Nematodes 1/2/3 Flashcards
Important factors for disease manifestation
- 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)
Basic body plan of nematodes
- 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.
Nematode developmental stages
Egg > Larva L1 > L2 > L3 > L4 > Adult
Type of lifecycle: Intestinal nematodes
Direct (usually soil-transmitted)
Major classes of anti-helminthics
Benzimidazoles Piperazine Levamisole Pyrantel Ivermectin
Enterobius vermicularis
Pinworm/threadworm Not soil transmitted Broadest range of any helminth 300 million cases worldwide Easy to treat, difficult to control
Trichuris trichiura
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
Diagnosis of various STHs
Direct smear
Kato Katz thick smear
Formol-ether concentration
FLOTAC
Ascaris lumbricoides
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
Hookworms
Necator americanus
Ancylostoma duodenale
Hookworm Lifecycle
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
Hookworm Treatment
Benzimidazole
Iron therapy (alleviates anaemia)
Mass chemotherapy campaigns
Strongyloides stercoralis
Female worms found in humans - asexual reproduction
L1 larvae hatch in the gut
Autoinfection - invading L3 larvae heart-lung migration = new adults in gut
Disseminated Strongyloidiasis
Overwhelming numbers of L3 larvae can cross the capillary bed of the lungs to infect all organs
Occurs following immunosuppressive therapy
Predisposing factors:
- corticosteroid use
- HTLV-1 infection
HTLV-1 and Disseminated Strongyloidiasis
- 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
S. stercoralis Pathogenesis
Skin - itchy dermatitis, autoinfecting L3s
Lung - pneumonitis
Intestine - acute and chronic phrase
S. stercoralis Diagnosis
Direct faecal smear
Concentration methods - formol-ether/Baermann
Culture methods - charcoal culture/nutrient agar plate
Factors of S. stercoralis Persistence
- Adequate source of infection in population (N.B. human is the only definitive host)
- Defecation habits or fertilizing with night soil (→ eggs in favourable conditions for development)
- Appropriate environmental factors - moist, shade, warmth.
- Opportunity for infective stages to be ingested or penetrate skin
Zoonotic Nematodes - Develops fully in humans
Trichinella spp.
Capillaria philippinensis
Zoonotic Nematodes - Arrest at larval stage in humans
o Toxocara canis
o Angiostrongylus cantonensis
o Anisakis spp.
o Gnathostoma spinigerum
Trichinella spiralis Lifecycle
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!)
Sources of infection - T. spiralis
Pigs Horses Feral cycles Artic cycles African cycles
Trichinella spp. Phase
Acute phase - gastrointestinal symptoms, inflammatory response
Chronic phase - chronic inflammatory cyst stage
Trichinella Diagnosis
Clinical picture
Dietary history
Lab - eosinophilia
Serology
