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58 Cards in this Set
- Front
- Back
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Malaria: Protozoa or Hemolinth
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Protozoa (single cell)
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How is malaria transmitted?
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Female anopheline mosquito
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Beginning and ending with a blood meal, describe the life cycle of plasmodium.
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Female anopheline mosquito takes blood meal (spits anti-coagulant and sporozoites)
Injects 1-30 sporozoites Infect hepatocytes Sporozoite-->trophozoite-->Schizont (1000's of nuclei) Cytoplasm wraps each nucleus in schizont-->Merozoites 6-18 days later: 10K merozoites (asexual reproduction) rupture from hepatocyte Merozoites can infect hepatocytes or RBC's In RBC: 25 merozoites form and burst cell Infect other RBC's or dx/dy into gametocytes Mosquito blood meal takes in gametocytes Gametocytes fuse-->Ookinete Ookinete attaches to gut wall Dx/dy-->Sporozoite-->salivary glands |
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How does the life cycle of p. falciparum differ from p. ovale and p. vivax?
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p. falciparum doesn't have a latent liver stage
p. ovale and p. vivax produce hypnozoites which lay dormant in liver |
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Which forms of plasmodium produce hypnozoites?
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p. vivax
p. ovale |
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What stage of parasite are associated with the pathology and clinical manifestations of malaria?
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Asexual erythrocytic stage parasites
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What are the clinical manifestations of a malarial paroxysm?
What event does the paroxysm correspond to? |
Paroxysm: sudden uncontrollable attack
Sudden onset of chills & vigorous shivering (cold stage) despite high temp Intense heat with severe headache, fatigue, myalgia (muscle pain), profuse sweating [hot stage] Paroxysm corresponds to rupture of infected erythrocyte, release of merozoites (antigens, toxins as well), which result in an immune response (TNF-alpha-->fever) |
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Why isn't the absence of periodic fevers enough to exclude the diagnosis of malaria?
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Naive individuals, i.e., those who have never been exposed to malaria before, do not exhibit synchronous development of the parasite, thus they don't have periodic fever paroxysms
Synchronous development - all of parasites within host are at same stage (ring, trophozoite, schizont) |
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Why does falciparum malaria exhibit an increased morbidity and mortality?
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-all erythrocytes invaded
-large number of merozoites -sequestration of parasite via adherence in small postcapillary vessels -immune evasion -complications |
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What form of malaria is associated with splenic rupture?
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p. vivax
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What form of malaria is associated with nephrotic syndrome?
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p. malariae
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What is hemozoin and how is it related to hetpatic/splenic enlargement?
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Hemozoin is a malaria pigment released during rupture of RBC's
Macs in liver and spleen try to ingest RBC's infected with parasite/containing hemozoin, also ingest normal RBC's, and just hemozoin |
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Clinical presentation of cerebral malaria?
Cause? |
Diffuse encephatlopathy with LOC (stupor-->coma), may be rapid or gradual
Patient is unresponsive to pain, visual, and verbal stimuli Caused by sequestration of RBC's infected with p. falciparum in cerebral microvasculature |
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What is the advantage of RBC sequestration for malaria? How is it mediated?
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Avoidance of spleen and subsequent elimination of infected RBC's
Mediated by electron-dense protuberances on surface of infected RBC ("knobs") Knobs expressed during trophozoite and shizont stages and are restricted to p. falciparum Knobs serve as contact poitns between infected RBC and endothelium |
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Thick Smear vs Thin Smear: Parasitic Diagnosis
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Thick blood smear: superior for overall detection of parasite
Thin blood smear: preferable for species identification |
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A patient presents with fevers, chills, malaise, anemia, and a history of being in a malarial endemic area.
Blood smear comes back negative for parasites. Next step? |
Additional smear every 6-12 hours for 48 hours.
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Fast-acting blood schizontocides:
site of action, use, examples |
Act upon parasite within RBC's
Quickly relieve clinical syx Chloroquine Quinine Mefloquine Artemisinin Derivs (quinhaosu) |
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Tissue schizontocide: site of action, use, examples
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Act on schizontocides (hypnozites) in hepatocytes
Use to prevent future relapses in p. ovale and p. vivax Primaquine |
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Slow-acting blood schizontocide: example
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doxycycline
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Prophylaxis for resistant and non-resistant strains of malaria?
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Non-resistant: chloroquine (Central America above Panama Canal only)
Resistant: Malarone (atoraquone-proguanil)--a combination drug Mefloquine Doxycyline |
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Treatment for non-falciparum malaria?
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Chloroquine + Primaquine
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Treatment for resistant p. falciparum?
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Quinine (can be delivered IM)
Artemether (Artemisinin) |
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What is presumptive treatment for malaria? Under what circumstances would it be appropriate?
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Presumtpive Tx = Standby Tx
Take chloroquine prophylaxis and carry a drug like Fansidar, mefloquine, or quinine (take only if exhibit syx of malaria) Appropriate for prophylaxis in regions of chloroquine-resistant malaria |
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What is the basis of chloroquine resistance?
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Reduced chloroquine accumulation in parasite's food vacuole
Chloroquine mechanism is to enter food vacuole and interfere with hemozoin (malaria pigment) formation |
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How does mass administration of a drug contribute to spread of drug resistance?
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Increases drug pressure by exposing a larger parasite population to drug
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How does a long drug half-life contribute to spread of drug resistance?
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Drugs that are slowly eliminated will lead to a longer exposure of parasite to sub-therapeutic drug concentrations.
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Primigravid vs Multigravid: Vulnerability to Maternal Malaria
Why is there a difference? Treatment? |
Primigravid>>>Multigravid
Multigravid women can block the infected RBC interaction with CHONDROITIN SULFATE A via Ab's because they've had prior exposure Can vaccinat primigravid women with parasite protein that binds to CSA to mimic multi-gravid state |
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What is the vector for leishmaniasis?
What are the different forms? Which species contribute to each one? |
Female phlebotomine sandfly
Cutaneous: Leishmania tropica, L. major, L. mexicana, L. braziliensis Visceral: L. donovani Mucocutanous: L. braziliensis |
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What is the geographic distribution of Leishmaniasis (include different forms)?
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Cutanoues: middle East, Brazil
Visceral: Middle east, Brazil Mucocutanoues: Brazil L. tropica sis found in middle east, NOT Brazil |
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Beginning and ending with a blood meal, describe the life cycle of leishmaniasis.
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Infected female phlebotomine sandfly injects promastigote (flagellated)
Macs phag promastigote Enter amastigote stage (non-motile) Infect other macs Sandfly takes up other macs infected with amastigotes Transform into promastigotes, develop in gut Migrate to proboscis |
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Leishmania: Protozoa or helminth?
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Protozoa
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Visceral leishmaniasis:
AKA Reservoirs Strains |
Kala-azar
Dogs (feral or domesticated) are reservoir for L. chagasi L. donovani, L. chagasi, L. infantum |
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Cutaneous leishmaniasis:
Subtypes and Strains |
Old World: L. tropica, L. major, L. aethiopica
New World: L. Mexicana, L. braziliensis |
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Strains causing diffuse cutaneous leishmaniasis?
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L. aethiopica, L. mexicana
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Strains causing mucocutaneous leishmaniasis?
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L. braziliensis
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Visceral Leishmaniasis:
Clinical presentation Complications Laboratory findings Diagnostics |
Prolonged fever (CHRONIC!!!)
Pronounced Splenomegaly(!!!) Anemia Leukopenia Hypergammaglobulinemia Complications: progressive wasting, inter-current infections (pneumonia, Tb, diarrhea) Lab findings: leukopenia, hypergammaglobulinemia, hypoalbuminemia, thrombocytopenia Dx: BM or splenic aspirate, blood/nasal secretions contain organism; skin test only positive after active dz |
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Leishmania:
Treatment |
Antimony (Stibogluconate--STB; IV or IM)--HIGHLY TOXIC
For antimony-resistance: Miltefosine (PO)--WONDER DRUG 2nd Line Defense: Amphotericing B (IV) |
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Leishmaniasis:
Preventive Methods Diagnosis |
Prevention:
Suppress reservoirs (dogs, rats, gerbils, small mammals/rodents) Suppress vector: Sandfly Prevent sandfly bites: long sleeves, insect repellent w/DEET, permethrin treated bed nets (sand fly is small enough to fit through bed net; need to be treated!) Dx: Biopsy! of ulcer, BM, liver, spleen, LN showing leishmania Dx of mucocutaneous may require PCR as very few parasites present in ulcers |
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What is the most common vector of trypanosomes?
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Tsetse fly
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Beginning with the vertebrate host, describe the life cycle of trypanosomes.
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Parasite grows and reproduces as trypomastigote in blood (motile form)
Vector ingests trypomastigotes during blood meal Transform into epimastigotes, reproduce in gut/salviary glands Transform into trypomastigotes to infect a new host |
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African Sleeping Sickness:
Eastern vs Western Strains Symptoms Diagnosis Treatment |
East African (more severe): T. rhodesiense
West African (slowly progressing): T. gambiense Syx: Indurated, painful ulcer (heals in 2 wks), LAD, INTERMITTENT fevers, CNS involvement: daytime drowsiness, bhvrl changes, coma, death Healing of ulcer = blood stage, usually asymptomatic LAD = lymphatic stage (WINTERBOTTOM'S SIGN--LAD in posterior cervical triangle); CACHEXIA is part of lymphatic stage CNS involvement due to parasite crossing BBB (meningoencephalitis) Dx: Blood: several days--thin/THICK smears LN or CSF aspirate Treatment: Early, i.e., no CNS involvement: suramin, pentamidine (good prognosis) Late: Melarsapol (arsenical! HIGH TOXICITY!), eflornithine (RESURRECTION drug) |
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What is zoonosis and which strain of trypanosomes exhibit it?
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Zoonosis: infection naturally transferable between animals and humans
T. rhodesiense (bush buck = wild animal reservoir) |
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How does infection from the tsetse fly bite differ from other insect bite transmissions?
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Tsetse is a pool feeder: metacyclic trypomastigotes in saliva and blood pool they feed off, enters bite wound (not an injection!)
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Why does African Sleeping Sickness exhibit intermittent fevers and parasitemia?
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Trypanosomes covered with VARIABLE SURFACE GLYCOPROTS (VSG)
Contain genes that makes 1000's of different types of VSG's Thus immune system will continually mount immune response (new Ab formed for each new VSG) VAT = variant antigenic types of VSG |
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American Trypanosomiasis:
AKA Trypanosome Strain Vector Route of Entry Strain Symptoms |
AKA Chagas' Disease
Vector: Kissing Bug (reduviid bug; TRIATOMINE)--eats and poops! Feces contains trypomastigote Enters via wound or mucous membrane, even hair follicle Strain: T. Cruzi (Tom Cruise is an American actor) Syx: damage to neural plexi (Meisner's, Auerbach's) that control gut motility, thus, MEGA COLON; damaged conduction system of heart-->DILATED Cardiomyopathy |
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Describe the life cycle of T. cruzi.
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Enters via wound or mucous membrane, enters blood-stream (trypomastigotes are non-dividing), invades host tissue and transforms into amastigotes (binary division), reuptake of trypomastigotes in blood stream by kissing bug
Convert to epimastigote and replicate in bug gut |
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Chagas' Disease:
Diagnosis Treatment |
Parasite Detection via blood smears, inoculation into mice, XENODIAGNOSIS
Serum Testing Treatment: Acute: Nifurtimox, Benidazole (less effective for chronic) Chronic: Treat syx |
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Amoeba: protozoa or hemolinth
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Protozoa
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Entamoeba hystolytica:
Symptom Progression Carriers Route of Entry Life Cycle |
Symptoms (most people clear the disease and are asyx):
-if invade intestinal mucosa-->diarrhea (dysentery) -penetrate portal circulation-->hepatic abscess -penetrate diagphram into lung-->pulmonary abscess (death!) Homosexual men Fecal-Oral transmission: Trophozoite-->Binucleate Precyst with CHROMOTOID bodies (aggregates of ribosomes), food vacuoles--> Tetranucleate Cyst (mature) sans food vacuoles |
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Where in the gut do entamoeba tend to reside?
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Colon
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Where in the gut do giardia tend to reside?
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Upper GI
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Encystation vs Excystation
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Encystation:
Trophozoite-->Cyst (chromatoid bodies, protective coat), passed in feces Note: cysts are infectious form Trophozoites cause disease Excystation: Cyst-->Trophozoite (motile) |
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Non-Invasive vs Invasive Amebiasis
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Non-invasive: ameba colony ion intestinal mucosa, asyx cyst passing, non-dysenteric diarrhea
Dysenteric Diarrhea must have blood and/or mucous in stool, 2-3 times per day Invasive Amebiasis: necrosis of mucosa (ulcers, dysentery), ulcer enlargement (severe dysentery, colitis), metastasis (extraintestinal amebiasis) |
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What is an amoeboma?
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Inflammatory thickening of intesetinal wall around abscess (can be confused with tumor), granulomatous
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How would peritonitis affect a stool exam screening for amoebiasis?
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Cessation of cyst production means (-) stool exam
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Cause of cutaneous amebiasis? Clinical presentation?
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Intestinal or hepatic fistula (abnormal connection between anatomic structures)
Mucosa bathed in fluids containing trophozoites Ulcers may be perianal, urogenital |
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Amoebiasis:
Diagnosis Treatment |
Dx:
Intestinal: Stool exam (need at least 3; diagnostic sensitivity is low because poop has crud in it), sigmoidoscopy, lesion aspirate, Ag detection (detects old and new infections) Extraintestinal (Hepatic): RUQ pain Imaging Abscess aspiration (not recommended for risk of dissemination) Tx: Asyx/Luminal Parasite: Iodoquinol or Paromycin Extraluminal: Metronizadole followe by luminal agents--metro won't clear luminal parasites on its own Drain liver abscess if high prob rupture |
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Giardia Lambia:
Route of Entry Reservoirs Life Cycle Symptoms Diagnosis Treatment |
Fecal-Oral transmission (poor hygiene, poor sanitation, male homosexuals: oral-anal contact)
Reservoir: beaver Life Cycle: Cyst ingested with contaminated water or food Cysts excyst and trophozoites (replicative stage) colonize small intestine Cysts passed in feces Syx: After 1-2 week incubation-->EXPLOSIVE, watery diarrhea (foul smelling), NO BLOOD OR MUCOUS! (possible mech: obstruction of fat absorption) Dx: Stool test for 3 non-consecutive days Aspirate, biopsy Enterotest (string test) Tx: Metronizadole WASH YOUR HANDS, BOIL WATER, etc. |
