Intestinal Nematodes Flashcards
Adenophora class
T. trichura & T. spiralis
Truchuris trichura AKA
also known as the “whip worm”
T. trichura adults live inside
the large intestine and rectum
Embryonation of T. trichura eggs occurs in:
moist, warm, shady soil
Infection of T. trichura
ingesting embryonated eggs on salad vegetables, fruit, in water or in soil
T. trichura Larvae to adults:
Larvae hatch in small intestine and become adults in the cecum
Adults burrow inside mucosa, where they consume RBCs
2 requirements for the worm to become a serious health problem
poor sanitation (human feces are deposited on the soil)
physical factors that allow their survival and development (warm climate, high rainfall and humidity, moist soil and dense shade)
T. trichura adults pass ________
unembryonated eggs in feces
_____ may coexist with _____
Trichuris
Ascaris
It’s the 2nd most common infecting nematode in the US
Trichuris
Pathogenesis in Trichuris
Trauma to the mucosa can cause chronic hemorrhage that may result in anemia and bloody stools
Symptoms on Trichuris
Abdominal pain, insomnia, vomiting, prolonged diarrhea, weight loss, nausea, rectal prolapse
Dx of Trichuris
ID of a worm or egg in the stool
Eggs have 2 distinct opercular plugs
Treatment of Trichuris
Albendazole and mebendazole
Prevention and control of Trichuris
thorough washing of salad vegetables
Washing hands
Sanitary disposal of feces
smallest nematode parasite of humans
Trichinella spiralis
Trichinella spiralis causes a ____ infection called _____
Zoonotic
Trichinosis
Trichinella spiralis is _____ in host specificity
Low
In Trichinella spiralis uterus is filled with _______ in _______ region; _____ region contains ___________
developing eggs; posterior
anterior; fully developed, hatching juveniles
In trichinella Life cycle is unusual in that the same animal serves as:
both definitive and intermediate host: larvae and adults are found in different organs
human infection of T. spiralis is contracted from:
the consumption of poorly cooked pork, infected with larvae (nurse cells)
T. spiralis larvae to adults:
Larvae are swallowed, reach SI where they excapsulate, molt and then enter the intestinal mucosa
Copulation occurs, Males die after. Females give birth and then die shortly after
After juveniles are birthed:
T. spiralis
Juveniles are carried away by the hepatoportal system –> the liver –> the heart –> lungs –> arterial system, which distributes them throughout the body
Through out migration (T. spiralis):
Juveniles can become lodged in any tissue
If T. spiralis juvenile end up in striated muscle tissue:
diaphragm, jaws, larynx, eyes, tongue
they penetrate individual muscle fibers and begins to grow, eventually forming a nurse cell
Most susceptible are muscles to least
eye and tongue, then the jaw muscles, then diaphragm, and finally muscles of the arms and legs
After ~1 year:
T. spiralis
host reactions begin to calcify the cyst walls and eventually the worms themselves
Sylvatic trichinosis
occurs between wild carnivores and their prey. Bears, foxes and raccoons are often infected
Urban trichinosis
It occurs primarily as a triangle between humans, rats, and pigs
Trichinosis triangle
rats maintain infection via cannibalism
Pigs get infected by eating rats
humans get infected by eating pigs
Trichinosis is rare in:
jews, hindus, muslims and vegetarians
Pathogenesis of T. spiralis in 3 stages:
(1) mild during penetration of adult females into the mucosa
(2) severe during migration of juveniles, (constituting the primary symptoms)
(3) moderate during penetration and encystment in muscle cells
Symptoms of stage 1 in T. spiralis
intestinal inflammation and pain, nausea, vomiting, sweating and diarrhea
red blotches on skin, facial edema, fever
Symptoms of stage 2 in T. spiralis
damaged blood vessels, pneumonia, pleurisy, encephalitis, meningitis, nephritis, deafness, and loss of vision
Death occurs via:
myocarditis or heart and kidney failure and respiratory complications
Symptoms of stage 3 in T. spiralis:
intense muscular pain
difficulty breathing and swallowing, and cardiovascular, excretory, and nervous disorders
dx in T. spiralis:
Immunological tests
Xenodiagnosis
Treatment of T. spiralis:
mebendazole (against muscle larvae) & pyrantel pamoate (against adult worm)
Prevention and Control
Fully cook pork before eating
Education on fully cooking pork before serving
Laws preventing feeding of uncooked waste to pigs have greatly reduced the disease in the US
Hook works spp
Ancylostoma duodenale (old-world) Necator americanus (new-world)
Buccal capsule in A. duodenale
2 pairs of teeth on the ventral wall of its capsule
Buccal capsule in N. americanus
pair of dorsal and a pair of ventral cutting plates surrounding the smaller buccal capsule
Life cycle of hookworms (eggs - L3 stage)
eggs are passed in feces
in the proper envt, they will develop and hatch into rhabditiform larvae (L2) (feeding stage)
molts into filariform larvae (L3) (non-feeding stage) which moves to surface when soil is wet where they penetrate human skin
Migration (hookworms)
human skin –> lymphatic system –> lungs (via heart and pulmonary circulation) –> alveoli –> glottis –> coughed up and swallowed
Once adult hook worms are swallowed:
They arrive in SI and attach to mucosal lining where they molt into L4 stage they feed off of blood and sexually mature
4 factors lead to hookworm infection:
shaded sandy and loamy soil
moisture in form of precipitation
poor sanitation
contact with contaminated soil
3 stages of hookworm disease:
1) Invasive
2) Pulmonary
3) Intestinal
Invasive:
hookworm
hemorrhage and swelling with intense itching at entry site
Secondary infection possible
ground itch
Pulmonary:
hookworm
pneumonitis, burning sensation in the chest, dry cough, and other symptoms of bronchial pneumonia
Intestinal:
hookworm
most important period of pathogenesis.
Cause bleeding and ulceration of mucosa
Anemia resulting in geophagy
Intermittent abdominal pain
loss of appetite
Heavy infection of hookworm:
malnutrition, anemia and mental dullness
Chronic malnutrition from hookworm infection often causes irreversible damage, resulting in:
weakness, stunned growth and below-average intelligence
Dx of hookworm
presence of eggs or worms in feces
Smear of feces on filter paper stored in tube allows to observe hatching larvae
Treatment (hookworm)
Mebendazole
Iron therapy
Prevention (hookworm)
Wear shoes
Wear protective clothing while gardening
Washing salad vegetables or fruits well
Control (hookworm)
Control involves an increase in sanitary conditions
regular chemotherapeutic campaigns
proper elimination of dog feces for N. a.
broad public education
Creeping eruptions
Caused by A. braziliense (cat) or A. caninum (dog)
Penetrate human skin but are incapable of migrating to the intestine
Cause trauma to the skin before they are killed by immune system
Largest nematodes
Ascaris lumbricoides
Ascaris lumbricoides eggs in uterus
Uteri may contain > 27 million eggs at a time, with 200,000 being laid per day
Ascairs eggs have a ______ outer layer which allows them to be _______
Mammilated
Resilient
Ascaris lifecycle
Unembryonated eggs passed in feces, in soil they develop if optimal conditions are present
Although the eggs are resistant to ____ temperature, ________, and strong _____, _________ is retarded by such factors
low
desiccation
chemicals
embryonation
Infection with Ascaris occurs when
embryonated eggs are swallowed with contaminated food and water
Once Ascaris eggs are ingested
Eggs containing 2nd stage larva hatch in the small intestine, penetrate mucosa/submucosa, enter lymph/circulatory system and migrate from liver –> right heart –> lungs
During ascaris migration:
many worms get lost and accumulate in every possible organs of the body, causing acute tissue reactions
Ascaris in lungs:
juveniles molt twice and emerge from pulmonary capillaries –> alveoli –> trachea –> glottis –> SI via coughing and swallowing
Ascaris in SI:
4th stage larvae mature and sexually reproduce
Proposed reasons why ascaris travels back to intestine where they originated
(1) migration simulates an intermediate host
(2) ancestor was a skin penetrator for which the migration (L2 -> L3 -> L4) was a developmental necessity
Prevention/control for Ascaris
Organism is difficult to control because eggs are so resistant and eggs can be carried by wind-borne dust
Avoid/wash raw vegetables
Proper disposal of feces
Regular chemotherapy to carriers
Pathogenesis in Ascaris (lungs)
When juveniles emerge from capillaries they cause hemorrhage
Ascaris causes what type of pneumonia
Loeffler’s pneumonia - small pools of blood clog air spaces, accumulation of WBCs and dead epithelium add to respiratory congestion
In heavy intestinal Ascaris infections:
In children, protein malnutrition is common.
Intestinal obstruction results in severe abdominal pain, loss of appetite, nausea and vomiting
Dx for Ascaris
ID of eggs in feces as well as egg counts
Xray of abdomen
Treatment for Ascaris
None for juveniles piperazine citrate for adults Albendazole and mebendazole Surgery IV fluids
Enterobius vermicularis AKA
Pin worm or Seat worm
Does Enterobius vermicularis have an intermediate host?
NO
Adult Enterobius vermicularis live in:
ileocecal region of intestine
Enterobius vermicularis adults commonly travel throughout:
GI tract (stomach to anus)
Infection of E. vermicularis usually occurs via:
ingestion of eggs containing 3rd stage juvenile
Adult E. vermicularis feed off of :
Bacteria and epithelial cells
Life cycle (E. vermicularis):
Gravid female migrates out of the anus and lays sticky eggs at night
Female and male survival (E. vermicularis)
Males die after copulation females die shortly after they lay eggs or sometimes burst open while laying eggs
Eggs deposited on the anal skin in E. vermicularis:
Causes pruritus - intense itching and swelling
Eggs can be ______
Inhaled
When inhaled, eggs may remain in the nose until they hatch
retroinfection
If the perianal or vaginal folds are unclean for long periods, the attached eggs may hatch and juveniles wander into the anus and back into the intestine
If E. vermicularis is ingested:
the larvae slowly move down the small intestine, molting twice to become adults by the time they arrive at the SI-LI junction
Heavy infections of E. vermicularis in children result in:
sleeplessness, weight loss, hyperactivity, grinding of teeth, abdominal pain, and vomiting
e most common nematode parasitizing humans in the U.S.
E. vermicularis
Dx of E. vermicularis
finding eggs and worms
Examining under flash light either early or at night
Treatment of E. vermicularis
Albendazole and mebendazole
How to confirm treatment in E. vermicularis:
cellophane tape is pressed against the perianal skin, then removed and pressed against a glass slide for exam.
Negative results for 7 consecutive days means the patient is cured
Prevention and control in E. vermicularis:
Frequent washing of hands, bed sheets and clothes in hot water are strongly recommended.
Since eggs can survive for days in moist, cool home, everyone in the infected household should be properly treated
