L17: Intestinal nematodes Flashcards
What is Trichinella spiralis
smallest nematodes, unusual
not host specific
def host/int host/resevoir: pigs, bushpigs, wild carnivores, rats
humans are acciedntal deadend hosts, cause tirchnellosis zoonosis
what are nurse cells
a single larva penetrates and occupies each contractile muscle fiber => penetration they form a complex nucleated mass called nurse ccell
larva coil and absorb nutrients from te host muscle sarcoplasm, also obtaining
oxygen and nutrients from the new blood vessels
During encapsulation, larva can enter developmental arrest and survive indefinitely => can calcify
Distinguish between Trichinella male and female
female
* monodelophic, ovoviviporous, larger, blunt round posterior
male
*smaller, curved postera with 2 lobe alae appendages
what is nurse cell formation consit of
- Myofilaments disappear
- Mitochondria degenerates
- Smooth endoplasmic reticulum increases
- The nuclei enlarge
- Collagen production by neighboring fibroblasts
- Angiogenesis (formation of new blood vessels)
Life Cycle of Trichinella spiralis
The domestic cycle most often involves pigs and rodents
* The sylvatic cycle involves a wide range of animals
* A second host is required to perpetuate the life cycle
1. Trichinellosis is caused by the ingestion of undercooked meat containing
encysted larvae of T. spiralis
2. After exposure to gastric acid and pepsin, the larvae are released from the cyst
3. Larvae then invade the mucosa of the small intestine where they develop into
adult worms within 24-30 hours. The life span at this site is ~4 weeks
4. Soon after copulation, the male passes out of the host. The females burrow
deeper into the mucosa and submucosa and begins depositing larvae (up to
1500 in 5-10 days). Eventually, the female dies.
5. Larvae are carried by the lymphatic and blood vessels to the heart. From the
heart, larvae enter the peripheral circulation and are carried to various tissues
of the body. Larvae develop into the infective stage only in striated muscles
(especially of the eye, tongue, diaphragm, jaws and larynx) and become
encapsulated in host material
When muscle harboring the encapsulated larva is eaten by a carnivorous mammal,
the larva excyst and the life cycle is reinitiated
T. spiralis is one of the largest known intracellular parasites
generally what are Clinical Presentation of Trichinellosis
light can be asympto but symptoms arise from larval invastion of muscle and hyper immune reaction of host metabolic products and larva secretion
Symptoms appear in 3 clinical phases Trichinellosis
- Mild symptoms in the intestinal stage: Adult worms penetrating the intestinal mucosa and submucosa. Inflammation causes gastrointestinal symptoms
- Severe symptoms in the migration stage:
Migrating larva cause damage to blood vessels resulting in localized edema. They may cause pneumonia, myocarditis, encephalitis,
hemorrhages, meningitis, rheumatism, rashes, fever, conjunctivitis, eosinophilia, etc. - Moderate symptoms after encapsulation
nurse cells and larval encapsulation may cause muscle pain and weakness, after which symptoms usually subside
also cause resp complication
Epidemiology of Trichinellosis
common in europe and US. most reportable disease
rare in subtropics
T. native polar bears
Diagnosis of Trichinellosis
asympto but suspected based on clinical symptoms, patient history and eosinophilia
confirmatry by antibody detection and muscle biopsy
Trichinella is an intestinal nematode. As such, adult worms and
eggs should be detectable in stool specimens.
t/f
Treatment of Trichinellosis, WHY
mebendazole or albendazole
✓ This is essential to kill adult worms and prevent release of larvae. WHY?
Steroids may be administered to relieve symptoms due to the intense
Strongyloides stercoralis
thread worm
def host: humans
complex life cycle, alternate between:
1. Direct, parasitic cycle
2. Indirect, free-living cycle
worlwide, tropics/subtropics, summer transmission in cold places
S. stercoralis causes strongyloidiasis - opportunistic parasite
Life Cycle of Strongyloides stercoralis
Free-living Cycle
1. The rhabditiform larvae are passed in the stool of an infected definitive host
2. The larvae develop into free-living adult males and females in moist soil. Larvae may also develop into infective filariform larvae (direct
development ⑥)
3. The free-living adult males and females mate and produce eggs
4. Eggs hatch in the soil to release rhabditiform larvae.
5. Under unfavorable environmental conditions, rhabditiform larvae molt twice to become infective filariform larvae (L3
)
6. The filariform larvae cannot mature into free-living adults and must find a new host to continue the life cycle
In an uninterrupted free-living cycle, eggs hatch in the soil to release larvae which actively feed on organic debris, pass through four molts and develop
into sexually mature adults
Parasitic Cycle
6. The filariform larvae in contaminated soil penetrate the skin of a human, or other suitable host when skin contacts soil
7. These larvae then migrate via the bloodstream and lymphatics to the lungs where they are coughed up and swallowed to reach the small intestine
8. In the small intestine, larvae molt twice and become adult female worms
9. The females live embedded in the submucosa of the small intestine and produce eggs via parthenogenesis (parasitic males do not exist). Eggs yield
rhabditiform larvae
10. The rhabditiform larvae become infective filariform larvae that can penetrate either the intestinal mucosa or the skin of the perianal area,
resulting in autoinfection. Filariform larvae enter the circulatory system and continue their parasitic lives without ever leaving the host.
Alternatively, rhabditiform larvae can be passed in the stool ①and continue the ‘free-living cycle’ if the environmental conditions are favorable
What is clinical presentation of Strongyloidiasis
mostly asymp with three phases
1. cutaneous:
slight hemorraging, swelling ,ground itch
- pulmonary
larval migration to lungs, dry cough - intestinal
female in mucossa, with heavy infection u get abdominal pain, anorexia, vomitting
What are the more severe stages of strongyloidisais
becomes chronic due to dysentarty and weight loss
auto infcection
*untreated cases persist even after not living in endemic region for a long time
*get a rash from migration of filariform larva, rash on butt, perineium and thighs
hyperinfection
*can be fatal
*invasion of tissues by filaform larvae = disseminated strongloidiasis
*secondary infections
*immunosuprresion => more autoinfection
