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Protozoans Trichomonas Vaginalis Basic Characteristics Flagellated Protozoan Exists mainly in trophozite stage and can’t survive outside of host Organism only resides in female lower genital tract and male urethra. It is noninvasive so can’t cause systemic infection. E. Histolytica (Amebiasis) Single nucleus org. with ingested RBCs Naegleria Fowieri Acanthomoeba Giardia Frothy discharge (yellow green) Strawberry cervix Pruritis, vaginitis Eosinophilia pH>4.5= malodorus Transferred via fomites Think Abscesses (anchovy paste) Associated with poor water quality and travel Disseminates into brain, liver, etc. and for abscesses Symptoms: acute infection causes dysentery with abdominal pain, chronic infection causes recurrent episodes with dysentery & dissemination to liver, brain, lung. Flask Shaped Ulcers on biopsy Treatment Metronidazole Safe Sex Treating partner very important since males are often asymptomatic Metronidazole for symptomatic iodoquinol for asymptomatic Must use both Paromomycin is the drug of choice amphotecerin B shown to work in vitro infects the brain (meningitis) Patient comes in obtuntded, very sick with eosinophilic meningitis points to naegleria, toxoplasma, or Cryptococcus Altered sense of smell early in disease process Causes keratitis, contact lenses predispose Destroys cornea Think Keratitis when you think acanthamoeba Difficult, some topical regimens available Polyhexamethylene biguanide, and many more Campers drinking from mountain stream is classical presentation Abdominal distension, diarrhea, flatulence Metronidazole In pregnant women use paromomycin as replacement (1st trimester) Motile trophozoites in a wet mount Life Cycle a) Starts with a mature cyst that is ingested & travels to small intestine b) Traveling into small intestine there is transformation back into trophozites that multiply & are excreted in the small intestine c) Main stages of trophozites are diagnosed either in stool as mature cysts or as trophozites from different organs d) Can have either asymptomatic infections, intestinal dz or extra intestinal abscesses Diving and swimming in warm waters An amoeba THINK CONTAMINATED CONTACT LENS An amoeba Most common parasite in US Animals are a reservoir Manifests in small intestine, not dysenteric ds! (unlike E.Coli and Shigella) Fatty stools THINK of bad smelling, floating stool (CAMPING) Clinical Presentation Cryptosporidium Trypanosome Brucei Think community outbreak with cryptosporidium Haploid and diploid stages (oocystssporozites which differentiate into merozoites in GI tract) Voluminous diarrhea More severe in immune-compromised Leads to dehydration Acid Fast Oocysts (same as Giardia, but more commonly associated with immune compromised) Treat with nitazoxanide (new drug) Requires a vector (tse-tse fly in Africa) Genetic variation is a big deal with this (host-organism fight back and forth with Ag variation, eventually host loses) KNOW ABOUT ANTIGENIC VARIATION WITH THIS BUG African Sleeping Sickness Happens when parasite enters CNS Blood stage use pentamidine (has a lot of toxicities hypoTN, nephrotoxic, etc); can’t penetrate CNS CNS stage use melarsoprol (can have reactive encephalopathy); if you can’t Tx E. African brucei w/ first dose multiple won’t do anything (W. African is effected w/ multiple dosing) Can use eflornithine for W. African T brucei Trypanosome Cruzi Found primarily in S. America Think C’s Cruzi, Chagas, Cardiac, megaColon, Children Chagas disease Cardiomyopathy, megaesophagus, megacolon ANS ganglia destruction Inflammatory response ds. Swelling around eye is one of the first signs (Romana Sign) Leishmania donovoni Toxoplasmosis Transmitted by sand fly Macrophages take up promastigote which then differentiate into amastigote, infection propagated by amastigotes Rarely manifests in immunocompetent Most of population is seropositive Intracelluar replication thus CMI response Spread by cat feces and pork CNS disease in AIDS patients (ring enhancing lesions) THINK pregnant woman w/ cats 3 forms of Leishmaniasis, each caused by a different organism Visceral is most serious form (internal organs affected) Cutaneous forms skin ulcers Mucocutaneous is disfiguring Think: Congenital defects! Part of ToRches Generalized lymphadenopathy, thrombocytopenia is associated with this infection Also associated with chorioretinitis (loss of eye sight later life due to congenital defect earlier in lfe) Falciparum, vivax, ovale, and malariae are subtypes Damage is from immune system Spread by Mosquito (anopheles) livershizontmeroziteruptures invades bloodstreamerythrocytic shizontruptures Febrile periods follow cycle of red cell lysis Vivax, ovale hang out in liver Falciprum and malariae don’t hang out in liver Duffy blood group antigen is receptor for vivax Unique because it infects blood Plasmodium (malaria) IF someone comes from a third world country with high fever and respiratory distress think malaria Falciparum binds to postcapillary endothelial cells and noninfected RBC’s. Can cause occlusion of blood flow. Sickle cell patients have protection against malaria Falciparum gives the worst clinical picture Malariae has 72 h fever spikes, has rosette shizonts Falciparum, vivax, and ovale have 48 h fever spikes Falciparum has crescent shaped gametes and trophozoate sometimes look like signet cells. Stibogluconate Sodium (affx redox sys of bug) Side effx: pain at injection site, chemical pancreatitis, BM suppression, muscle and joint pain Treat with TMP-SMX or atovaquone for prophylaxis Pregnant women should avoid cat litter (only causes congenital defects if mother infected while pregnant, being seropositive before being pregnant doesn’t cause congenital defects) Avoid cat litter Quinine derivatives for RBC stage(won’t kill gametes of falciparum), quinidine is used for lifethreatening falciparum , Primaquine for vivax and ovale in liver stages (give w/ food to mimze GI distress; can cause hemolytic anemia in G6PD def pts) Falciparum is resistant to chloraquine often Mefloquine resistance in N. Thailand Tx p. falciparum w/ Malarone (atovaquone/proquanil) Metazoans (nematodes, flatworms, flukes) Ascaris lumbricoides Basic Characteristics Large intestinal round worm Clinical Presentation Treatment Degree of disease related to number of organisms present Larva move from lungs to small intestines Mebendazole inhib tubulin dimer formation; teratogen, pyrantel pamoate Asymptomatic with eosinophilia Symptoms: Purpura, eosinophils in lungs, intestinal problems Eggs not in stool, they hatch in intestines Filariform larvae penetrate skin and initiate infection, or can have autoinfection from larvae in intestines If immunosuppressed, then preexisting infection can become apparent Think about this in G-sepsis, travels back up then down into GI system from respiratory (re-infection) Ivermectin inhib glutamate gated Cl- channels and GABA gated channels, which are located in bugs but in CNS in humans (selectivity) Egg of Acaris lumbricoides Strongyloides stercoralis Enterobius vermiculars Taenia saginata & solium Autoinfection Hyperinfection in the immunocompromised (disseminated infection with abdomen/respiratory distress and GNR sepsis) Pinworm infection Most common helminth infection in US THINK perianal itchness Perianal irritation Dx. By finding adults/eggs in perianal region “Scotch tape test” No eosinophilia because no tissue invasion. Pyrental pamoate binds nicotinic receptors and causes spastic paralysis Sanitize bedclothes Treat entire family Cestodes Scolex=head with sucking part Proglottids= segment that produce eggs Prazinquantel Saginata has very little symptoms unless infection is heavy (beef) Solium eggs are infectious, cystiercosis can develop (pork) Dx. By eggs in stool Schistosoma spp. Trematode Blood fluke S. mansoni (Africa), japonicum (Asia), haematobium (Africa) Life cycle involves snails (intermediate hosts) and mammals (primary hosts) Snail control is important for disease control. Infections often occur after swimming in fresh water. Get dermatitis due to penetration of infectious forms S. haematobiumbladder granulomas (also associated with bladder cancer squamous cell) S.mansoni/japonicumperiportal fibrosis/hepatosplenomegaly Hypersensitivity to eggs is major cause of pathology dx. with egg in urine or stool dx. by egg in stool (classic pics below) Female sexual parts are inside male S. mansoni. Remember: shistosoma mansoni has a subterminal spine S. haematobium. Remember: shistosoma haematomium has a terminal spine S. japonicum. Praziquantel incr permeability to Ca++ (hepatic metab via CYP 450)