
  • Food contaminated with eggs
  • Eggs on skin/fingers
  • Eggs in bedding/underwear
80
Q

Anthroponosis

A

Pathogen only lives in humans, includes enterobius

81
Q

Eggs visualization

A

small, flat on one side, dome on the other

82
Q

Life cycle - pinworm

A
  1. when consumed stomach juices allow them to hatch
  2. cecum - where they have reached maturiy
  3. Female fertilized and moves to rectum = crawl out through anus along perianal skin and leave goo behind which is microscopic - sticky eggs are irritating so it becomes itchy
83
Q

Pinworms must exit body to complete life cycle

A

Yes they move to perianal space

84
Q

Children are affected by pinworm more often (T/F)

A

True

85
Q

Symptoms

A

Often asymptomatic
Itchy butt/pruritis ani in heavy infection

Young kids symptoms
Irritability, wet beds, insomnia

86
Q

Perianal rash in kids can occur due to

A

Perianal rash, - can be due to eggs themsevles/ due to secondary infection /superinfection - on the superficial area

87
Q

Vaginal discharge occurs why?

A

Migration of worms to vagina

88
Q

Immune response - pinworms

A

None - since they dont invade tissue - hides from GALT

-Eosinophil - no response - no vaccine

89
Q

Standard sign of pinworms

A

Pruritis ani

90
Q

Diagnosis

A

Cellophane tape prep in morning
Fingernail scrapings
Adult female can be seen outside perianal area at night

91
Q

Treatment - enterobius

A

Albendazole - penetrates tissue
Pyrantel pamoate - stays in gut
Both highly effective

92
Q

Prevention - enterobius

A

Keep hands clean

Parasitology (10 decks)

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