DISEASE



|INTESTINAL PROTOZOA | | | | |

|Entamoeba histolytica | | | | | |

|Amebic dysentery (bloody, |Acute: lower abdominal discomfort, |Transmission: ingestion of cysts via |•No animal reservoir |•identification of the |Metronidazole |•Avoid fecal |

|mucus diarrhea) and liver |flatulence, tenesmus, constipation |fecal-oral route in contaminated food |•Trophozoites invade |organism in the stool or |(Flagyl®) = a |contamination of food &|

|abscess |Chronic: low-grade symptoms - |& water (also oral-anal) |colonic epithelium & |tissues via: |mixed amebicide |water |

| |occasional diarrhea, weight loss, |Lifecycle: |secrete enzymes »» local |O & P Test: trophozoites in |effective against | |

| |fatigue |•Ingestion of cysts (4 nuclei (central|necrosis »» “teardrop” |diarrheal stool or cysts in |both luminal and |•Observe good personal |

| |90% infected = asymptomatic carriers|dot w/ dense peripheral chromatin & |ulcer »» may disseminate, |non-diarrheal stool; note that|systemic forms of |hygiene (hand washing) |

| |Amebic abscess of liver (ameboma): |chromatoidal bars=ribosomes), |esp. to right lobe of |there will not be large |the disease plus a| |

| |RUQ pain, weight loss, fever, |nonmotile, rigid cell wall, |liver where it causes |numbers of polymorphonuclear |luminal amebicide |•purify water supplies |

| |tender, enlarged liver |nondividing, 10-20 microns in |abscesses |leukocytes in stool (vs. |like diloxanide |(boiling/filtration is |

| | |diameter) |•worldwide (tropical, poor|shigellosis, salmonellosis, |furoate |effective, but |

| | |•Trophozoites (motile, phagocytic for |sanitation is most common)|ulcerative colitis) | |chlorination is not) |

| | |RBCs & bacteria, disease-causing, |•1-2% in USA |Biopsy | | |

| | |amorphous, 1 nucleus=located | | | | |

| | |eccentrically w/ evenly distributed | |Distinguish between: | | |

| | |chromatin) excyst in small intestine | |Entamoeba dispar | | |

| | |(1 cyst »» 8 trophozoites) | |(nonpathogenic, | | |

| | |•Trophozoites invade tissues of colon | |morphologically identical) by | | |

| | |•Trophozoites encyst in colon OR cause| |PCR or monoclonal Antibodies | | |

| | |pathology (liver abscess, brain | |Entamoeba hartmani: cysts have| | |

| | |abscess, flask-shaped ulcer) | |4 nuclei, but are 95% |after mosquito bite (coincide w/ |transplacentally, blood transfusion, |(merozoites & spleen) |(for species id) |•kills merozoites |OR chloroquine + |

|•P. malariae ~4% |cycle between RBCs) |IVDA |•P. falciparum is more |Giemsa-stained smears |•does not affect |Fansidar |

|•P. ovale is very rare |•periodic cycle of CHILLS, then | |severe: children/elderly |•ring-shaped trophozoites can |hypnozoites |•mosquito netting, |

| |FEVERS, then SWEAT (due to |Highlights of Lifecycle: |most @ risk |be seen within infected RBCs | |window screens, |

| |erythrocytic phase) develops several|•Asexual cycle (schizogony »» |•Hg is degraded to provide| |Primaquine to |protective clothing, |

|>200 million infected |days after onset (note that |schizonts) in humans (intermediate |aa’s for protein |Diffs between P. falciparum & |prevent relapses |insect repellents |

|>1 million die each yr |parasites synchronize themselves) |hosts) |biosynthesis »» heme |others: |•kills hypnozoites|•protection more imp. |

| |•fever spike (37°C to 41°C) |•Sexual cycle (sporogony »» |released »» Heme |•gametocytes are | |during the night |

| |w/nausea, vomiting, & abdominal pain|sporozoites) in mosquitoes |polymerase of plasmodium |crescent-shaped, whereas |Mefloquine or |•drainage of stagnant |

| |»» drenching sweats as fever breaks | |makes insoluble hemozoin |others are spherical |Quinine-Fansidar |waters |

| |•Splenomegaly (most) |•schizogony=nuclear division without |(malarial pigment) |•infects all RBCs »» higher |(sulfadoxine-pyrim|•partial immunity based|

| |•Hepatomegaly (1/3) |cell division | |parasitemia level (Note: P. |ethamine) |on humoral antibodies |

| |•Hemolytic Anemia (prominent) |•P. vivax & P. ovale (48hr |•Susceptibility: |vivax infects reticulocytes, |combination for |that block merozoites |

| |•Renal damage, esp. P. falciparum |cycle)-benign tertian (recurs every |blacks < whites |whereas P. malariae infects |chloroquine-resist|from invading RBCs |

| |•GI problems |3rd day) |•Sickle-cell trait |mature RBCs only) |ant strains of P. |occurs in infected |

| |•Superinfections |•P. falciparum (48hr cycle)-malignant |provides protection from |•produces more merozoites via |falciparum |individuals |

| |P. falciparum untreated: |tertian (every 3 days) |malaria (RBC does not |asexual reproduction | |•determine what causes |

| |•brain/kidney involvement may be |•P. malariae (72hr cycle)-benign |support growth) |•destroys more RBCs »» | |multi-drug resistance |

| |fatal |quartan (every 4 days) | |decrease in tissue oxygen is | |•no vaccine |

| |Other threee: | | |bigger problem | | |

| |•usually self-limited | | |•sticky knobs cause adherence | | |

| |P. vivax & P. ovale: | | |to & plugging-up of | | |

| |•Relapses may occur up to several | | |capillaries & vessels which | | |

| |yrs after initial illness due to | | |may lead to life-threatening | | |

| |hypnozoites latent in liver | | |hemorrhage & necrosis | | |

| |•Recrudescence=controllable # of | | |(brain»»cerebral malaria) | | |

| |parasites remain latent in RBC and | | |•extensive hemolysis/kidney | | |

| |reactivate upon physical | | |damage »» hemoglobinuria »» | | |

| |trauma/immunosuppression | | |dark urine = “blackwater | | |

| | | | |fever” | | |

|Toxoplasma gondii | | | | |

|Toxoplasmosis |Immunocompetent: |Transmission: contact with cat feces |•may infect any mammal & |Dx is based mainly on clinical|Congenital (with |•cook meat thoroughly |

| |•most are asymptomatic/self-limiting|or ingestion of cysts in undercooked |any nucleated cell |manifestations, serologic |or without |to kill the cysts |

|•infects 10% of world |»» chronic with cysts persisting for|contaminated meat; also transplacental| |procedures (IgM), the |symptoms) AND | |

|•intracellular parasite |years |transmission |High Risk Groups: |demonstration of cysts in |Immunocom- |•pregnant women should |

|•Apicomplexan, so has |•some resemble infectious | |•Immunosuppressed |tissues, or inoculation of |promised: |avoid undercooked meat |

|specialized structures @ |mononucleosis (heterophil negative) |Lifecycle: |•Fetus: only if mother is |infected materials into |•sulfadiazine & |& contact with cats |

|anterior end of cell that | |•Domestic cat ingests cysts in raw |infected for first time |animals |pyrimethamine |(they should esp. |

|aid in invasion |Congenital infection: |meat (mice) |during pregnancy; 35-40% | |combination |refreain from emptying |

|(=rhoptries) |•abortion, stillbirth (1st |•Bradyzoites fromed in cat small |transmission rate, with |Tachyzoites have been found in| |cat litter boxes) |

| |trimester) |intesttine |10% of those infants |bronchoalveolar lavage | | |

| |•neonatal disease w/encephalitis, |•Mucosal cells infected |becoming symptomatic |specimens from HIV pts. | |•cats should not be fed|

| |chorioretinitis (»blindness), & |•Male & Female gametocytes formed | | | |raw meat |

| |hepatosplenomegaly |•Gametocytes fuse to form oocysts |•worldwide |Acute & congenital: | | |

| |•fever, jaundice, intracranial |which are then shed in cat feces | |•immunofluorescence assay for | | |

| |calcifications and hydrocephalus |•Human ingests/makes contact with |•1% of domestic cats in |IgM antibody is used | | |

| |•most infected newborns are |oocysts |USA shed Toxoplasma cysts | | | |

| |asymptomatic though, BUT may develop|•Cysts rupture in small intestine and | |•Microscopic examination of | | |

| |chorioretinitis or mental |release forms that invade gut wall | |Giemsa-stained preps shows | | |

| |retardation months to yrs later |through receptor mediated process | |crescent-shaped tachyzoites | | |

| | |•Macrophages ingest into phagosomes | |with dark-staining nuclei | | |

| |Immunosuppressed: |where Toxoplasmosis inhibits lysosome | | | | |

| |•life-threatening disseminated |fusion with phagosome | | | | |

| |disease |•Forms differentiate into rapidly | | | | |

| |•primarily encephalitis |multiplying trophozoites | | | | |

| | |(=tachyzoites) | | | | |

| | |•Tachyzoites kill macrophages & invade| | | | |

| | |others | | | | |

| | |•CMI limits spread | | | | |

| | |•Parasite enters host cells in brain, | | | | |

| | |muscle, liver, eyes...where they | | | | |

| | |develop into pseudocysts containing | | | | |

| | |dormant organisms (bradyzoites) | | | | |

| | | | | | | |

|Pneumocystis carinii (actually a fungus) | | | | |

|Pneumonia in |•sudden onset of fever, cough, |Transmission: airborne inhalation, |High Risk Groups: |•sputum specimen (usually less|Trimethoprim-sulfa|Chemoprophylaxis with |

|immunocompromised |dyspnea, and tachypnea is typical of|spread by respiratory droplets; not |•premature infants |suitable) |methoxa-zole |trimethoprim-sulfametho|

|(PCP) |Pneumocystis pneumonia (an |transmitted from person-to-person |•infants under 3 months | | |xazole for |

| |interstitial plasma cell pneumonia) |though |•malnourished children |•bronchial brushing/lavage or |Pentamidine & |immuno-compromised |

|•mortality rate >80% if |•bilateral rales & rhonchi | |•immunosuppressed |transbronchial biopsy |atovaquone are | |

|untreated, ~50% if treated|•chest X-ray » diffuse interstitial |•extracellular organism found in lungs| | |alternative drugs | |

|•normally a commensal |pneumonia | | |Giemsa-stained lung smears: | | |

|•first disease diagnosed |•more gradual onset in infants |Lifecycle: | |•look for trophozoites & | | |

|in >50% of AIDS pts | |•cysts inhaled into alveoli | |intracystic bodies (opposed | | |

|•worldwide (up to 70% of | |•inflammatory response causes frothy | |comma-like particles) which | | |

|people have been infected)| |exudate that blocks oxygen exchange | |are diagnostic | | |

| | |•organism does not invade lung tissue | | | | |

| | |•pneumonia results when host defenses | |•no serologic test exists | | |

| | |are reduced | | | | |

|Trypanosoma cruzi | | | | |

|Chagas’ disease (American |acute phase: |Transmission: through bite of |•most common in children |Acute: |Acute: |•protection from bite |

|trypanosomiasis) |•facial edema & a nodule |reduviid bug (Triatoma & Rhodnius); | ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download