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346 Cards in this Set
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What is the standard lab order for a pt suspected to have a worm infection?
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microscopic exam of the feces. sweet. Looking for O&P. ova and parasites. wooot.
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What types of round worms are there?
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intestinal roundworms and tissue roundworms
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What types of flatworms are there?
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tapeworms and flukes
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What cell plays a major role in the immune response against worms?
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Eosinophils. Eosinophilia doesn't necessarily occur when there are worms in the intestins or infections with protozoa but it is commonly associated with worm infection.
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Structural overview of round worms
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A number of tubes within an outer tube. Outer tube is an impermeable cuticle and within the outer tube are tubular gonads and intestines.
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In what form do round worms release offspring
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most lay eggs. Some release live larvae.
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Host of enterobius vermicularis
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humans only
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type of infection enterobius vermicularis causes?
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asymptomatic or minor intestinal worm infection
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sx of infection with enterobius vermicularis
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usually none of anal itch
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Describe the life cycle of Enterobius Vermicularis
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1) Human is infected by ingesting infectious (embryonated) eggs. The eggs hatch in the small intestine and become mature adtuls in 6 weeks migrating to the cecum.
2) The adults mate and the female produces ~10,000 eggs. The pregnant female crawls through the anal sphincter and deposits all of her eggs on the perianal skin then dies. THESE EGGS ARE UNEMBRYONATED (and therefore non infectious). 3) However, in 6 hours these eggs become infectious (thus embryonated). Some components cause a perianal itch which results in contamination of kids' fingers and thus ingestion and continued infection. Infectious eggs may become widely disseminated but the enviro eggs remain infectious for less than 2 weeks. 4) The cycle continues with the eggs hatching in the small intestine. |
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Epidemiology of enterobius vermicularis infection
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COMMON!!
30% of kids 15% of adults. Kids have an average of 50 worms. |
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What is a complication of enterobius vermicularis?
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Pinworm neurosis.
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What is a common name for enterobiius vermicularis?
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pinworm.
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How should enterobius vermicularis be treated?
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Mebendazole cures most infections and the whole family should be treated and retreated about 3 weeks later.
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What is ascaris lumbricoides?
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intestinal roundworm that can grow up to 35cm in length.
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Describe the lifecycle of ascaris lumbricoides
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1) humans ingest embryonated eggs from human fecal contamination.
2) tiny larvae hatch in the small intestine AND penetrate the portal circulation. 3) The larvae move through the circulation and are trapped in lung capillaries. They then break out into the alveoli and do most of their maturing here. 4) The larvae then make their way up the respiratory tree to the mouth and are swallowed. (you can imagine the coughing that is helping this movement). 5) The larvae mature to adults in the small intestine (their second stay here). 6) Once mature they mate and begin producing eggs about 2 months after the original infection. 7) The eggs are excreted in the feces and mature to the fully embryonated infectious form in about 3 weeks. **If you don't have a mature female and male in the intestines at the same times then you don't have mating happening. |
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What is the diagnostic stage of ascaris lumbricoides?
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It is the egg in the feces. Unmated females lay non fertilized eggs. You will see an undeveloped unicellular embryo with a thick, yellow-brown bile-stained shell and a lumpy-bumpy surface.
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What kind of symptoms may be present in light infections in children?
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often asymptomatic.
May show malabsorption of ingested nutrients. |
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What are symptoms of heavy infections with ascaris lumbricoides?
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substantial malabsorption, intestinal obstruction by a knotted mass of worms, biliary obstruction from a worm in the bile duct, pancreatic obstruction, and hemorrhagic pneumonitis (can happen during the phase of larval migration)
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General signs and symptoms of infection with ascaris lumbricoides besides being asymptomatic
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passage of an adult worm through the anus.
abdominal pain, nausea, vomiting fever eosinophilia (only during larval migration through the lung) pneumonitis (only during larval migration and only in heavy infections) Obstructions. |
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epidemiology of ascaris lumbricoides
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very common in the tropics and occasionally seen in the USA (especially southeast). The female produces ~200,000 eggs per day and they are stable to freezing but destroyed by sunlight or drying. They can remain infectious for months!!! Most ascaris infections in NE are due to pig worms.
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Tx of ascaris lumbricoides
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mebendazole
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How do you prevent ascaris lumbricoides?
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sanitary disposal of feces
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What are ancylostoma duodenale and necator americanus?
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They are hookworms!! Just depends on your location for what kind is more likely to be plaguing you. Ancyclostoma- mostly Europe and Asia. Necator- mostly Africa and western hemisphere
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What is the life cycle for the ancylostoma and necator hookworms?
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1) Infectious larvae in soil or wet vegetation penetrate the skin and enter the blood.
2) The larvae exit from the alveolar capillaries and partially mature in the alveoli (similar to ascaris). 3) The late stage larval worms ascend the respiratory tree and are swallowed (also similar to ascaris). 4) Mature is completed in the small intestine. It is here that the male and female mate and the female lay eggs. 5) the eggs are excreted in the feces and hatch to release the free-living larvae. 6) the free-living larvae mature into infectious larvae that survive less than 6 weeks. |
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What is the diagnostic stage of ancylostoma and necator hookworms?
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The egg in the species is the diagnostic stage. Looks the same in both species. Thin shell with early stage of devolopment. Looks like a blastocyst or something. Older eggs contain a larva.
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What is ground itch / dew itch that is seen in ancylostoma and necator infections?
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it is the site of entry. The larvae produce a papule and erythema. If there is heavy infections may even give rise to transient pulmonary symptoms with eosinophilia.
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How big are hookworms when they are adults and what do they do once in the body?
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Females are about 1cm long, the male is slightly smaller.
The adults attach to the mucosa of the small intestine by their mouth and secrete an anticoagulant while sucking blood. Females lay about 10,000 eggs a day. adult worms live like this for about 5 years. |
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What are the sx of light and heavy hookworm infections?
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Light- often asymptomatic.
Chronic, heavy- often cause anemia esp. with marginal iron deficiency to begin with. Children may be physically and mentally retarded as a result of severe chronic anemia. |
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epidemiology of hookworm infections
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prevalent in tropical and warm temperate regions. In the rural southeastern US only a few percent of kids are infected but that is decreased from 100 years ago when it was much more prevalent in this country.
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Tx of hookworm infection
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mebendazole.
May need other measures to treat the anemia such as iron supplements or transfusion. |
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prevention of hookworm infection
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sanitary disposal of human feces and wearing shoes.
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Host of strongyloides stercoralis
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humans
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What makes the lifecycle of strongyloides stercoralis so very complicated?
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the fact that it is 3 lifecycles interrelated and connected to each other. it's crazy talk.
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Describe the strongyloides stercoralis parasitic lifecycle
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This part is a lot like the hookworm cycle.
1) infectious larvae penetrate the skin and enter the blood stream. 2) larvae exit at the alveoli and partially mature there. 3) partially mature larvae ascend the respiratory tree to the mouth and are swallowed 4) larvae mature into adults that are hermaphrodites!!! They don't need anyone else for their sexual mating fun. 5) one month after infection the fertilized adults burrow in the mucosa of the small intestine and start laying eggs. These eggs hatch in the intestine and newly hatched larvae are excreted in the feces. 6) excreted larvae mature into infectious larvae. |
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Describe the free living cycle of strongyloides stercolaris
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1) Excreted larvae differentiate into non-parasitic males and females.
2) these free living gender differentiated adults mate and lay eggs which hatch and yield more free-living forms that mate and lay more eggs etc. 3) some larvae progeny of the free living forms differentiate into infectious larvae and infect humans. |
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Describe the autoinfection (hyperinfeciton) life cycle of strongyloides stercolaris.
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1) newly hatched larvae mature into infectious larvae in the intestine and penetrate the intestine wall or the perianal skin.
2) These larvae then enter the parasitic cycle where they end up in the alveoli by following the bloodstream. 3) Most people infected by S. stercoralis have a long (lifelong?) infection maintained by the autoinfection cycle. |
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diagnostic stage of strongyloides
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larva in the feces
the larve is about .25mm. It has a short buccal cavity, an hourglass esophagus and genital promordium and an anus identifiable under a microscope |
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How large is the adult strongyloides?
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2mm
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Sx of light and heavy strongyloides infections
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light- asymptomatic
heavy- mild cutaneous and pulmonary sx associated with the pulmonary phase of the life cycle. Intestinal sx predominate with diarrhea, nausea, abdominal pain, and eosinophilia. |
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What is one of the consequences of adult strongyloides persisting in the intestine even after they die?
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low grade infection with eosinophilia even decades later because of autoinfection. Often those with autoinfection also have recurrent gram negative bacteremia resulting from E. Coli carried by larvae penetrating the intestinal mucosa.
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If a person is infected with strongyloides and they are immune compormised and continue to autoinfect... what is one potential consequence?
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They can get a HYPERINFECTION which includes high fever, dyspnea, and gram negative septicemia.
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Tx of strongyloides infections
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REQUIRED even if asymptomatic b/c of the danger of hyperinfection.
Thiabendazole is used. (ivermectin is the best but don't care about this for the exam) |
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What is the geographic distribution of strongyloides?
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same as that of the hookworm.
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How do you prevent strongyloides infection?
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control fecal contamination and wear shoes.
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What is larva migrans?
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series of syndromes caused by human infection w/ larvae of an intestinal roundworm species that do not recognize humans as natural hosts. Because of this there is no intestinal phase. There are 2 forms: visceral and cutaneous.
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What are accidental hosts?
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unnatural hosts that do not allow parasites to progress through the life cycle. Larvae wander until they die.
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What causes visceral larva migrans?
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ascaris-like intestinal round worm of dogs (sometimes but less commonly from cats).
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What is the life cycle of the worms involved in visceral larva migrans?
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similar to that of ascaris lumbricoides... it crosses the placenta which is why nearly all puppies and kittens have to be de-wormed.
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Whom is most infected with viceral larva migrans?
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children under the age of 4 who ingest embryonated dog or cat round worm eggs
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What happens after a child ingests an embryonated round worm egg in visceral larva migrans?
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the larvae penetrate the intestinal mucosa and enter the portal circulation.
they exit at the liver and elsewhere and begin wandering through the tissues. Many infections are asymptomatic. |
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If a child has symptomatic visceral larva migrans what sx might present?
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Eosinophilia
fever hepatomegaly eosinophilic granulomata surrounding dead larvae. retinal involvement can occur and may mimic retinoblastoma. |
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How is dx of visceral larva migrans made?
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hx of dog contact and / or pica, positive tests for antibody to specific worm antigens and a liver biopsy to detect migrating larvae
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Tx of visceral larva migrans
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albendazole. Most symptomatic cases are self-limiting in less than a year as the larvae become enclosed in granulomata
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Prevention of visceral larva migrans
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avoiding dog feces and treating dogs to eliminate their round worms.
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What causes cutaneous larva migrans?
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dog and cat hookworm... life cycle like the hookworm cycle in humans
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How does cutaneous larva migrans work in humans?
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humans are infected by infectious larvae which creep along making intracutaneous tunnels with attendant local itching and inflammatory response. They move 1cm per day or less. The disease is self-limiting. The larvae die in less than 2 months. The larval track leaves a scar.
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What is another name for cutaneous larva migrans?
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creeping eruptions
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How is cutaneous larva migrans diagnosed?
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observing the characteristic lesions
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What is the geographic distribution of cutaneous larva migrans?
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It is worldwide but prevalent in the southeastern USA
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Tx of cutaneous larva migrans
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thiabendazole.
Dogs should be checked for hookworms and treated if positive!!! |
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What female roundworms release live larvae instead of laying eggs?
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Trichinella spiralis
Dracunculus medinensis (guinea worm) Filarial infections: -wuchereria bancrofti (elephantiasis) -Onchocerca volvulus (river blindness) |
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What is the host and target tissue of trichinella spiralis?
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Carnivores and omnivores... target the skeletal tissue.So when each host eats skeletal muscle from a previous host it ends up with adult worms in the intestine and then encysted larval progeny in the skeletal muscle
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What causes symptoms in trichinella spiralis infection?
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larval migration and encystment in muscle
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Describe the life cycle of trichinella spiralis
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1) Humans eat undercooked pork or bear or other carnivore (LION! haha kidding) with encysted T. spiralis larvae in the muscle cells.
2) Larvae are released in the small intestine, invade the mucosa, and mature. The male fertilizes the female about 2 days after infection, and she burrows in to the intestinal mucosa. 3) 5 days after infection, the female begins to release live larvae, which enter the blood and are disseminated throughout the body. Larvae are released for about 1 month. 4) Larvae enter cells of straited muscle and grow to maximal size in the next 3 weeks. The larvae are enclosed a fibrous capsule of host cell origin. Larvae die and are calcified with 2 years. |
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What is the diagnostic stage of trichinella infection?
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larval form in the muscle. You will see a coiled larva (potentially calcified around the edge) surrounded by an inflammatory infiltrate in the midst of striated muscle.
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What can mucosal invasion by adult trichinella worms cause?
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diarrhea and gastroenteritis
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What are sx of light trichinella infection?
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mild or asymptomatic (often)!
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What are sx and signs of infection with trichinella?
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pain from larval invasion of skeletal muscle 1-4 weeks after infection.
migration into other tissues that don't support encystment like the heart and brain can cause death eosinophilia periorbital edema diplopia muscle pain headache fever |
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How can dx be made of trichinella?
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Must demosntrate migrating larvae (super difficult) or encysted larvae (usually easy) in a skeletal muscle biopsy. Various serological tests support this dx
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tx for trichinella
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albendazole but doesn't seem to have a proven effect. Steroids may be useful.
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Prevention of trichinella?
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thorough cooking of pork (and the meat of other flesh-eating animals). Freezing for several days kills most larvae. Prevention at the population level depends on not feeding uncooked pork scraps to pigs. This is now illegal in all states but doesn't mean compliance is universal. USDA inspection does NOT TEST FOR THIS VOMIT IN YOUR MOUTH GROSS.
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Incidence of trichinosis?
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fallen a lot in the USA.
can be found worldwide except for Australia and some Pacific islands. |
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Host of filariases
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Intermediate host is a blood-sucking insect.
In the human varieties the human is the definitive host which means we harbor both the adult worms AND their newborn larvae |
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microfilariae aka
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newborn filariases larvae
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Lifecycle of filarial roundworms
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1) Human are bitten by an insect, and mature larvae are injected.
2) Larvae become adults and mate. 3) female releases live first stage larvae (microfilariae) which circulate in the blood or migrate to tissues depending on the style of their species. 4) blood sucking insect lands on an infected host and sucks their blood sucking up some microfilariae which become mature larvae in the insect. They fly off to bite another person and the cycle continues! |
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What does infection with Wuchereria bancrofti cause?
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elephantiasis- results from adult worms all up in the lymphatics
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Intermediate host of Wuchereria bancrofti?
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mosquitoes.
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Sx of light and heavy infection with Wuchereria bancrofti
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Light- asymptomatic
Heavy chronic infection- leads to lymphatic obstruction and elephantiasis. |
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What is the diagnostic stage of wuchereria bancrofti?
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microfilaria in the blood.
Clinical dx of elephantiasis is generally reliable but a definitive parasitological confirmation may be difficult b/c the microfilariae are few in chronic disease. |
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What is the epi of wuchereria bancrofti?
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found in all tropical regions. It is possible that the disease can be eradicated by universal chem over 5 years
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tx of wuchereria bancrofti
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ivermectin
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What is a complication of Wuchereria bancrofti?
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tropical pulmonary eosinophilia... it is a potentially fatal, rare complication characterized by pulmonary infiltrate. Wuchereria bancrofti is a common cause of the syndrome (though that's not to say that this is a common occurrence)
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Prevention of suchereria bancrofti
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protection from mosquito bites
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Intermediate host of onchocerca volvulus
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black fly
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What does onchocerca volvulus cause?
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river blindless- the major pathology is caused by the microfilariae which migrate in tissue.
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How big are adult onchocerca volvulus worms?
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35cm!!!!! (females... males are smaller).
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Where adult onchocerca volvulus worms found in humans?
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subcutaneous nodules at the site of the infecting black fly bite
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What sx do onchocerca volvulus microfilariae cause?
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Dermatitis with severe itching
blindness from chronic keratitis and fibrosis of the cornea, atrophy of the iris and chorioretinitis all caused byt the microfilariae in various parts of the eye. It is thought that the ocular damage has an autoimmune mechanism though too. |
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Geographic prevalence of onchocerca volvulus
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focal areas of tropical Africa, Central and South America
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Dx of onchocerca volvulus
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must demonstrate microfilariae in a skin snip or adult worm in a biopsy of nodules
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tx of onchocerca volvulus
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once a year ivermectin b/c it kills microfiliariae before they can do harm. More efficacious than surgical removal of nodules b/c some nodules may not be detected but the ivermectin does NOT kill adult worms
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prevention of onchocerca volvulus
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protection from fly bites or eradication of black flies
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What are flukes?
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parasitic flatworms that reproduce sexually in humans or other hosts and also multiple asexually in the snail which is an obligatory intermediate host!!!
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Classification of flukes?
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blood flukes with separate male and female forms
hermaphroditic tissue flukes |
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What are schistosomes?
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blood flukes!
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What are the 3 important schistosomes of humans?
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Schistosoma mansoni
Schistosoma haematobium Schistosoma japonicum |
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Describe the life cycle of schistosomes. (same for the 3 species important to humans)
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1) Human skin is quickly penetrated by free-swimming freshwater cercariae.
2) cercariae (infective stage!!!) transform to larval worms and migrate to the lungs and then to the hepatoportal system where they mature further. 3) They enter the mesenteric venules (S. mansoni and S. japonicum) or the bladder venules (S. haematobium) as mated pairs and the females lay eggs in the venules. 4) Some of the eggs make their way to the intestines and are excreted in the feces (S. mansoni and S. japonicum) or make their way to the bladder and are excreted in the urine (S. haematobium). 5) In fresh water, the eggs hatch to yield a ciliated stage. These infect the proper species of snail and multiply extensively to yield many cercariae. |
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What is the diagnostic stage of schistosomes?
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egg in the feces urine or rectal biopsy
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What does the schistosoma mansoni egg look like?
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The diagnostic stage egg has a large lateral spine. Depending on how the egg is turned it may be obvious or not. May be difficult to distinguish. Will see the ciliated stage inside.
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What does the schistosoma haematobium egg look like?
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The diagnostic stage egg has a large terminal spine. Therefore no matter how the egg is turned the terminal spine should be visible. The ciliated stage will be seen inside the egg.
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What does the schistosoma japonicum egg look like?
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The diagnostic stage has a small lateral spine. It looks more round instead of oval like the S. mansoni egg that has a large lateral spine. inside will be seen to look like a ciliated stage.
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What is the timeline for schistosomal infection sx emergence?
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3-6 weeks.
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How do patients with acute schistosomiasis present?
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typically travelers.
Present ~6 weeks after exposure: fever, flu-sx (malaise, fever), hepatosplenomegaly, lymphadenopathy, eosinophilia, respiratory, urticaria |
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What causes pathology in schistosomiasis?
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chronic damage caused by the immune response to eggs in various tissues. The worms live for decades. They cloak themselves with human antigens to avoid an immune response.
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How many eggs do female schistosomas produce?
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1,000 eggs / day.
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In schistosomiasis, what happens to the migrating eggs that don't make it to the intestine or bladder?
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They become trapped in veins or tissues (most of them don't make it). They are especially trapped in the liver and provoke an intense cell-mediated response with granuloma formation. This damage compromises blood flow which causes other damage.
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What is one of the major complications of schistosomiasis eggs in the liver?
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Eggs that are trapped in the liver cause portal fibrosis aka pipestem fibrosis which results in portal HTN and esophageal varices with hepatomegaly and sometimes splenomegaly. Portal-systemic collateral circulation may circumvent the liver and deposit eggs in the lungs. A few eggs may escape deposition in the lungs and end up trapped in the CNS vasculature where they cause severe damage.
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What do eggs of S. haematobium cause?
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They cause chronic urinary tract disease and induce bladder tumors. Obstructed urine flow yields hydronephrosis. Calcification of S. haematobium eggs in the bladder reduces its ability to expand.
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What 4 sx should make you suspect schistosomiasis?
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Eosinophilia
hepatosplenomegaly bloody vomit hematuria |
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What is most important aspect of hx in schistosomiasis?
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geographic hx- traveling? recent move?
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geography of S. mansoni
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Northern Africa
Arabia South America some Caribbean islands |
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geography of S. haematobium
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Africa
Middle East |
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geography of S. japonicum
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China
Japan Southeast Asia |
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Besides geography what other piece of hx is very important in schistosomiasis infection?
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Hx of contact with fresh water. Not momentary contact though.
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How do you diagnose schistosomiasis?
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look for eggs in stool, urine, or rectal biopsy. the 3 eggs have distinctive morphologies so pay attention when looking under the microscope.
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How do you prevent schistosoma infection?
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avoid contact with contaminated water. The life cycle can be broken by sanitary disposal of feces and urine.
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How do you tx schistomiasis?
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Praziquantel
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What is another name for schistosome dermatitis?
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Swimmer's Itch
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What causes schistosome dermatitis?
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by infection with the cercariae of schistosomes that can mature only in their normal avian or mammalian species.
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What is the host of schistosome dermatitis?
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Not humans.
Birds or other animals. |
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How does schistosome dermatitis cause problems in humans?
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the cercariae in humans, which is not their normal host (foreign), penetrates the skin, but dies there in the skin and can cause itchy dermatitis.
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What is the geography of schistosome dermatitis?
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Worldwide distribution in fresh or salt water depending on the type of snail involved.
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What are the 3 main parts of an adult tapeworm?
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1) Scolex (head) with specialized structures for attachment to intestinal mucosa.
2) The neck, in which growth forms new reproductive segments (called proglottids) 3) Proglottids- the segments involved in egg formation. The end-most one is most mature whit the one near the neck is most immature. Each proglottid is HERMAPHRODITIC. |
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Where does an adult tapeworm get it's food?
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gets food from the contents of the intestinal lumen. It is absorbed through the entire surface of the worm.
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What are the tapeworms for which humans are the definitive host?
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Taenia saginata (beef tapeworm)
taenia solium (pork tapeworm) diphyllobothrium latum (fish tapeworm) |
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What is the tx for the 3 adult tapeworms that use humans as a host?
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praziquantel
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What is Taenia Saginata?
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giant tapeworm of humans
aka beef tapeworm |
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Describe the life cycle of the taenia saginata.
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aka beef tapeworm.
1) humans ingest encysted larvae (cysticerci) in raw or under cooked beef. 2) the larvae attach to the wall of the small intestine and grow to mature, 12-30 feet hermaphroditic adultsi n several months. 3) mature proglottids containing 50,000 to 100,000 eggs are passed in the feces or occasionally leave even when not defecating (farting? anal sex?) 4) The intermediate host is the cow which ingests the eggs. The larvae hatch, penetrate the intestinal wall and become encysted in the muscle of the cow as larvae (cysticerci). Remember that humans are the definitive host. |
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What is the diagnostic stage of Taenia saginata?
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mature proglottid in the feces or free eggs.
Egg looks like it has an embryo inside with radial striations on yellow-brown egg shell... kind of looks like the ciliary muscle. The gravid proglottid has 15-20 branches on each side coming off of the central stem. Count one side only. |
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What are the sx of taenia saginata?
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There does not seem to be any evidence that taenia saginata causes sx.
Although pts present b/c they notice a proglottid in their feces or sense a motile worm forcing itself through the anal sphincter. |
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What is importance in the dx of taenia saginata?
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Proglottids super important.
If not proglottids then geographic and dietary histories are important. T. saginata is found where ever cattle and extensive human fecal contamination co-exist. It is highly prevalent in Africa. |
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How do you prevent taenia saginata?
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thorough cooking of beef and protecting cows from human fecal contamination.
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What stage of taenia saginata is the infectious stage?
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larval stage aka oncosphere stage but remember LARVAL!!!
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Where do taenia saginata live in humans?
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small bowel
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What is taenia solium?
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pork tapeworm, giant tapeworm of humans
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Describe the life cycle of Taenia Solium.
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**Humans are the definitive hosts, but they can also be the intermediate hosts***
1) Humans ingest encysted larvae (cysticerci) in raw or undercooked pork. 2) The larvae attach to the wall of the small intestine and grow to mature 12-30 foot hermaphroditic adults in several months. 3) Mature proglottids containing 50,000-100,000 eggs are passed in human feces 4) The intermediate host (pig) ingests the eggs or gravid proglottids from human feces. The larvae hatch , penetrate the intestinal wall and become encysted in muscle as larvae (cysticerci) 5) If humans ingest the eggs (human fecal contamination) then cysticerci are formed in the tissues (cysticercosis) This can be a serious or life-threatening disease. The cysticerci can form in lungs, brain, eye, and CT. |
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How can you distinguish the beef and pork tapeworm?
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view of the scolex and proglottid
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What does the beef tapeworm scolex look like?
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4 suckers on it.
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What does the pork tapeworm scolex look like?
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4 suckers and then this 5 area with hooklets
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What does the pork tapeworm proglottid look like?
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fewer branches of the uterus but they are thicker. only 8-13 branches
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What should you consider in new onset epilepsy in adults?
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cysticercosis
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What is the dx stage of taenia solium?
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mature proglottid with the fewer, thicker branches or eggs in the feces. The eggs look like that of taenia saginata... embryo with hooklets surrounded by radial striations on yellow-brown egg shell.
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What are the sx of T. solium infection?
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no distinct sx UNLESS THE EGGS ARE INGESTED!!! then you have cysticercosis which damage the eye, heart, or brain. The larvae die and calcify. Pt will have eosinophilia and may cause epilepsy or visible nodules, etc. Once calcify can see on x-ray unlike trichinella which is too small to really see on x-ray.
Infection with the adult worm will NOT cause eosinophilia |
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How do most infections with T. solium present in the united states?
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usually asymptomatic and not cysticercosis. Thus, pts usually present b/c a multi-proglottid segment of the worm is found in feces.
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What is diphyllobothrium latum?
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giant tapeworm of humans
aka fish tapeworm |
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How large can diphyllobothrium latum be?
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BIGGER than the beef and pork tapeworms.
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What is a rare cause of vitamin B12 deficiency that mimics pernicious anemia?
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Diphyllobothrium latum
interferes with vit B12 absorption. Can use schilling test to figure things out. |
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What does the scolex of the diphyllobothrium latum look like?
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sort of long vertical opening and such. with a V shaped opening and 2 long folds on the side.
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What do the proglottids of the diphyllobothrium latum look like?
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broader than they are wide. Hermaphrtoditic but not as busy as the beef and pork tapeworms.
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Describe the lifecycle of Diphyllobothrium latum.
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1) human ingest raw freshwater fish containing encysted larvae
2) larvae attach to the wall of the lower small intestine and grow to maturity in a few months. 3) mature proglottids release eggs (one million per worm per day) that are excreted in the feces 4) In fresh water, the egg hatches into a free living ciliated stage. 5) Ciliated stage is eaten by a copepod and develops into a large stage larva 6) copepod is eaten by a fish and the larva encysts in the fish muscle. ** can be several intermediate hosts (cats, dogs, pigs) though humans are the definitive host. |
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What do the eggs look like in D. latum?
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standard egg. very large size. undeveloped ciliated stage.
hatch on one end or trap door... where the larvae gets out. knob on the other. hatch |
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What is anisikiasis?
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fish roundworm that infects marine mammals but passed through fish.
humans are accidental hosts--ingested larva cause eosinophilic granuloma of the stomach wall. people show up in the ER with 72 hours of abdominal pain. Can scope them and find eosinophilic granuloma with these in and can remove them. |
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Where is Diphyllobothrium latum often seen (geography)?
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USA (in the Great lakes region and alaska)
Also very prevalent in Finland. |
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How do you prevent D. latum infection?
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thorough cooking or freezing of fish and keeping human feces from fresh water in which the copepods live.
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What is Echinococcus granulosus?
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dog tapeworm... causes a serious cystic disease in humans
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What kind of host are humans for echinococcus granulosus?
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accidental intermediate hosts
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Describe the normal life cycle of Echinococcus Granulosus.
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1) sheep (or other animal destined to be eaten by a dog) ingests eggs from dog fecal contamination
2) early stage larvae hatch from the eggs in the intestine and penetrate the intestinal mucosa to enter the portal circulation. 3) most are trapped in hte liver and devo into cysts with an inner germinal layer. The germinal layer grows, vesciulates, and differentiates to form larval scolices (rudimentary heads). The cyst grows slowly over years and contains many progeny larval scolices. This is asexual multiplication by a larval stage worm in the intermediate host. The diameter of the resulting cyst may exceed 20 cm. 4) the sheep or other animal dies and its viscera are fed to dogs. In the dog intestine, the larval scolices attach to the small intestine well and mature into small tapeworms that release 500 eggs per gravid segment. |
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What is the prevention for E. granulosus?
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avoiding dog feces in endemic areas, preventing dogs from being infected and treating infected dogs.
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What are the sx of echinococcus granulosus?
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Majority are asymptomatic.
Asymptomatic infections are often detected by routine x-ray showing calcified cysts. The usual location is the liver (65%) or lung (35%) but any organ can be affected. Bone in some cases! |
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How does echinococcus granulosus cause sx?
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Cause sx by gradual expansion.
hepatic cysts may cause pain and enlargement of the liver. Pulmonary cysts may cause cough and dyspnea. Cysts in other organs cause the sx of space-filling lesions. A ruptured cyst may precipitate anaphylactic shock. |
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What do you do if you suspect Echinococcus cysts?
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x-rays and a scan looking for space-filling lesions are essential. Specific serologic tests for antibody to E. granulosus antigens support the dx.
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Where are echinococcus cysts found geographically most often?
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prevalent in sheep and cattle livestock areas of south america, USA, south africa, and the mediterranean basin. Remeber that infection may have occurred decades earlier especially for liver and other visceral cysts.
Dogs can be infected by eating wild animals! |
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Where is Taenia solium endemic?
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NOT the USA but it is widespread wherever pigs have contact with human fecal contamination.
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How do you tx taenia solium?
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You tx it with praziquantel.
Tx is MANDATORY b/c cysticercosis can be caused by ingestion of eggs present in proglottids and in fecal contamination. |
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How do you dx neurocysticercosis?
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Radiologic imaging to demonstrate calcified cysts (easy) or live cysts (more difficult)
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Tx of neurocysticercosis.
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Praziquantel or Albendazole is often preferred now b/c of more recent studies.
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How do you prevent taenia solium infection?
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Thorough cooking of pork and protecting pigs from human fecal contamination inaddition to protecting humans from human fecal contamination.
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How do you treat ecchinococcus granulosus?
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Asymptomatic patients may or may not require tx.
Symptomatic patients are generally tx'ed surgically by excision of the cyst. The contents of thecyst and its germ layer must be sterilized with ethanol or another disinfectant before removal to prevent initiation of new cysts by a scolices that happen to be released. |
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What is the infective stage of echinococcus granulosus?
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Embryonated egg in feces
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How are humans infected with ecchinococcus granulosus and what happens as a result?
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Humans are infected (just like sheep are) by ingested eggs from contamination with dog feces and the early stage larvae form slowly-growing cysts containing many larval scolices (asexual multiplication).
The cysts are called hydatid cysts and the laval scolices within them are called hydatid sand. Lots of protoscolices are in the body in hydatid cysts but there are not multiple worms!!! |
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What is Echinococcus multilocularis?
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dog / fox tapeworm
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Where is echinococus multilocularis endemic?
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It is endemic in the far northern climates ( like Alaska). A few cases have recently been seen in Minnesota and adjacent northern states.
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What is the lifecycle of echinococcus multilocularis?
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same as echinococcus granulosus.
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What are usually the intermediate host of echinococcus multilocularis?
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usually rodents.
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What are the nature of the cysts in echinococcus multilocularis?
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The cysts are multi-compartment alveolar cysts that can give rise to metastatic growth at distant sites of the body (lung and brain).
B/c of the nature of the cysts surgical cure is much more difficult~~~ tx with albendazole may be useful though. :) |
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What are the 3 potential chemotherapeutic agent targets active against worms?
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neural and neuromuscular transmission
cytoskeletal structure, especially microtubules energy metabolism |
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What 3 drugs used against worms are important?
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-bendazoles
ivermectin praziquantel |
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What are filiarial infections tx'ed with?
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Ivermectin.
Diethylcarbamazine is preferred for many of them, but ivermectin is used for all except Loa loa. |
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What are most roundworm infections treated with?
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Mebendazole or thiabendazole
true of all roundworm infections except filarial infections. Not the first choice for all roundworms but often used. |
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What can all fluke infections and adult tape worm infections be treated with?
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praziquantel
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What are protozoa?
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single celled eukaryotes
most are not pathogenic or parasitic. |
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What are differences between worms and protozoa?
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all protozoa that cause disease must multiply in humans
eosinophilia is not a usual sign of protozoal infection. |
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Are Entamoeba histolytica, giardia lamblia, and trichomonas vaginalis anaerobic or aerobic?
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anaerobic.
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What is a suitable tx for the 3 anaerobic protozoa?
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metronidazole
E. histolytica, G. lamblia, T. vaginalis |
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What causes amebiasis?
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Entamoeba histolytica
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Entamoeba histolytica
intra or extracellular? aerobic or anaerobic? |
Extracellular
grows anaerobically |
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Describe the life cycle of entamoeba histolytica?
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** life cycle only involves humans!!**
1) humans ingest cysts of E. histolytica (human fecal contamination) 2) The cysts open in the intestine and the progeny parasites multiply as trophozoites in the large intestine. 3) As the bowel contents lose water and become formed stools, the trophozoite changes to a cyst. The cysts excreted in stools are resistant to most environmental conditions and survive for weeks! |
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How does the E. histolytica multiply?
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binary fission
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What is a trophozoite?
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gneeral term for the actively multiplying stage of parasitic protozoa. It is used with a number of different parasitic protozoa. It is used with a number of different parasitic protozoa.
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What is the dx stage of the E. histolytica?
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cyst in formed stools or the motile trophozoite in diarrhea or the stained trophozoite in diarrhea stools.
**microscopic dx is being replaced with monoclonal-antibody -based tests for E. histolytica antigens in fecal extracts. This test is specific for pathogenic species. |
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What does the cyst of E. histolytica look like?
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There is a dark oblong oval chromatodial body... with 4 nuclei in the mature cyst.
Circular |
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What does the trophozoite of the E. histolytica look like?
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May see several ingested RBCs, tear drop shaped. one nucleus.
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What kind of sx does entamoeba histolytica cause?
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May be asymptomatic
Sx when occur are due to invasive disease of the colon mucosa which causes sx of pain and dysentery (bloody and mucous stools). Often can see cysts or trophozoites here!! (under microscope) You can observe the ulcerating lesion (flask shaped)on endoscopy. |
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What is the geographic distribution of E. histolytica?
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worldwide with an increased prevalence in the tropics.
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What human cells do E. histolytica look like and act like?
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macrophages!
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What do the E. histolytica trophozoites do in the human GI tract?
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Kill pmns, liquefy tissues, cause a sterile abscess (but this is terrible wording)
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How do you prevent E. histolytica?
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avoid fecal contamination
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How do you treat amebiasis?
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metronidazole in combo with other drugs (not necessary to learn those now).
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Besides the intestinal tract, where else can E. histolytica spreadi n a human? What problems result?
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Sometimse they spread to the liver and cause an amebic abscess. This causes pain, fever, enlarged and tender liver. Only 10% of liver abscess pts continue to excrete cysts or trophozoites and only 50% have a hx of dysentery.
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How is E. histolytica diagnosed?
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Serology for anti- E. histolytica antibody, liver scan, search for trophozoites in an aspirate from the abscess. Amebic abscess are only occasionally seen in other organs like brain or lung.
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What is another name for amebic meningoencephalitis?
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naegleria
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What are naegleria?
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free-living soil/water amebas
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People who are infected with naegleria have what common thread in their histories?
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nearly all have hx of swimming in stagnant warm water
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How do naegleria reach the brain?
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neural route that involves penetration of hte cribriform plate
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What are the sx of naegleria?
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meningitis or encephalitis
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What is a chromatodial body in E. histolytica?
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crystallized ribosomes
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Routes of infection with amebiasis
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contaminated food or water
sexual transmission contaminated GI procedures |
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How is naegleria dx?
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usually made histologically at autopsy.
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Guidelines / Tips for avoiding food and water-borne infections.
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1) avoid water unless it is boiled or disinfected by halogen tx or filtration (not as good). ICE IS ONLY AS SAFE AS THE WATER!!. Bottled carbonated water, sodas, beer, and wine are usually safe.
2) Avoid contact with fresh water in areas in which schistosomiasis is prevalent 3) Avoid uncooked fruits and vegetables unless you peel them yourself 4) avoid undercooked meats 5) avoid dairy products 6) hot cooked foods and canned foods are generally safe. |
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What causes giardiasis?
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Giardia lamblia.
an extracellular protozoan |
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What should you NOT give a patient with amebiasis or strongyloides?
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It makes them amped up
with amebiasis your colon will PERFORATE!!!!! DONT DO IT |
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Describe the life cycle of Giardia lamblia
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** identical to that of E. histolytica EXCEPT that it is not only in humans. Animals can be infected and excrete cysts that are infectious for animals.
1) Ingest a cyst from fecal contamination 2) The cysts open in the small intestine and the released parasites multiply as trophozoites in the duodenum and jejunum. 3) As the stool mass is dehydrated, the trophozoites become encysted and are excreted in the feces. |
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What is an amebic sterile abscess not sterile nor an abscess?
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amebae are on the edge (why people thought it was sterile) but they are there just on the edge eating away at the normal tissue.
Center is not inflammatory cells bu cellular debris |
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How do you distinguish E. histolytica from the non-pathogenic ameba?
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stool antigen... would also not see RBCs ingested in the trophozoite of the nonpathologic one but not as reliable.
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What is the diagnostic stage of the G. lamblia?
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the cyst in stools or the trophozoite in diarrhea
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What needs to happen to metronidazole before it is activated?
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it has to be reduced and so iti s really only affective in organisms that are existing in an anaerobic metabolic state.
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What does the cyst look like in G. lamblia?
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It looks like an oval with a wall and 4 nuclei (eyes) with a sperm looking like structure in the middle.
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What does the trophozoite look like in G. lamblia?
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Looks like a crazy owl creature with hair.
2 nuclei (looks like eyes), tear drop shaped body... many flagella, sperm looking line running in the center. |
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Where is giardia lamblia infection endemic?
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Most if not all parts of the world.
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What are the sx of G. lamblia?
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some are asymptomatic
sx include diarrhea, foul smelling greasy stools, abdominal discomfort, nausea. Chronic infection can result in wt loss from malabsorption. |
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In what population is chronic infection of giardia most common?
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people who have a congenital defect in IgA
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What is different about giardia and it's interactiosn with humans compared to E. histolytica?
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It does not spread from the GI tract.
It is not invasive. |
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What are infectious cysts of giardia resistant to?
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chlorine! how many places purify water. Use large sand filtration devices.
This is responsible for focal epidemics in towns worldwide! |
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What is the tx for giardia?
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Metronidazole
There is a new drug now though called nitazoxanide but we don't need to know it. |
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How do you prevent giardia?
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Avoiding human and animal fecal contamination of water and food.
Beavers are a common cause of municipal water contamination when open reservoid are the source (asi n hanover!!!) other naimals may also be involved. |
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How do you dx giardia?
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microscopy
IF antibody detection |
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What is trichomonas vaginalis?
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it is a flagellate, extracellular protozoan parasite.
Causes an STD |
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Describe the lifecycle of trichomonas.
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Trophozoites in the vagina of the female or the urethra/prostate of the male are transmitted by sexual contact or poor hygiene.
Multiply by binary fission. There is no cyst stage and the trophozoites are relatively hardy. |
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What is the diagnostic stage for trichomonas?
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For women it is the motile trophozoite in vaginal secretions and in urine.
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What are the symptoms of infection?
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10-20% of women have inflammation, burning, itching, and a purulent discharge. Most who are infected are asymptomatic. Some may have a nonspecific urethritis.
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Tx for trichomonas?
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metronidazole and MUST TREAT SEXUAL PARTNERS TOO
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Prevention of trichomonas
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mechanical barriers... i.e. condoms
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What is toxoplasma gondii?
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obligate intracellular parasite
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Describe the natural life cycle of toxoplasma
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Humans are accidental intermediate hosts that do not play a significant role in the life cycle.
1) member of the cat family (only definitive host) eats the intermediate host, a mammal with tissue cysts that contains dormant paraiste in muscle and brain. 2) in the feline intestine, the parasite grow intracellularly in the intestinal mucosa and produces male and female gametes 3) gametes fuse to form a zygote which is excreted in the feces (only feline feces) as noninfectious fecal cyst 4) at ambient temperature, the fecal cyst becomes infectious, a process that requreis at least 2 days 5) a non-feline animal ingests infectious fecal cysts and survives an acute infection with trophozoites (actively growing stage) to have tissue cysts that contain dormant paraiste in muscle and brain. These tissue cysts in the intermediate host are different from the fecal cysts excreted by infected cats. They are totally different stages in the life cycle. |
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What is the infectious stage of trichomonas?
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trophozoite! the only real stage.
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How does trichomonas affect HIV transmission?
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It's inflammatory qualities (as with other STDs) increase the risk of HIV transmission.
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How are humans infected with toxo?
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Two ways:
1) Eating undercooked or raw meat that contains tissue cysts. Tissue cysts are common in pork and also found in beef and other meats. 2) ingesting infectious fecal cysts from feline fecal contamination In either case the ingested parasites turn into trophozoites that produce an often asymptomatic acute infection followed by chronic infection with tissue cysts in muscle and brain |
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What is the dx stage of toxo?
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THERE IS NO DIAGNOSTIC STAGE.
Dx is generally serological looking for a rise in specific antibody titer between acute convalescent sera or the presence of anti-toxoplasma IgM. Various serological tests are available. 1) Sabin-Feldman dye test: complement mediated lysis of parasites in the presence of anti-toxo antibody) 2) ELISA or fluorescent antibody tests Consider PCR too! |
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Tx for toxo
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1st choice is pyrimethamine (blocks dihydrofolate reductase) plus sulfadiazine (blocks dihydrofolate synthesis) which act synergistically.
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Sx of toxoplasmosis
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Most are asymptomatic if immune system is intact. (about 1/8 of the US population is infected)
If symptomatic though, Lymphadenitis, myalgia, HA, fatigue, fever Encephalitis, myocarditis, hepatitis, pneumonia in the more severe or fatal cases |
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Toxo and AIDS
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Toxoplasmic encephalitis is a common opportunistic infection in AIDs characterized by HA or confusion with focal neuro deficits on exam.
Typically a result of reactivation of paracytes in the brain. Often they are seropositive but may lose it late in AIDs. On CAT or MRI scans will see RING ENHANCED CNS lesions. Dx confirmed with trial of pyrimethamine-sulfadiazine which should yield a prompt response. |
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Toxoplasmosis and transplacental infection
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Causes severe or mild chronic damage to the fetus if mom has primary infection during pregnancy. If it occurs earlier in gestation than there is a more severe outcome.
Sever cases can cause microcephaly, hydrocephalus with intracerebral calcifications, mental retardation, or blindness Milder manifestations are visual defects (recurrent chorioretinitis) and mental subnormality of gradual onset. Outcome of congenital infection is improved by chemotherapy during pregnancy and after birth. (pyrimethamine plus sulfadiazine) |
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How do you prevent toxo infection?
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cook meat well and avoid cat fecal contamination especially important during pregnancy.
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What are the characteristics of the "...spor..." intestinal parasites?
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they are all obligate intracellular parasites
they all cause mild-moderate self-limiting diarrhea in pts with a normal immune response. all 4 cause severe and protracted diarrhea in AIDS and in other immunosuppressed pts. All 4 are transmitted by the fecal-oral pathway all 4 are resistant to chlorination used in municipal water supplies. |
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How are the ",...spor..." parasites dx?
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look for fecal cyst by microscopy though it is being replaced by PCR diagnosis.
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Cryptosporidium is what?
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an intracellular parasite that forms lumps protruding from the plasma membrane of intestinal epithelial cells.
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Dx cryptosporidium
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acid-fast (red stained) cyst in feces
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Clinical manifestations of cryptosporidium
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mild- moderate diarrhea in pts (especially kids) with normal immune system
severe protracted diarrhea in AIDS patients and other immunosuppressed pts |
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Parasitic diseases in AIDS patients in order of frequency
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1) Pneumocystis (pneumonia) not actually protozoan but originally thought to be)
2) Toxo (encephalitis) 3) Cryptosporidiosis (diarrhea) 4) Amebiasis (dysentery and invasive disease) 5) Visceral leishmaniasis (only where the disease is endemic) 6) strongyloides hyperinfection- surprisingly rare even when infection is endemic. |
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What are anaerobic protozoa treated with?
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Metronidazole... it needs to be reduced to work so treats anaerobic creatures.
Anaerobic protozoa include: Entamoeba histolytica, Giardia lamblia, and trichomonas vaginalis |
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What protozoa are treated with pyrimethamine and a sulfa drug?
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Toxoplasma gondii and chloroquine resistant malaria
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What can you use to treat pneumocystis and cyclospora?
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Bactrim
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What are 4 drugs used to treat malaria?
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chloroquine, mefloquine, pyrimethamine sulfadoxine, and primaquine
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How do we treat hemoflagellates?
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Super hard to tx
most of the drugs that work are too toxic we don't care about their names. |
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What does babesia microti cause?
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babesiosis... an erythrocytic infection with endemic foci on Nantucket island, MA and other places on the coastal northeast where the ecology is similar.
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What is babesia microti related to?
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distantly related to the plasmodia and can be mistaken for malaria on blood films
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Describe the life cycle of babesia microti
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involves the same tick that transmits lyme disease! Gamete fusion takes place in the tick which is the definitive host.
1) babesia is injected by tick during bite (into human, rodent, horse, cattle, dogs, and other vertebrates) 2) babesia penetrates the RBCs, forms a tetrad which then releases them and they infect other RBCs and it continues. |
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What is the diagnostic stage of babesia?
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trophozoite in stained blood films... look for tetrads. Some RBCs have just the ring stage which can be mistaken for malaria so look around just to check for tetrads.
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What are risk factors for overt babesiosis?
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old age
immunosuppression asplenia |
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What are the symtpoms of babesiosis?
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hemolytic anemia
fever chills |
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How many residents of coastal New England are sero positive for babesia microti?
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5-20%, largely from subclinical infections though.
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What are qualities common to all the hemoflagellates?
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1) found in the blood in some stage in the life cycle
2) have flagella 3) have an insect host in their life cycle Some species also have an obligate intracellular stage called the amastigote in vertebrate hosts. |
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Where does the flagellum of the hemoflagellate originate?
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in an organelle (mitochondria!)
It is called the Kinetoplast , which is rich in tiny circular DNA molecules and also contains the usual small circular mitochondrial genome |
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What is an amastigote?
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it is the obligate intracellular form of hemoflagellates
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How can African trypanosomes, Leishmania species, and Trypanosoma cruzi be classified?
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Hemoflagellates.
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What African sleeping sickness?
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African trypanosomiasis.
an extracellular protozoan parasite. |
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Describe the life cycle of African trypanosomiasis.
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requires the tsetse fly ( genus Glossina)
1) An infected fly bites a human and transmits the trypanosomes in its saliva. Sometimes particularly in tourists local multiplcation of the parasites produces an ulcerating cutaneous lesion. 2) in humans, the trypanosomes multiply in the blood, lymph, CSF and tissues. 3) An uninfected tsetse fly bites a person with parasitemia. In the insect gut, the trypanosomes multiply and migrate to the salivary glands, where they multiply more. |
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What is the diagnostic stage of African trypanosomiasis?
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The flagellated form in the blood, lymph node or CSF
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What is the clinical course of African trypanosomiasis?
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1) a local ulcerating nodule apperas a few days after the bite of an infected fly.
2) 6. Two weeks after the bite: parasitemia, fever, and lymphadenopathy (especially posterior cervical nodes -WINTERBOTTOM’S SIGN). The parasites multiply in blood, lymph nodes, and other tissues. Splenomegaly is common. 3) Invasion of the CSF with parasite multiplication in the CSF which then leads to lethargy, coma, and death. |
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How do you treat African trypanosomiasis?
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highly toxic drugs (we don't care about exact names)
You can try to prevent by controlling the tsetse fly poulation and trying to identify cases and IMMEDIATELY tx. **Travelers should avoid fly bites**!!! |
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What is Leishmaniasis?
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It is a disease caused by several different species of the genus Leishmania.
** in humans they are intracellular parasite that are predominantly located in the reticuloendothelial system. |
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What is the lifecycle of Leishmania?
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1) Sandflies of the genus Phlebotomus (or another genus in the New World) regurgitate extracellular flagellated forms at the site of a bite.
2) This flagellated form enters mononuclear phagocytes, loses its flagellum, and multiplies as an intracellular amastigote. The progeny amastigotes are released by lysis of the host cell and enter more mononuclear phagocytes in successive cycles. 3) An uninfected Phlebotomus fly ingests macrophages containing amastigotes. They become extracellular flagellated forms and multiply extracellularly in the insect digestive tract. After one to two weeks the sandfly can transmit the parasites. **Leishmaniasis is often a zoonotic infection. Human infections play a role in the natural cycle in Leishmania donovania. ** |
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What is the diagnostic stage of leishmania and how can it be diagnosed?
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dx stage is the intracellular amastigote.
It can be detected microscopically in clinical specimens A delayed-hypersensitivity skin test detects current or previous infection. |
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How do you tx Leishmaniasis?
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Tx is difficult b/c many of the available drugs are toxic.
mostly they're trying things but they suck so just avoid sand flies instead. |
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What causes Visceral Leishmaniasis?
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Leishmania donovani
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What causes Kala-Azar?
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Leishmania donovani
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Where (in the world) does Leishmania donovani live?
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Asia, tropical Africa, and focally in the Mediterranean basin
There is another species in South America that causes the same disease but the creature is a little different. ** Also note that most infected sandflies acquire the Leishmania donovani from infected humans |
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What is the clinical picture of Kala-azar?
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Incubation period is 2-6 months (sometimes longer)
Insidious onset with fever, enlarged spleen and lymph nodes and hypergammaglobulinemia. It is fatal if left untreated. |
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When would you suspect kala-azar in a patient?
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protracted fever (nonprostrating though) and splenomegaly with a geographic hx that makes sense for this parasite.
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How do you dx Kala-Azar?
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bone marrow biopsy.
The original cutaneous lesion is almost always healed before the visceral sx appear and often no organisms can be found in blood. |
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In what population is Kala-azar common?
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AIDS patients in areas where leishmania donovani is endemic.
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What is the source of cuteanous leishmaniasis?
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Different Leishmania species in the eastern and western hemispheres. Reservoir hosts ( especially domestic dogs but other rodents and mammals too) are the source of most fly infections.
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What is the "oriental sore"?
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It is a sore of cutaneous leishmaniasis that is usually seen on arms, legs, and face. It can be found in Central Asia, India, Mediterranean basin, and Western Africa.
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What is the chiclero ulcer?
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It is an ulcer on the head that is caused by Leishmania in Central and South America.
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What is the clinical picture of cutaneous leishmaniasis?
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Incubation period 2-8 weeks
Papule at site of bite slowly becomes 1-2cm in diameter Papule becomes an ulcer that lasts 6 months to several years Scar and reasonably good immunity. |
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When should you suspect cutaneous leishmaniasis?
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Patients with a chronic wet or dry ulcer and an appropriate geographic history.
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How do you diagnose cutaneous leishmaniasis?
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Microscopy review of a biopsy of the margin of a lesion.
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How do you tx cutaneous leishmaniasis?
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The drugs used are dangerously toxic!! Often if not progressive, it is self-limiting and not treated. You will end up with immunity to it but may have a significant scar to show for it.
Not treating in the western hemisphere is problematic b/c the lesion may represent the stage of mucocutaneous leishmaniasis... which is disfiguring. |
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Clinical picture of mucocutaneous leishmaniasis
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Starts out like cutaneous leishmaniasis
Weeks to years later, in about 3% of patients the parasite disseminate to produce progressive massive necrotizing lesions at the mucocutaneous junctions of mouth or nose (less commonly at other mucocutaneous junctions) |
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What causes mucocutaneous leishmania?
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Leishmania species in south and central america. Dogs and other mammals are important reservoir hosts
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How do you diagnose mucocutaneous leishmaniasis?
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microscopy inspection of a biopsy of the margin of the lesion often fails. You need to try PCR.
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How do you avoid Leishmaniases?
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Prevention is by avoiding sand flies.
DDT controls the fly population very well. |
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What parasites cause malaria?
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The intracellular protozoan parasites in the genus Plasmodium
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Describe the lifecycle of plasmodium (includes in the mosquito and in humans)... start with mosquito bite.
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1) The Anopheles mosquito injects SPOROZOITES as it bites humans.
2) The sporozoites enter parenchymal cells of the liver and divide repeatedly to yield MEROZOITES. This is the liver stage (asymptomatic) of infection. Since each sporozoite destroys only one hepatocyte there is no significant pathology. The merozoites are released into the circulation and 3) Begin the erythrocytic (symptomatic) stage by entering the blood stream and infecting red cells. 4) The malaria parasites grow within the red cell through an unusual sequence of events to produce more merozoites. In these notes, several of these events are given trivial names that should not be learned. These names are designed to be sufficiently obvious to allow easy communication about Giemsa-stained smears. 5) Shortly after entering an RBC the merozoite becomes a RING STAGE (official nomenclature; learn this term) 6) The ring stage synthesizes a large volume of cytoplasm but remains uninuclear. Our trivial name for this stage is “cytoplasm synthesis”. 7) When cytoplasm synthesis is complete, multiple replications of the nucleus yield a multi-nucleate cell. Our trivial name for this stage is “nuclear replication”. 8) When nuclear replication is complete, each nucleus acquires its share of cytoplasm to become a mono-nuclear merozoite (trivial name for this stage “cytoplasm division”) 9) The progeny merozoites are released by lysis of the RBC and go on to infect more RBCs. 10) Some merozoites enter RBCs and (instead of making more merozoites) differentiate into male and female gametocytes, the precursors of the gametes. 11) The gametocytes are taken up by an infected mosquito with its blood meal. 12) In the mosquito (the definitive host), the male gametocyte differentiates into flagellated male gametes The female gametocyte becomes the female gamete. 13) The male and female gametes fuse to form a zygote which matures through a number of stages to produce many SPOROZOITES that migrate to the salivary gland. |
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What is the intermediate host of plasmodium ?
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humans
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What is the definitive host of plasmodium?
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Anopheles mosquito
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plasmodium sporozoites comes from? infects? progeny become?
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Comes from mosquito
infects liver cells progeny become merozoites |
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plasmodium merozoites come from? infect? progeny become?
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Comes from: liver cells or red cells
Infects RBCs Progeny become merozoites or gametocytes |
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plasmodium gametocytes come from? infect? progeny become?
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Comes from RBCs
Infects mosquitos Progeny become sporozoites (after a # of intermediate stages, including gametes and a zygote) |
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What stage of plasmodium does the anopheles mosquito pick up from sucking the blood of humans?
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gametocytes
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What are 3 species of protozoa that cause human malaria?
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Plasmodium falciparum
plasmodium vivax plasmodium malariae |
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What is the diagnostic form of plasmodium?
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various erythrocytic forms observed in blood smears. Easy if you THINK OF DOING IT!!!! Use thick and thin blood smears
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Why does the female anopheles mosquito require blood proteins?
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It requires them to make and mature eggs for reproduction to occur. MUST DRINK BLOOD TO PROCREATE.
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What are the steps for prepping a thin and thick blood film on the same slide? Why would you do it?
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To look for malaria!
1. The drop of blood is touched with a clean slide. 2. Spread the drop of blood with the comer of another slide to make a circle or a square about cm. 3. Touch a new drop of blood with the edge of a clean slide. 4. Bring the edge of the slide carrying a drop of blood to the surface of the first slide, wait until the blood spreads along the whole edge. 5. Holding it at an angle of about 45°, push it forward with a rapid but not too brisk movement. 6. With a pencil, write the slide number on the thin film. Wait until the thick film is quite dry. |
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What is the incubation period of plasmodium?
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The incubation period is usually relatively short 10-40 days.
But it can be longer in P. vivax (6-12 months) b/co f a dormant stage in the liver. P. malariae can have a much much longer incubation period of years or decades. |
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When you're looking for malaria in someone's blood, would you see gametocytes?
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probably not. Rarely in the large vessel circuation and instead sit preferentially in small peripheral blood vessels
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What is the shape of the P. falicparum gametocyte?
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banana shaped or slipper shapped and still within cytoplasm of RBC although may not look like it.
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What does Plasmodium falciparum cause?
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malaria... the most serious malaria. IT IS A MEDICAL EMERGENCY requiring immediate dx and tx.
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What is the incubation period of plasmodium falciparum?
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~ 2 weeks.
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What is a characteristic of plasmodium falciparum infection (in the blood)?
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HIgh parasitemia=many infected red cells. IT is characteristic because red cells of all ages are infected.
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What is the clinical picture of plasmodium falciparum infection?
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primary attack merges into fever spikes every second day and then subsides to a low parasitemia in about three weeks. relapses with lower parasitemia and renews febrile episodes may take place over the next few months.
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What are alternative ways that plasmodium species can infect humans?
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-can be transmitted by blood transfusion.
-they can be transmitted perinatally or transplacentally to a newborn but it is a rare form of transmission. |
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What are the prodromal sx of malaria?
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headache, anorexia, fever, joint pains
These sx lead to a false dx of influenza in places where malaria isn't common. |
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What is special about the fevers in malaria?
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The distinctive primary attack begins with a shaking chill of about 1 hour followed by a longer hot stage with headache and often nausea and vomiting.
A heavy sweat ends this cycle, which eventually begins to recur with characteristic periodicity as the blood stages become synchronized. However, in the early days of disease daily fever spikes are common. **Returning travelers with malaria often do not have the characteristic fever cycles because synchronous growth has not yet been established. |
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What are some other major sx of malaria besides fevers?
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Anemia due to red cell destruction by the parasites.
Chronic reinfection in endemic areas which result in splenomegaly. |
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What causes the most severe sx of plasmodium falciparum?
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They result from the presence of one class of parasite specific proteins exported from the intracellular parasites to the surface of the infected red cell because these antigens form knobs that cause infected RBCs to bind to vascular endothelial cells.
AT a high parasitemia, capillaries are blocked with masses of infected RBCs which produce micro-infarcts. The resulting anoxia causes tissue damage, especially in the brain (cerebral malaria) with headache, coma, paralysis, or death. Other organs such as intestine ( with GI hemorrhage) or kidney (tubular necrosis) are also affected. |
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What is the geography of P. falciparum?
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almost entirely tropical. The P. falciparum has no mechanism for relapse or delayed response and can not survive the mosquito-less winters of the temperate zone.
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What are the diagnostic features of a blood smear for plasmodium falciparum?
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peripheral blood usually only contains early forms rings and gametocytes (banana shaped).
The later stages are not found in the peripheral blood because the "knobs" cause them to stick to the capillary endothelium. The later stages can be found in blood films when there is an overwhelmingly heavy infection. Cells with 2 rings are common! gametocyte is pathognomic for falciparum malaria. |
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What are the clinical features of plasmodium vivax infection?
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Fever spikes seen every 2nd day. The parasitemia is lower than that of P. falciparum b/c reticulocytes are preferentially infected. Anemia is common too.
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What plasmodium species can have relapse of infection?
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Plasmodium vivax
Either relapse can occur or initial sx can be delayed for 6-9 months and occasionally for up to 5 years.b/c dormant liver stage (hypozoite). This allows P. vivax to survive mosquito-less winters. Thus vivax is the most common malaria of temperate zones, but is also common in the tropics. |
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What are some diagnostic features of a blood smear?
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1) large-sized infected RBCs (reticulocytes)
2) all stages are seen ( contrast with p. falciparum) 3) SCHUFFNER's DOTS are prominent in some late-stage infected cells. The dots in other species of malaria are smaller and less distinct. MOST IMPORTANT FEATURE FOR OUR PURPOSES. |
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What stage of RBCs does plasmodium vivax prefer?
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reticulocytes!! Unlike P. falciparum which loves any RBC stage.
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What kinds of drugs are used to treat malaria?
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Many drugs are available which inhibits growth of the erythrocytic stage.
Examples: chloroquine, mefloquine, atoavaquone-proguanil (Malarone), artesunate, primaquine |
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What drug is a huge problem in treating malaria because of all the resistance against it?
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chloroquine
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What is the recommended drug of phophylaxis for travelers to areas where chloroquine resistant P. falciparum is endemic?
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mefloquine
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What drug is used to eradicate the hypnozoite of P. vivax after a traveler returns home? Contraindications?
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primaquine
You can NOT give this to patients with glucose-6-phosphate dehydrogenase deficiency. |
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What are 2 non-pharmacological recommendations for people traveling to or living in areas where malaria and other insect borne diseases are prevalent?
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Bed nets
Insect repellents on the skin |
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What kind of mosquito is always involved in malaria infection?
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Anopheles
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Where is eradication possible if anywhere? And how can it be eradicated?
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It is VERY difficult in tropical regions where malaria is highly endemic such as the tropics.
Eradication of malaria in temperate and subtropical areas is expensive but possible. Eradiation in these areas depends on: 1) mosquito control. Residual insecticides kill mosquitoes in houses 2) Mosquito bite protection. 3) Case finding and chemotherapy to reduce the number of infected humans. |
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What genes are prevalent in malarious regions?
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Sickle cell hemoglobin. Heterozygous humans are much less likely to die of their P. falciparum infections.
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Is immunity to malaria possible?
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Immunity to P. vivax and P. malariae is possible but may take years. Immunity is slow to arrise and typically requires repeated reinfections.
**immunity is species specific and may even be strain specific. A genetically engineered vaccine has been shown to produce significant reduction in childhood incidence. |
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What are reduviid bugs?
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blood-sucking bugs
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What causes Chagas' disease?
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Trypanosoma cruzi
It is a protozoan parasite with intracellular and extracellular stages. |
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What disease does Trypanosoma cruzi cause?
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Chagas' disease
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Describe the life cycle of Trypanosoma cruzi
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1) a. The infected reduviid bug bites, takes a blood meal, and defecates. The feces contains the infectious extracellular flagellated forms of T. cruzi. which enter at the site of the bite
2) b. The extracellular flagellated forms enter cells (RE system, skeletal muscle, cardiac muscle) and multiply intracellularly as amastigotes. 3) An uninfected reduviid bug ingests extracellular flagellated forms with a blood meal. The parasites multiply extracellularly in the gut and transform to infectious extracellular flagellated forms in the rectum of the bug. |
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Diagnostic stage of Trypanosoma cruzi
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The extracellular flagellated forms in the blood. May be hard to find in chronic disease. (Often C shaped... C for cruzi!!)
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What are the symptoms of initial infection with T. cruzi?
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Often mild or subclinical. Some people have a painless swollen lesion near the eye at the site of the bite (aka Romana's sign).
Some pts might die in the acute phase due to heart failure or meningitis. A lot of times though patients are asymptomatic and you detect infection through seroconversion. |
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What happens to 10% of sero positive Chagas Disease patients?
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They develop chronic Chagas' disease years or decades later.
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What does chronic Chagas' disease entail?
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1) myositis of cardiac muscle results in enlargement of the heart and congestive heart failure.
2) Marked destruction (probably by parasite-induced autoimmunity) of autonomic ganglia leads to mega-colon and mega-esophagus. 3) About 3% of chronically infected pregnant women will have transplacental infection of their fetuses. |
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Why is diagnosing Chagas' disease (chronic version) difficult?
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It is difficult b/c of the low parasitemia.
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What are some strategies to diagnose chagas disease?
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1) look for flagellated form in blood smears (only really reliable in acute disease)
2) Culture blood on blood agar for 3 months, looking for growth of the extracellular form that is found in reduviid bugs. 3) Inject mice with blood and look later for circulating flagellated form that is seen in human infections. 4) XENODIAGNOSIS is the most reliable test in chronic disease. This test is not generally available. Feed laboratory-raised reduviid bugs on the patient, and check bug rectum for fecal parasites 1-2 months later. Xenodiagnosis will be replaced by PCR. 5) A C-fixation test detects previous infection, but with poor sensitivity. |
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How do you prevent Chagas' disease?
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Requires reduviid bug control and avoiding bug bites. Upgrading rural housing helps to reduce bug-human contact. Bug-trasnmitted Chagas' disease has been nearly eliminated in Argentina, Chili, Brazil, and Uruguay
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What is the geography of Chagas' disease?
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Found only in South and Central America and Mexico.
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How does the US prevent Chagas' disease spread in the blood?
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It screens blood donations for Chagas' disease by PCR now to prevent transfusion transmission.
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Where do reduviid bugs live? (not geography but more location in the places where they're endemic?
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Reduviid bugs live in substandard houses that provide crevices and cracks in the walls in which they must hide. Thus, Chagas’ disease is more common in the rural poor. Increasingly Chagas disease has spread to urban slums where shanty town housing provides a suitable habitat for reduviid bugs.
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