6/17- Helminths I: Intestinal Nematodes Flashcards

1
Q

What are Neglected Tropical Diseases (NTDs)?

A

The most common afflictions of the “bottom billion”

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2
Q

What are the 3 most common afflictions of people living in poverty? Relative sizes?

A

(Intestinal Helminth Infections: soil-transmitted)

1. Ascariasis (2 in)

2. Trichuriasis (2 ft, largest)

3. Hookworm (cm, smallest)

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3
Q

What are the Millenium Development Goals?

A
  1. Combat HIV/AIDS, malaria, and other diseases
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4
Q

Prevalence of “worms” in Guatemalan kids? (chart)

A

Basically, all kids are infected; kids are disproportionately affected (adults have them too, but not as much)

  • Peak just under 10 yo (practically 100%)
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5
Q

What is this a symptom of?

A

Ascaris infection

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6
Q

Symptoms of hookworm and other soil-transmitted helminth infections?

  • Hookworm leads to __% _____________
A
  • Stunting
  • Impaired memory
  • Decreased school performance
  • Debilitating and limit potential, but typically not fatal

Hookworm leads to 40% reduction in future wage earnings

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7
Q

What is this? Characterisics?

A

Trichuris trichiura (Whipworm)

  • Male on left
  • Female on right

Thinner end is anterior (internal existence), while fatter back end is external in gut

  • Causes inflammation
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8
Q

Structure of Tirchuris trichuria (whipworm) in environment?

A

Thinner end is anterior (internal existence), while fatter back end is external in gut

  • Causes inflammation
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9
Q

What is this?

A

T. trichiura egg

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10
Q

Life cycle of Tirchuriasis?

A
  • Eggs ingested
  • Larva hatch in small intestine
  • Larvae migrate to colon
  • Adults mature in colon
  • Unembryonated eggs pass out in feces
  • Eggs embryonate in soil
  • Eggs ingested (May cause prolapsed rectum)
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11
Q

What is this?

A

SEM of T. trichiura with its intracellular and extracellular existence

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12
Q

What are the clinical sequelae of Trichuriasis?

A
  • Trichruis dysentery syndrome
  • Trichuris colitis
  • Rectal prolapse

(because feel like something is in rectum and straining hard)

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13
Q

Life cycle of Ascaris lumbricoides?

A
  • Eggs ingested
  • Larvae hatch in small intestine, enter bloodstream, go to liver (then to IVC)
  • Larvae migrate to the heart (right side)
  • Larvae reach lung capillaries (via pulmonary a.)
  • Larvae enter alveolar spaces; will have eosinophils and IgE in the lung (induces asthma)
  • Larvae migrate up trachea and are swallowed
  • Adults mature in small intestine
  • Cause penetration and obstruction in the gut
  • Eggs pass out in feces
  • Eggs embryonate in soil
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14
Q

What is this? Characteristics?

A
  • Eggs are very hardy
  • Sticky: mucopolysaccharide
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15
Q

Disease syndromes of Ascariasis?

A
  • Loeffler’s syndrome (pneumonitis)
  • Impaired nutrition
  • Growth retardation
  • Acute Intestinal Obstruction
  • Biliary Tract Obstruction: pancreatitis, cholangitis, hepatitis
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16
Q

What is this?

A

Ascariasis obstruction of gut

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17
Q

Treatment for intestinal worms? Exception?

A
  • Mebendazole
  • Albendazole

Except Strongyloides

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18
Q

What is the life cycle of Toxocariasis?

A

Toxocara canis and Toxocara cati (Ascaris homolog found in cats and dogs):

  • Animals eat embryonated eggs, acquires adults
  • Eggs pass in feces and embryonate in soil
  • Eggs are ingested by humans
  • Larvae hatch in small intestine and penetrate wall
  • Larvae migrate to all organs via bloodstream (don’t become adult worms in intestine cause kinda in wrong host; migrate elsewhere)
  • Causes pathology in eye, CNS, and liver (visceral larva migrans)
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19
Q

What is this?

A

Eggs of Toxocara canis or T. cati

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20
Q

Clinical Syndromes of Toxocarisis? Ages affected?

A

Visceral Larva Migrans (1-3 yo)

  • Pneumonitis (wheezing)
  • Hepatitis
  • Cerebritis
  • Eosinophilia
  • Hypergammaglobulinemia

Ocular Larva Migrans (>5 yo)

  • Strabismus (exotropia)

Covert Toxocariasis

  • Environmental cause of asthma- getting eosinophils, wheezing, maybe some cognitive deficits
  • Rise of asthma in our inner cities?
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21
Q

Toxocariasis in the US

  • Seroprevalence (by ethnicity)
  • Highest in what region?
  • Risk factors
A

Seroprevalence:

  • 21.2% in non-Hispanic blacks
  • 12% in Whites

Highest in American South

Risk factors:

  • Low household education
  • Poverty
  • Elevated lead levels
  • Toxoplasmosis
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22
Q

What are these? What are included in this category?

A

Hookworms:

- Necator americanus (85% of infxn)

  • Ancylostoma duodenale
  • Ancylostoma ceylanicum
23
Q

Global distribution of human hookworm infection?

What is the prominent species?

A

Necator americanus

Wherever rural poverty and adequate climate overlap

24
Q

Life cycle of Necator americanus?

A
  • Larvae hatch and develop in soil
  • Filariform larvae on blades of grass
  • Larvae penetrate skin, enter bloodstream, and reach heart (not always through feet, may also spread over skin- cause dermatitis)
  • Larvae enter lung capillaries and then alveolar spaces
  • Larvae migrate up trachea, and are swallowed
  • Adults mature in small intestine
  • Eggs pass out in feces
  • Larvae hatch and develop in soil
25
Q

What is the underlying mechanism/cause of disease from hookworms? Result?

A

Intestinal blood loss (attach to small intestine)

  • 25 worms = 1 mL blood loss = 0.55 mg Fe (a child’s daily iron intake)
  • Results in iron deficiency anemia and protein malnutrition
26
Q

What is this?

A

Hookworm embedded in intestine

27
Q

What is this?

A

Adult hookworms in situ (1 cm)

28
Q

What can be done to detect hookworms?

A

Adult hookworm antigens- hemoglobinases

(Ac-MEP-1, hookworm metalloendopeptidase 1)

29
Q

Symptoms of hookworm infections?

A
  • Iron deficiency anemia and severe anemia
  • Reduced growth, psychomotor development, physical fitness
  • Developmental delays, lower IQ
  • Reduced school performance and attendance
  • Pallor and facial edema
  • Anasarca
30
Q

At risk populations for hookworm disease? Symptoms?

A

Women and children: low iron stores

Children:

  • Physical growth stunting
  • Cognitive deficits and intellectual retardation

Women of child-bearing age:

  • Puberty
  • Menstruation
  • Pregnancy (adverse fetal outcomes)
31
Q

Comparison of typical age/intensity relationships of the three main infections?

A
32
Q

What can be used to treat these? (hookworms?)

A

- Benzimidazoles

  • Mebendazole
  • Albendazole Targeting the blood-feeding in the hookworm gut is in phase I trials in Brazil
33
Q

What drug fails to treat hookworm?

A

Mebendazole

34
Q

What is this?

Caused by?

Where is it found?

What at risk populations?

A

Cutaneous Larva Migrans, “Creeping Eruption”

  • Caused by A. braziliense
  • Found in Caribbean, Florida, Gulf Coast
  • Travelers from tropical resorts and Military person
35
Q

Distribution of Strongyloidiasis?

A
36
Q

How to differentiate hookworm larvae with Strongyloides larva?

A

Strongyloides have notched tail???

37
Q

Life cycle of Strongyloides stercoralis?

A
  • Reservoir hosts in dogs and monkeys
  • Free living soil cycle
  • Larvae penetrate unbroken skin
  • Larvae enter bloodstream and reach lung capillaries
  • Larvae enter alveolar spaces
  • Larvae are swallowed
  • Adult worms live in small intestine
  • Larvae develop to L3 in colon and enter bloodstream
  • Larvae pass out in feces
  • Free-llving soil cycle

There is a potential for auto-infection from gut into lungs

38
Q

What is this?

A

Adult S. stercoralis in crypts of small intestine

39
Q

Clinical features of Strongyloidiasis? Caused by what?

A

Clinical features:

  • Enteritis
  • Diarrhea
  • GI discomfort

Autoinfection:

  • Larva currens (creeping infection)
  • Eosinophilia present

Caused by Strongyloides stercoralis

40
Q

What is this?

A

Lava Currens from Strongyloides

  • Larva currens = autoinfection with Strongyloides filariform larvae
41
Q

Clinical features of hyperinfection with Strongyloides?

A
  • Intestinal perforation
  • Shock, sepsis, gram-negative meningitis
  • Hemorrhagic pneumoina
  • Eosinophilia often absent
42
Q

Risk factors for Strongyloides hyperinfection?

A

Steroids

  • Immunosuppressive therapy
  • Autoimmune disease, malignancy HTLV-1 infection (not HIV)

Malnutrition (especially children under 10 yo)

43
Q

Diagnosis of Human Strongyloidiasis?

A
  • Hunting in “black gold”- multiple fecal exams looking for larvae
  • Blood agar plate looking for larval tracks
  • Culture with charcoal to amplify through heterogonic life cycle
  • Serologic tests (“not yet ready for prime-time”)
44
Q

What is this?

A

First stage larvae of Strongyloides (NOT EGGS)

45
Q

Treatment for Strongyloides?

A

Ivermectin

46
Q

What is this?

A

Pinworm, or Enterobiasis

  • Enterobius vermicularis
47
Q

Life cycle for Enterobiasis (pinworm)?

A

Enterobius vermicularis

  • Eggs ingested
  • Larvae hatch in small intestine
  • Larvae migrate to colon
  • Adults mature in colon
  • Gravid adults migrate out of anus
  • Adults lay eggs on perianum
  • Eggs embryonate on perianum
  • Eggs contaminate fingers
  • Eggs are ingested
48
Q

Epidemiology of Enterobius vermicularis?

  • Geography
  • Transmission
A

Geography

  • Worldwide prevalence
  • Tropical and temperate climates

Transmission:

  • Re-infection
  • Person-to-person
  • Sexual
  • Fomite
49
Q

Adult habitat of Enterobius vermicularis?

A

Cecum and appendix

  • Gravid female nocturnally deposits eggs onto perianal skin
  • Eggs mature after 4-6 hrs of oxygen exposure
50
Q

Clinical features of hookworm infection (Enterobius vermicularis)?

A
  • Asymptomatic -> pruritus ani (itchy butthole)
  • Appendiceal inflammation
  • Female urogenital tract infection, granulomas
51
Q

Diagnosis of pinworm infection (Enterobius vermicularis)?

A

Unfrosted scotch tape over anus (early morning test)

52
Q

Treatment of pinworm infection (Enterobius vermicularis)?

A
  • Albendazole (1 dose)
  • Repeat in 2-4 weeks
  • Treat entire family
53
Q

What is this?

A

Enterobius vermicularis egg (?)