Nematodes 1/2/3

Question 1

Important factors for disease manifestation

Answer 1

• Number of worms infecting the host (related to level of exposure, cumulative after repeated exposures)
• Duration of infection (long life span of worms)
• Immune response to infection (may cause immune-mediated pathology)
• Location of worms (migration?)
• Age of host (children’s habits make them more likely to be exposed but they may also suffer more from disease, anemia etc.)
• Sex of host (women may suffer more from helminth-induced anemia)

Question 2

Basic body plan of nematodes

Answer 2

• Cylindrical body tapered at each end.
• Have a complete digestive system: mouth, intestine, and anus.
• Body is covered by tough cuticle that resists drying and crushing.
• Nematodes use longitudinal muscles to produce a sideways thrashing motion
• Most species are dioecious: separate males and females.
• Males are smaller than females and have one or two spicules on posterior end.

Question 3

Nematode developmental stages

Answer 3

Egg > Larva L1 > L2 > L3 > L4 > Adult

Question 4

Type of lifecycle: Intestinal nematodes

Answer 4

Direct (usually soil-transmitted)

Question 5

Major classes of anti-helminthics

Answer 5

Benzimidazoles
Piperazine
Levamisole
Pyrantel
Ivermectin

Question 6

Enterobius vermicularis

Answer 6

Pinworm/threadworm
Not soil transmitted
Broadest range of any helminth
300 million cases worldwide
Easy to treat, difficult to control

Question 7

Trichuris trichiura

Answer 7

Whipworm
STH - eggs need shade moisture and temp to become infective
Direct life cycle
Infection via ingestion of eggs
Pathogenesis = adults burrowing into the large intestine

Question 8

Diagnosis of various STHs

Answer 8

Direct smear
Kato Katz thick smear
Formol-ether concentration
FLOTAC

Question 9

Ascaris lumbricoides

Answer 9

Large/common roundworn
Eggs hatch in the duodenum but do not develop in gut
L3 larvae penetrate gut mucosa = lymphatics or veins = lungs/intestine/ectopic
Malabsorption leads to malnutrition

Question 10

Hookworms

Answer 10

Necator americanus

Ancylostoma duodenale

Question 11

Hookworm Lifecycle

Answer 11

Eggs hatch
L1 rhabditiform larvae feeds on bacteria in soil
L2 also feeds
L3 filariform infective larva - does not feed, penetrates humans (via feet)
In human - L4 > Adult > Produces eggs

Question 12

Hookworm Treatment

Answer 12

Benzimidazole
Iron therapy (alleviates anaemia)
Mass chemotherapy campaigns

Question 13

Strongyloides stercoralis

Answer 13

Female worms found in humans - asexual reproduction
L1 larvae hatch in the gut
Autoinfection - invading L3 larvae heart-lung migration = new adults in gut

Question 14

Disseminated Strongyloidiasis

Answer 14

Overwhelming numbers of L3 larvae can cross the capillary bed of the lungs to infect all organs
Occurs following immunosuppressive therapy

Predisposing factors:

1. corticosteroid use
2. HTLV-1 infection

Question 15

HTLV-1 and Disseminated Strongyloidiasis

Answer 15

• HTLV-1 → T cell leukaemia.
• Infected T cells produce higher IFN-γ (Th1 response) but less Th2 cytokines (IL-4 and IL-5).
• S. stercoralis specific IL-5 and IgE levels are significantly lower in HTLV-1 coinfected patients

Question 16

S. stercoralis Pathogenesis

Answer 16

Skin - itchy dermatitis, autoinfecting L3s
Lung - pneumonitis
Intestine - acute and chronic phrase

Question 17

S. stercoralis Diagnosis

Answer 17

Direct faecal smear
Concentration methods - formol-ether/Baermann
Culture methods - charcoal culture/nutrient agar plate

Question 18

Factors of S. stercoralis Persistence

Answer 18

1. Adequate source of infection in population (N.B. human is the only definitive host)
2. Defecation habits or fertilizing with night soil (→ eggs in favourable conditions for development)
3. Appropriate environmental factors - moist, shade, warmth.
4. Opportunity for infective stages to be ingested or penetrate skin

Question 19

Zoonotic Nematodes - Develops fully in humans

Answer 19

Trichinella spp.

Capillaria philippinensis

Question 20

Zoonotic Nematodes - Arrest at larval stage in humans

Answer 20

o Toxocara canis
o Angiostrongylus cantonensis
o Anisakis spp.
o Gnathostoma spinigerum

Question 21

Trichinella spiralis Lifecycle

Answer 21

Females produce L1 larvae→ intestinal wall → lymphatics and blood → skeletal muscles → penetrate a striated muscle cell → “nurse cell” containing a coiled L1 larva (cyst) (intracellular larvae!)

Question 22

Sources of infection - T. spiralis

Answer 22

Pigs
Horses
Feral cycles
Artic cycles
African cycles

Question 23

Trichinella spp. Phase

Answer 23

Acute phase - gastrointestinal symptoms, inflammatory response
Chronic phase - chronic inflammatory cyst stage

Question 24

Trichinella Diagnosis

Answer 24

Clinical picture
Dietary history
Lab - eosinophilia
Serology

Question 25

Capillaria philippinensis

Answer 25

Normal definitive host - marine birds
Ingested larva > patency > 3 weeks
Worms can multiply in gut = autoinfection/lots of worms

Question 26

Toxocara spp.

Answer 26

Cause of visceral larva migrans (VLM) i.e. ingestion of eggs or larvae of animal parasites leading to wandering larvae in the deep organs of the human body
Ocular larva migrans (OLM)

Question 27

Toxocara infection in humans

Answer 27

Children = covert toxocariasis is a mild, subclinical, febrile illness

Visceral larva migrans (VLM) = migration of larvae through the internal organs and the resulting inflammatory reaction

Ocular larva migrans (OLM) = migration of larva into the posterior segment of the eye

Question 28

Angiostrongylus cantonensis

Answer 28

Rat lung worm
Eosinophilic meningitis
Infective L3 larvae present in snail intermediate hosts
Larvaes migrate to brain/lungs/eye

Question 29

Anisakis simplex

Answer 29

Herring worm

Question 30

Pseudoterranova decipiens

Answer 30

Cod worm

Question 31

Gnathostoma spingerum

Answer 31

Spiny headed worm
Eggs hatch in water>L1 infects copepod>L2>L3
L3 larvae migrate around humans

Question 32

3 forms of Gnathostomiasis

Answer 32

Visceral larva mirgans
Cutaneous form
CNS form