[DISCUSSION] MODULE 3 UNIT 2 AND UNIT 3 Flashcards
The phylum Nematoda is divided into classes based on the presence or absence of “(?)’, which are caudal chemoreceptors.
phasmids
The two (2) classes were earlier called Aphasmidia and Phasmidia, but now have been renamed as (?), respectively.
Adenophorea and Secernentea
The origin of the name (Gr. trichos = hair + oura = the tail), is not quite correct because it is the (?) of the worm that is hair-like and not the tail.
anterior end
Whipworm
A. Trichuris trichiura
Infection is caused by ingestion of embryonated eggs.
A. Trichuris trichiura
Eggs – hatch in the small intestine.
A. Trichuris trichiura
larvae (L1) – released and penetrate the intestinal villi and undergo 4 molts in 3-10 days.
A. Trichuris trichiura
young adult – passively migrate to the cecum (also in the ascending colon) and mature in about 2-3 months
A. Trichuris trichiura
usually asymptomatic, except in heavy infection
Trichuriasis
Heavily infected individuals - those with a high worm burden (greater than 200 worms, >5,000 EPG)- are most likely to
develop clinical disease.
Trichuriasis
hypochromic, microcytic type
Iron-deficiency anemia
results from chronic blood loss at the attachment site coupled with the long life span of the worms
Iron-deficiency anemia
Small amounts of blood (0.005 ml per worm) are lost each day at the ulceration in the intestinal mucosa
Iron-deficiency anemia
worm may be found even up to the rectum in heavy infection
Rectal prolapse
mucosa of the rectum protrudes through the anal opening associated with the loss of muscle tone of the anus
Rectal prolapse
Children with severe trichuriasis have:
o growth retardation
o impaired mental development
o cognitive function
Sever Trichuriasis
Pudoc worm
B. Capillaria philippinensis
In 1967, an epidemic of Capillariasis took place in
Pudoc West, Tagudin, Ilocos Sur
B. Capillaria philippinensis
Infection is caused by ingestion of larvae in raw or
undercooked infected fish
B. Capillaria philippinensis
larvae - develop into adults in the small intestine
(jejenum) where they burrow into the mucosa
B. Capillaria philippinensis
Female worms - may produce two types of eggs:
o Unembryonated shelled eggs –
passed in the feces
o Embryonated eggs – hatches
within human host
B. Capillaria philippinensis
larvae - will re-invade and cause autoinfection.
B. Capillaria philippinensis
unembryonated eggs - ingested by fish when
passed into water.
B. Capillaria philippinensis
malabsorption syndrome with severe diarrhea
Intestinal capillariasis
borborygmi (gurgling stomach)
Intestinal capillariasis
abdominal pain (can become serious if not treated
because of autoinfection)
Intestinal capillariasis
Capillary liver worm
C. Capillaria hepatica
The nematode (roundworm) Capillaria hepatica (=Calodium
hepaticum) causes hepatic capillariasis in humans.
C. Capillaria hepatica
Nomenclature varies in use globally and by discipline; Capillaria
hepatica is most frequently used in medical literature.
C. Capillaria hepatica
zoonotic parasite with a low host specificity
o primarily exists in rodent and carnivore hosts
o Both true and spurious infections occur in
humans
C. Capillaria hepatica
Infection is caused by ingestion of embryonated eggs in fecally-
contaminated food, water, or soil
C. Capillaria hepatica
Adult worms - are located deep within the liver parenchyma of
the host, and lay hundreds of eggs in the surrounding
parenchymal tissue.
C. Capillaria hepatica
eggs - trapped in the parenchyma; can not be passed in the feces
of the host, and remain in the liver until the animal dies, or more
likely, is eaten by a predator or scavenger
C. Capillaria hepatica
o Eggs ingested by scavengers are
unembryonated (not infectious) and are passed
in through the digestive tract into and out in
feces, providing an efficient mechanism to
release eggs back into the environment
C. Capillaria hepatica
o Eggs embryonate in the environment, where
they require air and damp soil to become
infective.
C. Capillaria hepatica
Under natural conditions, embryonation is slow and may take
between 6 weeks and 5 months.
C. Capillaria hepatica
The cycle continues when embryonated eggs are eaten by a
suitable mammalian host.
C. Capillaria hepatica
Infective eggs hatch in the intestine, releasing first stage larvae.
C. Capillaria hepatica
The larvae penetrate the intestinal wall and migrate via the portal
vein to the liver parenchyma within 3-4 days.
C. Capillaria hepatica
Larvae take about 3-4 weeks to mature into adults and mate.
C. Capillaria hepatica
rare in humans
Hepatic capillariasis
typically manifests as an acute or subacute hepatitis with:
o peripheral leukocytosis and eosinophili
o hepatomegaly
o persistent fever (which may be as high as 40°C)
Hepatic capillariasis
Trichina worm
D. Trichinella spiralis
The name Trichinella is derived from the minute size of the adult (Gr. trichos =hair, ella suffix for diminutive) and spiralis refers to the spirally coiled
appearance of larvae in muscles.
D. Trichinella spiralis
Infection is caused by ingestion of raw/rare or undercooked meat containing encysted larvae
D. Trichinella spiralis
Adult worms and encysted larvae develop within:
o 1 vertebrate host
o definitive host and potential intermediate host : infected animal
o A second host is required to perpetuate the life cycle of Trichinella.
D. Trichinella spiralis
domestic cycle
o pigs
o anthropophilic rodents
o other domestic animals
horses
D. Trichinella spiralis
sylvatic cycle
o bear
o moose
o wild boar
D. Trichinella spiralis
After exposure to gastric acid and pepsin, the larvae are released from the cysts (excystation) invade the small bowel mucosa, molt four times and
rapidly develop into adults, either male or female, by the 2nd day of infection.
D. Trichinella spiralis
Within 5 days, they become sexually mature
D. Trichinella spiralis
The male dies after fertilizing the female.
D. Trichinella spiralis
After 1 week of infection, the fertilized females release larvae.
D. Trichinella spiralis
Larvae continue to be discharged during the remaining part of the lifespan of the female worm, which ranges from 4 weeks to 4 months.
D. Trichinella spiralis
These larvae enter the intestinal lymphatics or mesenteric venules and are transported in circulation to different parts of the body.
o They get deposited in the muscles, central nervous system and other sites.
D. Trichinella spiralis
The larvae die in most other situations, except in the skeletal muscles, where they grow.
D. Trichinella spiralis
Within 20 days after entering the muscle cells, the larvae encyst within nurse cells.
D. Trichinella spiralis
Encysted larvae lie parallel to the muscles of host and can survive for months to years and eventually calcify and die.
D. Trichinella spiralis
In man, the life cycle ends here.
o Man is a dead-end host of the parasite, as the cysts in human muscles are unlikely to be eaten by another host.
D. Trichinella spiralis
Trichinella spiralis has an unusual life cycle in that the same individual animal serves as both definitive and intermediate host, adults and larvae
located in different organs.
D. Trichinella spiralis
autoheteroxenous parasite
D. Trichinella spiralis
Cysts develop preferentially in muscles relatively poor in glycogen and in hypoxic environment.
o Therefore, the biceps, deltoid, gastrocnemius, pectoralis, masseter, extraocular muscles, intercostal muscles and diaphragm, which
are constantly active, are the ones mostly affected.
D. Trichinella spiralis
- gastrointestinal symptoms
diarrhea
abdominal pain
vomiting
Intestinal phase
high fever
periorbital and facial edema
conjunctivitis
blurred vision
myalgias
splinter hemorrhages
rashes
peripheral eosinophilia lasting 1 month in heavy infection
Occasional life-threatening manifestations:
myocarditis
central nervous system involvement
pneumonitis
Migration phase
myalgia and weakness o followed by subsidence of symptoms
Larval encystment
abdominal tenderness and pain
weight loss
weakness
mucoid or bloody stool
A. Trichuris trichiura
Cosmopolitan
Tropical and subtropical countries with warm and moist soil.
A. Trichuris trichiura
Global
604 to 795 million
o Children
A. Trichuris trichiura
Phlippines
4.5 to 55.1%
o preschool children
8.1 to 57.9%
o school-age children
A. Trichuris trichiura
Natural host: Humans
A. Trichuris trichiura
morphologically similar worms are found to infect:
o pigs
o dogs
o some monkeys
A. Trichuris trichiura
At risk: ↑ children
A. Trichuris trichiura
Area: poor sanitation practices are common
o open defecation
o night soil as fertilizer
A. Trichuris trichiura
Mechanical vectors:
o House flies
o Cockroaches
A. Trichuris trichiura
Symptoms
severe protein-losing enteropathy and hypoalbuminemia
malabsorption of fats and sugars
decreased excretion of xylose
low serum potassium, sodium and calcium
high levels of IgE
Serious cases may be fatal in 2 weeks to 2 months.
B. Capillaria philippinensis
Endemic
o Ilocos Norte, Ilocos Sur, Cagayan, La Union, Pangasinan, Zambales, Agusan del Norte, Leyte
o More: Zamboanga del Norte
o Few:
Zamboanga del Sur
Agusan del Sur
Misamis Occidental.
B. Capillaria philippinensis
Twice as many males as females become infected.
B. Capillaria philippinensis
Males are mostly fishermen who partake of the days catch.
B. Capillaria philippinensis
Definitive host/Reservoir: Fish-eating birds
Intermediate host
o fresh or brackish water fish
B. Capillaria philippinensis
Migratory birds
o parasite is widely distributed throughout Asia and elsewhere
B. Capillaria philippinensis
deposition of eggs in the liver parenchyma causes:
o granuloma formation and liver necrosis, which in heavy infections can lead to potentially fatal liver dysfunction
C. Capillaria hepatica
Cosmopolitan in wildlife
o Human cases have originated from all inhabited continents except for Australia, although it exists in wildlife
C. Capillaria hepatica
The prevalence in humans may be underestimated due to the nonspecific clinical presentation and difficulty of diagnosis
C. Capillaria hepatica
Typical host: rodents such as rats
o has a low host specificity
C. Capillaria hepatica
Infections have also been identified in:
o wild and domestic carnivores o humans
C. Capillaria hepatica
contaminated food is ingested
human feces are not the source of contamination
feces of carnivores or flesh-eating rodents are involved
C. Capillaria hepatica
Other symptoms vary depending on the location and number of larvae present
D. Trichinella spiralis
Cosmopolitan
o most common in Europe and America
o rarely reported in the tropics
D. Trichinella spiralis
It occurs particularly in members of the meat-eating population but the prevalence is low
D. Trichinella spiralis
pig
deer
bear
walrus
rat
D. Trichinella spiralis
ingestion of contaminated pork scraps by pigs
D. Trichinella spiralis
ingestion of contaminated infected rats by pigs – ubiquitous in pig farms
D. Trichinella spiralis
ingestion of contaminated meat by other animals
D. Trichinella spiralis
ingestion of contaminated pork meat by humans
o Cooking meat to 60ºC or freezing (20 days in a normal freezer or at - 20°C for 3 days) will kill larvae.
o Smoking, salting or drying the meat does not destroy the infective larvae.
D. Trichinella spiralis
The Trichinella cycle that is maintained in nature occurs among cannibalistic and carrion-feeding carnivores
D. Trichinella spiralis
Giant intestinal worm
A. Ascaris lumbricoides
Infection is caused by ingestion of embryonated eggs.
A. Ascaris lumbricoides
Larvae invade the intestinal mucosa, and are carried via the portal, then systemic circulation on to the heart, then into the lungs
A. Ascaris lumbricoides
The larvae break out of the capillaries into the alveoli.
A. Ascaris lumbricoides
The larvae (L4s) mature further in the lungs (10-14 days), after a molt, penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed.
A. Ascaris lumbricoides
Upon reaching the small intestine, they develop into adult worms.
A. Ascaris lumbricoides
Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female.
A. Ascaris lumbricoides
Adult worms can live 1 to 2 years.
A. Ascaris lumbricoides
Unfertilized eggs may be ingested but are not infective.
A. Ascaris lumbricoides
Larvae develop to infectivity within fertile eggs after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil).
A. Ascaris lumbricoides
Clinical manifestations of ascariasis are caused by the (?) of the:
o Larvae
o adult worms in the small intestine
o wandering adult worms
pulmonary migratory phase
The (?) causes allergic reaction.
larval migration