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140 Cards in this Set
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define definitive host?
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animal harboring the adult or sexually mature stage of the parasite
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define intermediate host.
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animal in which development occurs but adulthood is not reached
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define parasitic infection.
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invasion by endoparasites
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define parasitic disease
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invasion and pathology produced by endoparasities
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define parasitic infestation
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external disease by ectoparasites
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describe the drug chloroquine.
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for plasmodium and amaebae, widespread resistance, prevents the breakdown of toxic heme to non toxic hemozoin in RBC's as well as binding heme to form a toxic complex that disrupts the membrane function leading to cell lysis and then parasite death, bugs become resistant by setting up a pump to pump the chloroquine out of the cell
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descrieb the drug combo trimethoprim sulfamethoxazole.
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treats plasmodium and toxoplasma and pneumocystis carinii, folic acid antagonist, sulfas are competitive inhibitors of PABA while TMP prevent reduction of dihydrofolate to tetrahydrofolate, folic acid is needed to make uridine and thymidine
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describe the drug melaminophenyl arsenical.
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treat trypanosomes. prevents formation of 2 necessary enzymes for metabolism by using the orgs mechanism for reducing oxidized thiol groups
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describe the drug pentamidine.
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used in leishmaniasis and as prophylaxis from trypanosoma brucei gambiense, inhibits DNA and RNA, binds and aggreggates ribosomes, inhibits gluc metabolism, prottein and RNA synth, intracellular amino acid transport
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what antibiotics are used for parasities that block ribososmal peptide synthesis?
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clindamycin, spiramycin, paromomycin, tetracycline, and doxycycline are used to treat malaria, babesiosis, amebiasis, crypto, and toxoplasmosis
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describe metronidazole in parasite treatment.
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used for amebiasis, giardiasis, and trichomonas, enters the parasite cell, is reduced, and binds and breaks DNA
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what parasite can be treated with cipro?
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malaria
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describe the drug dufluoromethylornithine/
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treat african trypanosomiasis, inhibits ornitihine decarboxylase, interferes with polyamine metabolism and then DNA synth
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describe allopurinol in anti parasitic treatment
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leishmaniasis, alterantive substrate for HGPRTase that leads to incorporation of allopurinol riboside into RNA that leads to inhibition of protein synth
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describe the drug suramin
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treat african trypanosomiasis, causes decreased ATP synth
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describe the actions of the anti helminthic drugs
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inhibitions of microtubules causes irreversible block of glucose uptake, tubulin plymerization inhibition, depolarizing neuromuscular cascade, cholinesterase inhibition, increased cell membrane permeability, thus calcium loss and shrivel up
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describe the drug pyrantel pamoate
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treats ascaris, pinworm and hookworm. inhibits cholinesterase in worms so you poop them out
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describe the drugs piperazine and diethylcarbamazine.
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GABA agonists and thus paralysis of worm so you can poop it out
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describe the drugs albendazole, mebendazole, and thiabendazole.
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inhibit microtubule polymerization, which causes worm to starve to death
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describe ivermectin
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treat filarial infections, blocks neuromuscular action by binding selectively to glutamate gated chloride ion channels in worm nerves and muscle cells causing death
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describe praziquantel
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broad sppectrum antihelminthic. calcium agonist, permeability of cell effected, tetantic muscular contraction, drug also causes vaculolization and disintegration of the schistosome tegument.
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describe the drug niclosamide
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treats intestinal tapeworms, uncouples oxphos, thus inhibit ATP synth and the worm head and proximal segments are effected leading to detachment
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describe the typical lifecycle for apicomplexia.
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sexual cycle contains micro and macro gametes that join to form a zygote and then an oocyst which gives rise to sporozoites which infect a host cell and become trophozoites and then a schizont and then finally merozoites/tachyzoites that reinfect host cells and repeat the trophozoite to schizont etc.... wow
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how are cysts of intestinal protozoa killed?
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cannot be done by simple chlorination, need to filter or boil the water
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what is a characteristic of protozoal diarrhea compared to other form?
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it is longer lasting
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what are the clinical presentation of entamoeba infection?
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asymptomatic, dysentary, or liver abscess
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what is the mortality/morbidity of E. histolytica?
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2nd to malaria in protozoal death, millions of cases WW, 40K to 110K deaths a year, can get amebic colitis, necrotizing colitis, and intraperitoneal rupture in amebic liver abscess
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lifecycle of E. histolytica?
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fecal oral transmission of cysts, that turn to trophozoites in colon
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epi of E. histolytica?
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WW, tropical, main source of water and food contamination is asympto carrier
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what is the pathogenesis of E. histo?>
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usually diarrhea with slight blood, not inflamed, but 10% are virulent strains that make toxins and cause ulcerative lesions that cause dysentary and bloody diarrhea with leukocytes. It can then invade the host and go to the liver (rarely lung and brain) and cause liver abscess
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how can you diagnose E. histo?
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usually by cysts (4 nuclei is diagnostic) in stool, cysts are passed intermittently so check stool 3 times, can do EIA and PCR too
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how should pts with E. histo be treated?
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if asymptomatic use a luminal agent like iodoquinol, paromomycin, diloxanide furoate. If there is invasive amebiasis like colititis or liver abscess, use metronidazole or tinidazole plus a luminal agent to eradicate colonization
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would should E. histo patients be admitted to the hospital?
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severe colitis pts needing IV volume replacement, fulminant colitis that may need surgery, pts with liver abscess, not responding to therapy
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describe the symptoms of giardia infection.
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asymptomatic to non inflammatory diarrhea which is extra foul smelling, does not invade systemically
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what is the lifecycle of giardia
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cysts out in stool, then ingested, trophozoites in small bowel
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how is the cyst of giardia killed?
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heat and disseication and removed by filtration
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what are the properties of the giardia trophozoite?
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active motile feeding stage causing pathology in small intestine, anaerobic and can thus be treated by metronidazole, no invasive disease or inflammation, attaches to enterocytes via adhesive disks, cannot survive in the environment
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epi of giardia?
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endemic and epidemic disease worldwide, increased risk is MSM, kids in daycare, food handlers, mental patients, travelers, hikers, campers who neglect purifying their water, reservoirs are beavers, muskrats, dogs, other animals, most prevalent enteric pathogen in the US
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if infected with giardia, how long can you pass the cysts?
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up to 6 months
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how do you diagnose giardia?
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3 warm stool samples for trophozoites or cysts (not always reliable), ELISA or immunofluorescence, dudenal string test for trophozoites
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epi of cryptosporidium?
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WW, travelers diarrhea, epidemical, immunocompetenmcy is a major factor in determining severity, zoonotic and human reservoirs, fecal oral transmission
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clinical presentation of cryptosporidium?
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asymptomatic to non inflammatory diarrhea to volumous diarrhea and death in immunocompromised
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describe the hardiness of cryptosporidium cysts.
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very hardy, no water supply can guarantee removal, can remain viable for18 mos, boiled water is recommended for all immunocompromised patients
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lifecycle of cryptosporidium?
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apicomplexia... oocysts in stool, fecal oral transmission and ingestion of cysts, sporozoites in stomach, asexual life cycle in microvilli, merozoites released intraluminally, sexual forms develop in microvilli and then oocytes passed in stool
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how do you diagnose crypto infections?
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fecal smears with cysts lit up via acid fast stain or monoclonal antibody with immunofluorescence.
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treatment for cryptosporidium?
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immunologically normal pt will spontaneously recover while immunodeficient patiens need antidiarrheals and supportive care. nitazoxanide is new and may be useful in crypto and giardia esp in HIV patients
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clinical presentation of trichomonas?
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men: most asympto, 10% urethritis, women: foul smelling green/yellow discharge, vaginitis, cervicitis, half are asympto. neonates will be asympto with spontaneous clearance. This disease does not become invasive
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epi of trichomonas?
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very prevalent in US and WW
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pathophys of trichomnas?
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flagellated trophs adhere to UG tract epi cells and in men will be asympto with occasional non gonococcal urethritis, women will get vaginitis, cervicitis, and non gonococcal urethritis, congenital transmisssion leads to spontaneous clearance in newborn within few weeks
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how do you diagnose trichomonas?
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micr observation of orgs in urethral scraping, urine, or discharge
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treatment for T. vaginalis.
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only if symptoms are bothersome and persistant: metronidazole (note premature birth and no drinking) or if really bad symptoms: intravag clotrimazole tabs
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describe the life cycle of malaria.
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female anopheles mosquito injects sporozoites into blood, sporozoites travel to liver, shcizogony to make merozoites and then merozoites go to blood for asexual cycle of merozoites to intracellular rings (diagnostic for species), to troph, to schizont to merozoites. Male and female gametes are made in the blood, mosq eats em and then they make sporozoites in the gut of the mosquito
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clinical symptoms of malaria?
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chill stage, hot stage and sweating stage. fever spikes are due to schizont rupture and are at constant intervals in vivax, ovale, and malariae. note tertian (48 hr relapses) are in vivax, ovale, and falciparum and quartan (72 hour fever spike intervals) is seen in malariae
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mortality of malaria is due to what?
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cerbral malaria and resp distress: both due to falciparum bc of knob proteins on RBC that cause microvascular occlusions and hemorrhage, also can get anemia and glomerulonephritis (from immune complexes)
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release of hemozoin in malaria causes what?
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blackwater fever: black urine, black blood filters (spleen and liver)
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diagnosis of malaria?
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blood smear with giemsa stain and PCR for speciation
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malaria treatments...
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drug of choice is chloroquine if non resistant, dormant liver stage: primaquine (DNA binder and disrupter), bloodstage falciparum: mefloquine or quinine (increase intracellular pH) and tetra, doxy, pmt sulfa, or clinda. complications: quinidine gluconate (increase pH in organelles) with tetra, artemether is only for severe cases and is not FDA approved
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individuals at risk for T. gondii infection?
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fetuses, newborns, and immunologically compromised
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clinical presentation of toxoplasma infection?
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immunocompetent: lymphadenopathy
immunodeficient: fever, pneumonitis, altered mental status, impaired cardiac function |
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epi of toxoplasma?
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1/3 in US been infected, 65% of world infected, leading cause of MR if congenital
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describe the life cycle of toxoplasma.
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sexual reproduction in cat, oocyst in cat poo, to sheep, cow, goat to form tissue cysts AKA bradyzoites. Ingestion of either raw meat with bradyzoites or cat poo with oocyst causes sporozoite or bradyzoite (tissue cysts in muscle and brain) which can form tachyzoites that replicate and disseminate via blood stream, can go back to tissue cysts
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when is infection of the fetus serious?
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only in first trimester can it cause serious disease, in third trimester, it is no big deal
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the numerous tissue cysts formed in an immunocompromised host can lead to what?
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encephalitis, myocarditis, pneumonitis, and chorioretinitis. asplenics can have life threatening anemia
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diagnosis of toxoplasma?
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PCR or ELISA at 2 times (rising IgM and IgG means acute, high IgG means chronic )
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treatment for toxoplasma?
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note all treatments get the tachyzoites not the bradyzoites. none for immunocompetent, pyrimethamine and sulfadiazine in immunocompromized or clinda, atovaquone, and azithro. pregnant women get sprimycin or clinda
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vector for chagas disease? org? normal orgs infected?
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reduviid bug, T. cruzi, usually small mammals (sylvatic cycle)
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clinical presentation of T. cruzi infections...
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chagoma at site of entry, lymphadenopathy, myocarditis, and meningoencephalitis in acute phase. asympto in intermediate. cardiomyopathy, megacolon, and megaesophagus in chronic
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epi of T. cruzi?
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south america, lots cases, and 50K deaths each year mainly from cardiomyopathy, reduviid bug present in US but not the deficating lesion kind
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life cycle of T. cruzi?
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bug bites and deficates trypomastigotes into wound. tryps invade multiple cell types at bite site, amastigotes develope and replicate in many cell types (heart), cell ruptures and tryps spread via blood, can be ingested by reduviid bug. note metacyclic tryos are found in the reduviid and are more infective than the blood tryps and they replicate in the bug as epimastigotes and spheromastigotes are in the stomach of the vector
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pathophys of T. cruzi?
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more replication in acute phase. symptoms from inflammatory response, cellular lesions and fibrosis, in chronic phase infection is partially controlled by immune response
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what is romano's sign?
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seen in T. cruzi acute infections with uniocular bipalpebral edema and regional lymphadenopathy
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diagnosis of T. cruzi?
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travel history, acute is tryps in blood, chronic is ELISA
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describe the treatment of T. cruzi.
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benznidazole which acts on tryps and amastigotes
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orgs that produce African sleepng sickness?
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Trypanosoma brucei rhodiense in the east and T. b. gambiense in the west. Eastern are zoonotic while western are human only reservoirs
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life cycle of T. brucei?
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tsetse fly bite, tryps in blood, tryps replicate in blood and CNS (late)
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pathophys of T. brucei infections?
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infection leads to malaise, intermittent fever, rash, and wasting, eventually hits the CNS causing behavior and neuro changes like irritability then coma and death
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how does T. brucei infection produce waves of parasitemia?
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it changes its variant surface glycoprotein every 2 wks or so
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what is winterbottoms sign?
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at site of tsetse fly bite in T. brucei infections (large swollen nodule)
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diagnosis for T. brucei?
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micro observation of orgs in tissue of insect bite, lymph nodes, blood or CSF, also get travel history
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treatment for T. brucei?
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T. b. rhodesiense blood stage is suramin or eflornithine and CNS stage is melarsoprol or eflornithine. T. b. gambiense blood stage is pentamidine, suramin or eflornithine and CNS stage is melarsporol or eflornithine
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vector of leishmaniasis?
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female sand fly
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describe the epi of leishmaniasis.
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visceral leishmania is from the donovani (old world) species or chagasi (new world-infects canines and rodents usually). cutaneous leishmania is from tropica and major (both old world) and diffuse cutaneous is from mexicanna (duh new world). mucocutaneous is from braziliensis (new world)
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life cycle of leishmania?
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sandfly infects, promastigotes in skin, macs internalize, amastigotes grow in macs that are at optimal temp (37 C for visceral and 34 for cutaneous and mucocutaneous). amastigotes in blood after mac ruptures, sandfly gets a meal
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visceral leishmaniasis clinical symptoms?
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dissemination to RES, anemia, leukopenia, hepatosplenomegaly. Death is usually due to secondary bacterial infection
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diagnosis of leishmania?
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travel history, microscopic observation of amastigotes in skin biopsy or bone marrow, leishmanin test like PPD to check for exposure.
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treatment for leishmania?
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pentavalent antimonials like Na stibogluconate (pentosam) or meglumine antimoniate. Now amp B in its lipid form is choice bc of shorter course and lower toxicity
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epi of whipworm?
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WW, SE US, puertorico
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life cycle of whip worm?
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ingestion of egg in food contaminated with feces. larvae in small intestine, worms mate in cecum, gravid females secrete large number of eggs into feces
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what is the pathogenesis of trichurias trichuria?
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most are asympto, high worm burdens can lead to bloody diarrhea, rectal prolapse and growth retardation
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diagnosis of truchuris?
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micro observation of the eggs in the stool (football shape with polar plugs)
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treatment of trichuris?
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mebendazole, albendazole, possibly nitazoxanide
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which worm is seen in temperate zones and is the most common helminthic infection in the US?
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E. vermicularis or pin worm
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viability of E. vermicularis and eggs?
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short life span, eggs only infective for 2 weeks after deposition, long standing infection due to reinfection
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life cycle of pinworm?
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fecal oral, develop into adults in cecum and mate, gravid females migrate to perianal region for egg deposition, eggs wideley distributed over perianal area, embryonate for 6 hours then transferred to night clothes, bedding, and air
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treatment of entrobius?
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pyrantel pamoate 1st choice, mebendazole, wash clothes, bedsheets in hhot water, check the rest of the fam
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epi and risk factors for ascaris infection?
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seen in areas of poor sanitation, malnutrition, iron deficiency anemia, impairments of growth and cognition. ~4 mil in the US, WW is most common helminth infection...
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life cycle of ascaris?
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eggs passed in feces, eggs embryonate, eggs ingested, embryos hatch larva in SI, larva penetrate intestinal wall, migrate to liver, heart then lungs, via veins, break through blood lung barrier into alveolar space, migrate up bronchi and trachea, swallowed and return to intestine, develop into adults, adults mate, gravid females lay eggs in feces...
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pathogenesis of ascaris?
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loffler syndrome in lungs, eosinophilia in blood from larval antigens, intestine is generaly asympto but high worm burden can lead to nutritional problems in children and intestinal/biliary tree obstruction
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treatment of ascaris?
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albendazole, mbendazole, pyrantel pamoate, parlytic (piperazine citrate) for intestinal obstruction
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what are the hookworm species?
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ancyclostoma duodenale and necator americanus
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life cycle of hookworm?
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eggs in feces, eggs embryonate, larva penetrates skin (usually foot), larvae in venous blood, migrate to intestine, mature and mate then shed eggs
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pathogenesis of hookworm?
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grounditch, pnumonitis from larvae in lungs, adults in intestine cause nausea, vomiting, diarrheea, microcytic hypochromic anemia
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diagnosis of hookworm infections?
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observation of eggs in stool
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treatment for hookworm infection?
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albendazole, mebendazole, pyrantel pamoate
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epi of strongyloides?
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WW, in US in appalacian states
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describe the pathophys/life cycle of strongyloides.
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filariform infective larvae contacts skin and penetrates, migrates via lymph and veins to pulmonary system, alveoli, up trachea, swallowed, become adults and do parthogenic reproduction, eggs mature to rhabditiform larvae in the intestine, passed in feces and can become filariform or remain as a free living beast in the soil
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what is the cause of accelerated hyperinfections of strongyloides?
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in immunocompromised, autoinfection is possible, this is frequently fatal, note bacteria can hitch a ride on these migrate autoinfectious larvae... not too good...
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what is the pathogenesis of strongyloides?
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most asympto, ground itch. immunocompromised can get loffler syndrome, blood eosinophilia, diarrhea, epigastritis
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diagnosis of strongyloides?
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concentrate 7 stool samples to see the larvae, thus increasing sensitivity, blood eosinophilia is also present
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treatment for strongyloides?
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ivermectin with albendazole as the alternative...
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general structure of tape worms?
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head (scolex), integuement absorbs nutrients since they lack a digestive tract, segmented body contains both male and female gonads
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what tape worm causes cysticercosis? beef tape? fish tape? hyatid cysts?
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Taenia solium. T. saginata. Diphyllobothrium. Echinococcus.
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are humans definitve or intermediate hosts of tape worms? what species are what?
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can be both. definitive hosts are T. solium and saginata and Diphyllobothrium. Intermediate hosts are T. solium and Echinococcus
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what are the lifecycle of cestodes?
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eggs released from proglottids into feces, fecal oral transmission to intermediate hosts, eggs develop in GI tract, larva penetrate and disseminate via blood, tissue cysts form, cysts in tissue of intermediate host are consumed by definitive host, cysts uncoat in stomach and develop into adults in GI tract, proglottid formation and exit in feces.
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what is the pathogenesis of adult tape worms in definitive hosts?
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mild GI symptoms, anorexia and diarrhea can occur. Diphyllobothrium can cause megablastic anemia due to preferential uptake of vit. B12. Most do not realize infection until they notice proglottids coming out of their ass...
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diagnosis of adult tapes?
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T. saginata and solium are by micro observation of proglottids in stool and sometimes eggs. D. latum is by micro observation of eggs in stool since the proglottids rapidly disintegrate
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treatment for tapes?
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albendazole for echinococcosis; praziquantel for taeniasis
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pathogenesis of tape worm cysts?
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T. solium prefers the CNS, miuscle, eye or connective tissue. E. granulosis prefers the liver and E. multiocularis prefers the lung. size of cyst causes issues, if cysts rupture they induce lethal anaphylatic respinse. Echinococcus cysts grow in size and puncture will release larvae that can develop new cysts
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treatment of tissue cysts from tape worms?
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usually need surg for echinococcosis, then medication to keep it from recurring (albendazole)
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diagnosis of tape worm cyst disease?
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CT or MRI of cysts, ELISA for echinococcus
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epi of schistosomiasis?
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second most common tropical disease in the world. S. mansoni in africa and carribean, S. japonicum in SE asia, S. hematobium in africa, Middle east
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lifecycle of schistosoma?
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eggs hatch in water to release motile microcidia, goes in snail and becomes motile fork tailed cerceriae and emerges from snail, cerceriae penetrate skin of host, schistosomulae migrate to pulmonary then systemic circulation, mature into adult worms, S. japonicum and mansoni go to mesenteric vein and secrete eggs through the GI wall to the feces while S. hematobium goes to the vesical plevic plexus passes eggs in bladder and out the urine
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what is the condition in which schistosome cerceriae penetrate the skin causing a papular, pruritic rash and what species usually do this?
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swimmer's itch that usually happens via avian schistosomes and not human schistosomes
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describe the eggs of each schistosome species.
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hematobium is spine on the apex, mansoni is spine on the side, and japonicum has no spine
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pathogenesis of schistosoma?
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granulomas around eggs that get in the liver that block circulation leading to portal hypertension and possible vessel rupture, bloody diarrhea from migration of eggs across the colon or blood in urine from similar migration from bladder. Granuloma formation, fibrosis and secondary bac infections predisposes S. hematobium infected ppl to bladder cancer
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diagnosis of schistosoma?
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history and observe eggs in feces or urine
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treatment of schistosoma?
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praziquantel
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what are the cutaneous filirial parasites? lymphatic?
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Loa loa and Onchocera volvulus. Wuchereria bancrofti and Brugia malayi
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epi of filiarial parasites?
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W. bancrofti in tropics and sub tropics, Brugia in SE asia, O. volvulus in Africa, S America
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what are the vectors for the filarial nematodes?
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mosquito for wuchereria and brugia, horsefly for LOa loa, and blackfly for O. volvulus
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basic lifecycle of the filariae?
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microfilariae develop in vector and are passed to definitive host, larvae migrate to lymphatics or skin to become adults, then make more microfilariae that go to the blood, cause an immune response and eosinophilia
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pathogenesis of Los
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occasional microfilariae in eye, but not common
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pathogenesis of onchocerca?
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seen in the eyes, immune response leads to schlerosing keratitis and blindness. microfilariae are not normally present in the blood
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how do you diagnose the filiariae?
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all but onchocerca are by microfilariae in the blood, onchocerca has them in skin snips
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treatment of microfilariae?
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ivermectin, diethylcarbamizine, or albendazole
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pathophys/lifecycle of trichinellosis?
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ingest larvae in raw meat, gastric actions liberate larvae, larvae develop in duodenum and jejunum, mate and bear off spring adult worms go out in the stool. newborn larvae penetrate intestinal wall, enter lymph, go to bloodstream and move to areas of implantation. larvae encyst in striated muscle and induce the muscle cells to change into nurse cells. They remain encysted and viable for years.
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epi of trichinellosis?
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sporadic in US, rare, like 50 a year
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clinical disease of trichinellosis?
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light infection will have minimal to mild flu symptoms from migrating larvae, medium infection will have fever, GI distress, eosinophilia, and muscle pain. Heavy infection will have severe neuro symptoms including psychosis and meningoencephalitis. Lethal infection results when myocarditis, encephalitis and pneumonitis combine, resp arrest can be from heavy invasion pf teh diaphragm muscle
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diagnosis of trichinellosis?
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history of eating raw pork or bear. larvae in muscle biopsy, eosinophilia, ELISA
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treatment of trichinellosis?
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mebendazole during initial phase of infection. steroid treatment to reduce the immunologic response to the larvae
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