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56 Cards in this Set
- Front
- Back
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Describe basic characteristics of all nematodes that are human parasites
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Separate sexes (male smaller than female)
Egg production varies species to species |
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Describe the general life cycle of intestinal nematodes.
How mant stages? |
5 successive stages:
4 larval stages and adult stage |
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Describe the general life cycle of intestinal nematodes.
Infective stage? |
Usually 3rd stage larva
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Describe the general life cycle of intestinal nematodes.
How do eggs/larvae in intestine get out? |
Passed out by feces
Or can be deposite on the perianal skin by female worm |
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Describe the general life cycle of intestinal nematodes.
What happens when the eggs are passed out of the body? |
They are either fully embryonated or require an extended period of egg embryonation in the soil
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What happens if someone ingests a non-embryonated egg?
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Nothing, non-embryonated aggs arent infective
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What is the most common ascaris species that infects humans?
What disease does it produce? |
Ascaris lumbricoides
Disease: Ascariasis |
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Describe the development of Ascarids
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4 larval stages (L1-L4)
Larval morphology resembles adult worms Transition from one larval stage to the next requires shedding of surface cuticle (molting) Most species undergo 4 molts |
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Describe the Ascaris life cycle
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1) Female adult worm releases the eggs
2) Eggs passed out in feces: can be fertilized or no fetilized -->Unfertilized eggs don't undergo biological development Steps 1 & 2 are the diagnostic stages 3) Egg grows, contains larva (infective stage) 4) Ingest egg 5) Larva grow in intesting 6) Larva migrate out of intestine to lung 7) Larva migrate |
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What are the 3 clinical phases of ascaris infection?
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Lung phase
Intestinal phase Wandering worm |
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Describe the lung phase
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5-6 days after exposure
-Pneumonitis (Loeffler's penumonia) due to penetration of lung capillaries by juvenile parasite causing hemorrhage |
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Dsecribe the intestinal phase
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2-3 months after infection
-Abdominal pain, diarrhea -Malabsorption of nutrients -Stunted growth, cognitive impairment -Intestinal obstruction by high worm number |
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Describe how wandering worms cause pathogenesis
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Intestinal perforation: peritonitis
Blockage of bile ducts Obstruction of respiratory tract Liver abscesses |
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How is pathology really caused by Ascaris?
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Larva (wandering worms)
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How many ppl are currently infected with ascaris?
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>1.3 billion
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Where is ascaris infection prevalent?
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Tropical countries
Socio economic depressed areas of Europe, Latin America, Asia -73% of all infections in Asia -in some areas, 100% of ppl are infected |
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How is this worm transmitted?
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Ingestion of contaminated food, water, soil
Using human feces as fertilized --> contaminate vegetables |
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Which group of people have the highest rate of infection for ascaris?
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Children
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When does the intensity of this parasitic infection peaks?
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5-15 years follownig infection
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Describe the eggs of Ascaris
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Egg shell has a lipid layer
.: Extremely resistant to chemicals Long lived in soil (up to 15 years) Eggs are sticky and can be transmitted by windborn dust |
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How many ascaris eggs are produced/day worldwide?
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10^14
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What is the best diagnosis for this infection?
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Check for eggs in feces
->Female produces 200,000 eggs/day .: easy to find |
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What is the best chemotherapy for ascaris infection?
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Benzimidazoles: Mebendazole
or Ivermectin |
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What do benzimidazoles do?
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Bind to tubulin and block muscle action
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What are the beneficial effects of drug treatment on children?
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Weight and appetite gain
.: chemotherapy inc weight gain and appetite |
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What kind of immune response is associated with ascaris lumbricoides infection?
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Polarized cytokine response
-->Th2 response important |
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Which cells proliferate in response to ascaris antigens?
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PBMC
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What IL's are increased following ascaris infection?
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IL-4 and IL-5 produced by PBMC in infected ppl
(small increase in IFN-y, slight decrease in IL-10) |
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What is IL-5 responsible for?
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Eosinophilia
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What happens to the IL4/IL5 to IFN-y ration following ascaris infection?
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Increases ratio of cell produccing Th2 : Th1 cytokines
Get a lot more IL-4/5 than IFN-y |
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What happens to the frequency of PBMC producing IL-10, IFN-y?
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Nothing
Also no effect on IFN-y levels (its just that levels of IL4 and IL5 increases) ->Mixed Th0/Th2 response) |
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How can a Th2 environment effect host rsponses to other pathogens?
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L3/L4 are lung stage parasites
Th2 response in lung effect the host response to TB |
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Which Ab is increased in ppl infected with ascaris?
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IgE
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What are the 3 visceral larva migrans?
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Baylisascaris procyonis
Gnathostoma spinigerum Strongyloides stercoralis |
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Describe Baylisascaris procyonis
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Found in raccoons: causes serious disease in humans in N.A
Larva invade eyes (ocular larva migrans), spinal cord, brain (neural larva migrans) and in the intestine (Visceral larva migrans) ->NO effective treatment |
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Describe gnathostoma spinigeru
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Found in dogs and cats
Endemic in China/Phillipines Humans infected by ingestion of raw/poorly cooked/ pickled freshwater fish, chicken, birds, frogs or snakes Larva migration including pulmonary, GI, urogenital, ocular, otohinolaryngeal and cerebral tissues |
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What kind of infection is toxocariasis?
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Visceral larvae migrans (VLM)
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What causes toxocariasis?
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Infection of humans with ascarids of dogs (T. canis) or cats (T. catis)
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How is toxocariasis transmitted?
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Ingestion of embryonate Toxocara eggs in food/soil
-->Eggs are long lived (like Ascaris) |
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What happens if Toxocara larvae do not develop into the adult stage?
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Wander through the body
Migrate to soft tissues (liver, brain) or eye Can cause blindness |
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Describe the life cycle of Toxocara
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Eggs ingested by dogs
Larvae released in intestine (can be passed in feces) Goes through circulation Adults live in lumen of intestine Eggs passed in feces Eggs exposed to external env't, become embryonated with larva Eggs ingested by other hosts (ex Humans) Larvae released in intestine Goe into circulation Larvae migrate to various organs where their development is arrested In pregnant and lactating dogs, the larvae can be reactivated |
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What can happen following reactivation of larvae in pregnant/lactating dogs?
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Intestinal infection in mother
Infection of offspring, through transplacental and transmammary transmission |
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What happens when some larvae decide to wander in tisses?
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VLM
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What causes systemic visceral larvae migrans?
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Invasion of soft tissues by wandering larvae
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What pathogenesis is involved in systemic VLM?
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Hepatomegaly
Pulmonary/neurological symptoms eosinpophilia |
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What is ocular toxocariasis caused by?
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Invasion of the eye tissues by the larvae
Juveniles cause chronic inflammation Granulomas of retina (may cause blindness) |
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When do ascaris cysts become infective?
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Couple of days after shedding
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Where is Toxocarous most incident?
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Among children
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What increases the risk of human infection?
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Infection of dogs/cats
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How is toxocariasis diagnosed?
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Faecal egg count
ELISA using ES antigens high eosinophilia is suggested |
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What chemotherapy is used for Toxocariasis?
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Mebendazole
Also recommend: regular deworming of dogs/cats; dispose of feces and clean up after dog |
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Why is trichuris suis rising in importance?
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Might be safe and effective treatment vs IBD
->Causes a Th2 response that diverts Th1 response (which is responsible for the inflammation) |
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What kind of a worm is trichuris?
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Whip worm
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Compare Ascaris, Filaria and Schistosoma:
T cell cytokine responses |
A: Th0/2 in infected subjects
F: Th0/2 in asymptomatic, MF patients S: Th0/2 in resistant subjects |
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Compare Ascaris, Filaria and Schistosoma:Ab response?
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A: IgG1> IgG3, IgE, No IgG4
F: IgG1/4 > IgG2/3 S: high IgE, G1, G4 Low IgG2/4 |
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Compare Ascaris, Filaria and Schistosoma:
Correlation? |
IgG1/2 correlates with egg cpimts (infection). Suggests IgG1, IgG2 are non protective
F: High IgG4 linked to low pathology (IgG4 dampens pathology and disease) S: Low IgG4 linto to R to infection. IgE/G1/G3 protect against infection, not disease |
