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MD3002 - GI Disease/Pathology > Protozoal and Helminth Infections of the GI Tract > Flashcards

Protozoal and Helminth Infections of the GI Tract Flashcards

1
Q

What do infection levels of protozoa and helminths reflect?

A

Infection levels reflect hygiene/sanitation standards

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2
Q

How are protozoal and helminth infections usually acquired?

A

through ingestion of contaminated food or water

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3
Q

What is the most common symptom of protozoa and helminth infections?

A

acute to chronic diarrhoea and inflammation

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4
Q

What are the 2 main protozoa of the SI?

A
  • Giardia lamblia
  • Cryptosporidium
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5
Q

What is the main protozoa of the LI?

A

Entamoeba histolytica

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6
Q

What is Giardiasis a frequent cause of globally?

A

“travellers diarrhoea”

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7
Q

How is Giardia lamblia passed?

A

person-person

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8
Q

Describe the infective dose of Giardia lamblia

A

small; 10-15 cysts

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9
Q

How is Giardia lamblia diagnosed?

A

microscopy of stool samples

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10
Q

What are the 2 stages of the life cycle of Giardia lamblia?

A
  • Trophozoite
    • Flagellated and bi-nucleated
    • Lives in upper part of small intestine
    • Adheres to brush border of epithelial cells
  • Cyst
    • Formed when trophozoite forms resistant wall
    • Passes out in stools
    • Can survive for several weeks
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11
Q

Where is Giardia lamblia present?

A

duodenum, jejunum, upper ileum

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12
Q

Describe the pathogenesis of Giardia lamblia

A
  • Attaches to the mucosa via ventral sucker
  • Does not penetrate the surface
  • Causes damage to the mucosa and villous atrophy
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13
Q

What are the potential consequences of G. lamblia

A
  • Leads to malabsorption of food especially fats and fat-soluble vitamins
  • May swim up the bile duct to gall bladder
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14
Q

What are the clinical manifestations of G. lamblia?

A
  • Mild infections are asymptomatic
  • Diarrhoea is usually self-limiting (7-10 days)
  • Chronic diarrhoea presents in immunocompromised patients
  • Stools are characteristically loose, foul-smelling and fatty
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15
Q

How is Cryptosporidium parvum transmitted

A

through faecally-contaminayed drinking water

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16
Q

What is the infective dose of Cryptosporidium parvum?

A

as few as 10 cysts (small)

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17
Q

What type of condition is Cryptosporidium parvum?

A

AIDS defining condition

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18
Q

describe the life cycle of Cryptosporidium parvum

A
  • Asexual and sexual development within host
  • Ingestion of resistant oocysts
  • Release of infective sporozoites in small intestine
  • Invasion of intestinal epithelium
  • Division to form merozoites which re-infect cells
  • After sexual phase, oocytes released
19
Q

Describe the pathogenesis of Cryptosporidium parvum

A
  • Enters cells of the microvillus border of small intestine
  • Remains within vacuole of epithelial cell
  • May multiply to give large numbers of progeny, especially in immunocompromised hosts
20
Q

What are the clinical manifestations of C. parvum

A
  • Moderate to severe profuse diarrhoea
  • Up to 25 litres of watery faeces/day
  • Usually self-limiting disease
  • In HIV positive individuals CD4+ T-cell counts of <100/mm3, diarrhoea is prolonged and may become irreversible and life threatening
21
Q

Where is Entamoeba histolytica common?

A

Common in tropical and sub-tropical countries: prevalent in >50% of population

22
Q

What is the mode of transmission of Entamoeba histolytica?

A
  • Transmission via ingestion of contaminated food or water
  • Transmission also occurs through anal sexual activity
23
Q

What does Entamoeba histolytica give rise to? (life cycle)

A
  • Cysts pass through stomach and excyst in the small intestine giving rise to progeny
  • These adhere to epithelial cells and causes damage mainly though cytolysis
  • After mucosal invasion, cysts invade red blood cells giving rise to amoebic colitis
  • Trophozoite stages live in large intestine and pass out as resistant, infective cysts
24
Q

Describe the pathogenesis of Entamoeba histolytica

A
  • Adheres to epithelium and acute inflammatory cells
  • Resists host humoral and cell mediated immune defence mechanisms
  • Produces hydrolytic enzymes, proteinases, collagenase, elastase
  • Produces protein that lyses neutrophils, the contents of which are toxic to the host
25
Q

What are the clinical manifestations of E. histolytica?

A
  • Small localised superficial ulcers leading to mild diarrhoea
  • Entire colonic mucosa may become deeply ulcerated leading to severe amoebic dysentery
  • Complications include intestinal perforation
  • Trophozoites may spread to the liver, and other organs
  • Rarely abscesses spread to overlying skin
26
Q

What are the main methods used for the prevention of protozoal infections of the GI tract?

A
  • Improved hygiene and water supplies
  • Eating only freshly prepared food served hot
  • Avoiding salads and fruit which cannot be peeled
  • Avoiding tap water and ice cubes
27
Q

Describe bacillary dysentery

A
  • Many PMN in stool
  • Eosinophils absent
  • Many bacilli in stool
  • Blood/mucus present in stool
28
Q

Describe entamoeba dysentery

A
  • Few PMN in stool
  • Eosinophils present
  • Few amoebae in stool
  • Blood/mucus present in stool
29
Q

What are the main types of roundworms (nematodes)

A
  • Bisexual
  • Cylindrical
30
Q

What are the main types of tapeworms (cestodes)?

A
  • Elongated flatworms
  • Segmented
  • Hermaphrodite
31
Q

What are the main types of flukes (trematodes)?

A
  • Lead-shaped flatworms
  • Mainly hermaphrodites
  • Rare in humans
32
Q

What are the most clinically important worm and how are they transmitted?

A
  • Nematodes are the most clinically important intestinal worms
  • Often soil-transmitted
33
Q

How does infection by nematodes occur?

A
  • Swallowing infective eggs (Ascaris lumbricoides, Trichuris trichiura)
  • Active skin penetration by larvae and systemic migration through lung to intestine (Stronglyloides stercoralis)
34
Q

How are nematodes diagnosed?

A

stool microscopy

35
Q

Describe Strongyloides stercoralis and its actions

A
  • Pinworm
  • Disruption of small intestine mucosa
  • Villous atrophy
  • Marked loss of elasticity of intestinal wall
36
Q

Clinical Manifestations: S. stercaralis

A
  • Dysentery (persistent in immunocompromised hosts)
  • Dehydration
  • Malabsorption syndrome
  • Anal pruritis
  • Associated with appendicitis
37
Q

Describe Trichuris trichiura

A
  • Whip worm
  • Can live for 3 years in gut
  • Acquired through ingesting eggs on vegetables
  • 10,000 eggs produced daily
  • 800 million cases worldwide
38
Q

Describe Ascaris lumbricoides

A
  • Giant roundworm
  • Large thick white worm 20-30cm
  • Females produce approximately 20,000 eggs/day from 65 days after infection
  • Adults live in gut for 2 years
  • Causes 1 million clinical cases per year with 20,000 deaths
39
Q

What are the clinical manifestations of Ascaris lumbricoides

A
  • Allergic reaction in sensitised people
  • Digestive upsets
  • Protein/energy malnutrition
  • Intestinal blockages
  • Worm may invade mouth, nose etc.
40
Q

Describe Enterobius vermicularis

A
  • Threadworm
  • Small cylindrical nematodes < 1cm
  • Female migrates to anus at night to lay approximately 10,000 eggs, which may develop to infective stage within hours
  • Intense itching, secondary bacterial infection – mild catarrhal inflammation and diarrhoea, slight eosinophilia
41
Q

Describe Ancylstoma duodenale

A
  • Hookworm
  • Often picked up walking barefoot in infected areas
  • Attaches to small intestine, sucks blood and protein, often present in huge numbers
  • Causes hypochromic anaemia
  • Blood loss 0.03ml/day/worm (often 500-1000 worms)
42
Q

Describe Taenia solium

A
  • Tapeworm
  • Acquired from ingesting worms or eggs in undercooked pork
  • Reside in large intestine
  • Can grow to 7m long
  • Scolex – for attachment
43
Q

What is the main treatment and preventuon of intestinal helminth infections?

A
  • Improved hygiene and sanitation are important in prevention of infection
  • Drugs:
    • Mebendazole
    • Praziquantel
    • Ivermectin
    • Piperazine
44
Q

What are the major problems related to antiprotozoal and antihelminithic agents?

A
  • Pose particular problems because of:
    • Large variety of species
    • Complexities of their life cycles
    • Differences in their metabolic pathways
    • Drugs active against protozoa are inactive against helminths

MD3002 - GI Disease/Pathology (11 decks)

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