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95 Cards in this Set
- Front
- Back
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Cryptosporidiosis
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|Cryptosporidium parvum|
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C. Parvum-Life Cycle
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Fecal Contamination ●Infective Stage: Sporulated Oocyte-4 infectious units. ●Intestinal epithelial cells, internalize sporozite ●Differntiation into merozite and released into gut lumen ●Immunocompromised host replication occurs many time thus leading to Intestinal symptoms ●OBLIGATE Intracellular parasite ●Can differnetiate into male anf emale form which together produce oocyst ●Humans serve as both resoviors and intermediate hosts ●Zoonotic disease other animals as resoviors
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Cryptosporidiosis - Clinical Signs
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●Immunocompetent: Watery diarrhea, abdominal cramping, low grade fever short duration GI, flu-like resolves in short time. ●Immunocompromised: Replication is unlimited, severe water loss, may be fatal. Can loose upto 17L a day.
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C. Parvum - Epidemiology
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●Worldwide ●Waterborne ●Resistant to regular water treatment (ozone and cholrination)
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C. Parvum - Lab Diagnosis
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●Detection in unconcetrated stool specimens ●Modified Acid-fast stain ●Indirect immunofluorescece ●Assays often used
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C. Parvum - Treatment & Control
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●No broadly effective therapy ●Proper hygiene, and modern water treatment
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C. Parvum - Risk Groups
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●Animal care takers ●Vetenarians ●Day care center ●Health care workers ●Travel to epidemic regions ●Immunocompromised condition
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Pneumocytis
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|Pneumocystis jiroveci| also called PCP Pneumonia
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P. jiroveci - Life cycle
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●Fungus ●Thin walled trophozite ●Thick walled cyst
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P. jiroveci - Epidemiology
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●Infection in immunocompromised patient ●Resovior unknown ●Transmission uinknown
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Pneumocystis - Clinical Signs
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●Diffuse interstitial pneumonia i.e. PCP (Pneumocystis carnii pneumonia) ●Normal Immunocompetent Pts not generally treated since infection resolves on its own
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P. jiroveci - Diagnosis
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●Bronchial alveolar lavage sample observations ●Open lung biopsy
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P. jiroveci - Treatment
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●Prophylaxis and Tx: Trimethoprim-sulfamethoxazole (Bactrim)
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Toxoplasmosis
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| Toxoplasma gondii |
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T. gondii - Source
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●Raw or uncooked meat ●Feces from cats ●Congenital transfer ●Blood transfusion ●Tissue transplantation
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T. gondii - Life cycle
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●Cats are DEFINITVE hosts ●Man other mammal INTERMEDIATE hosts ●Sexual and asexual stagges ●Obligate intracellular parasite ●Ingestion of cysts ●Excyst in intestine release trophozites develop into Tachyozoite ●Internalized in intestinal epithelium ●Pseudocyst develop inside cells ●Macro and micro gametes develop inside intestinal cells ●Can form Pseudocyst, which has multiple progeny ●Gameste fuse to form oocyst ●Finally end up in MUSCLE tissue ●In all tissues
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T. gondii - Pathology
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●Congenital or Perinatal disease (Posterior chorioetintis) ●Major cause of death in Immunocompromised Pt.
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Toxoplasmosis - Clinical Manifestations
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●Acute acquired phase: Fever of Unknown Origin ●Congenital: Only if mother acquires primary infection in FIRST Trimester ●Ocular: Posterior chorioretinitis, Bilateral or Unilateral ●Immunosuppresed: Reactivation if become immuno suppressed
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T. gondii - Epidemiology
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●2-98% seropositive in World ●Outbreak related to eating raw meat ●Majority remain asymptomatic ●PREGNANT women kept away from Cats
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T. gondii - Treatment
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●Pyrimethamine w/ Sulfadiazine & Lecovorin in Chorioretinitis ●Use aggresive Tx in immunocompromised pt. ●Normal Pt. no Tx unless organ damage evident
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T. gondii - Control
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●Wash hands ●Protective wear during gardening ●House cats kept indoors ●Monitor children in "Sand boxes"
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Trichomoniasis
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| Trichomonas vaginalis |
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T. vaginalis - Life Cycle
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●Direct contact w/ secretions ●Common STI ● Humans ONLY natural host ●Flagellated protozoan (4 Ant., 1 Post.) ●Aerotolerant w/o mitochondria ●NO CYST sensitive outside body
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Trichomoniasis - Clinical Signs
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●Females: Severe Itching, Discharge, burning, Copious forthy discharge ●Males: Prostatitis, Ureteritis
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T. vaginalis - Diagnosis
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●Symptoms ●Direct recovery from vaginal discharge in Transfer pouch
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T. vaginalis - Epidemieology
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●Decreases in post menopausal females ●Humans only natural host
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T. vaginalis - Treatment
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●Metronidazole (250mg TID X7 days) ●For all sexual partners. ●Drug resistance may develop
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Types of Bacteremia
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●Transient ●Intermittent ●Continous
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Common Sources of Bacteremia
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●Genitourinary ●Respiratory tract ●Abscesses
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Microbial etiologies of Sepsis
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Gram Negative > Gram Positive > Candida, Rickettsia
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Continuous Bacteremia - Signs
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●Fever w/ shaking chills ●Sweat and cold, clammy skin ●Hypotension and Shock
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Bacteremia Diagnosis - Specimen Collection
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●Skin antisepsis and Venipuncture ●Direct draw vs. acutainer ●Anticoagulant, Sodium polyanetholsufonate (SPS) or liquoid ●AVOID citrate, oxalate, EDTA and Heparin
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Bacteremia Dx - Volume of Blood Cultured
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●Conventional: 1:10 blood to broth ratio based on 10% inoculum ●Current: 20% recommended, not useful for pediatric and neonatal
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Bacteremia Dx - Blood Cultures set
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●Adults: Conventional - 2 bottle 1 aerobic and 1 anaerobic, Contemporary - Place entire in aerobic since anaerobic <10% ●pediatric & Neonatal: Anaerobes not significant, so ENTIRE inoculum in aerobic
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Bacteremia Dx - Number of Blood Samples
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● Non-SBE: 20mL draw, I=80%, 2=90% 3=99%. ●SBE (Continous): 1=98-100%. ●IMP:Do not draw multiple from same venipuncture site
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Iatrogenic Anemias
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No more than 6 blood cultures set per Hospital Admissions (most cases)
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Blood Culture Mediums
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●Broth Medium: Trytic Soy, Columbia, Brucella broth etc.. ●Hypertonic media ● Resin containing media
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Fever of Unknown Origin Causes
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●Malignancy, lymphoma ●Q Fever (Coxiella burnetti) ●Other rickettsial disease ●Viral disease
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Giardiasis
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| Giardia lamblia |
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G. lamblia - Life Cycle
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●Flagellated protozoan ●INtestinal parasite ●Attaches to intestinal epithelium in Crypts ●Divides by Binary divison ●Cysts: Division and transmission
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Giardiasis- Clinical Signs
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●Epigastric pain ●Steatorrhea -Foul smell ●Flatulence ●Belching ●Upper abdomen distention ●Nausea ●Diarrhea
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G. lamblia - Epidemiology
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●True zoonotic disease ●Cyst resistant to Chloride - water Tx must have FILTRATION
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G. lamblia - Diagnosis
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●Stool specimen for trophozite or cyst ●Fecal antigen test
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G. lamblia - Treatment
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●Tinidazole, Metrondizole
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African Sleeping Sickness
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African Trypanosomas | T. brucei gambeiense - W Africa, T. brucei rhodesiene - E. Afrca | ●Tsetse Fly - Salvarian fly●
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African Trypanosoma - Life Cycle
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●Infective stage: Metacyclic trypanomastigote ●transforms in bloodstream to trypomastigote ●Evade immune system by Antigenic Variation
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African Sleeping Sickness - Clinical Signs
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●Chronic diseasse ●Stupor ●Coma eventually leading to Death
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African trypanosoma - Treatment
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●Pentamidine, Suramin, Melarsoprol ● Newer drug Eflornithine
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Chagas Disease
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American Trpanosoma | T. cruzi | Central, South America ●Kissing Bug - Reduvidae - Stecorarian tick●
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T. Cruzi - Life Cycle
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●Metacyclic trypomatigote ●Taken up by Macrophage, carried to other tissues ● Infection by feces when bite site stratched
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Chagas Disease - Clinical Signs
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●Chronic phase - Most important is imfection of myocardium
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T. cruzi - Diagnosi
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●Direct microscopic infection
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T. cruzi - Treatment
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●Nifurtimax ●Benznidalole
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Granulomatous Amoebic encephalitis (AM)
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| Acanthamoeba castellani | Free living amoeba
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Granulomatous amoebic encephalitis - Clinical Signs
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●Chornic/Subacute ecephalitis ●Foacl/multifocal necrosis of brain ●Keratisis of cornea ●Granulomatous sinusitis
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Granulomatous amoebic encephalitis - Treatment
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●Very difficult - resistant to common microbial agents
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Primary amoebic meningoencephalitis (PAM)
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| Naegleria fowleri | Free living amoeba
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PAM - Clinical Signs
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●Acute fulminating ●Rapidaly fatal ●Briain and Meninges infection
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N. fowleri - Epidemiology
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●Warm climates ● Young healthy adults swimming ●Hx of being outdoors and drinking "fresh water"
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PAM - Treatment
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●Difficult ●Amphotericin B - sensitive (antifungal)
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Plasmodium
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●Sporozoans Obligate Intracellular Parasite ●Asexual stage in vertebrate host ●Sexual stage in Feamle mosquito
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Plasmodium - Med Imporatant species
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●P. vivax ●P. Falciparum ●P. malariae ●P. ovale
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Plasmodium vivax
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●Benign Tertian malaria ●Most widely distributed ●Symptoms debilitating rarely fatal ●Paraoxysms occurs every 48 hours ●untreated notorious for reccuring
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Plasmodium falciparum
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●Malignant subtertian malaria ●Tropicla, subtropical regions Most of mortality assoc. with malaria ●Infect reticulocytes, RBCs and bock cappilaries ●Paraoxysms every 48 hrs, but generally irregular
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Plasmodium malariae
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●Quartan malaria ●Tropic & Subtropical areas ●Less prevalant than vivax ●Paroxysm every 4th day ●recurrence can occur decades after initial insult recur w/o Hypnozoite formation
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Plasmodium ovale
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●Tertian-type malaria ●Less distributed than vivax ●Similar to P. vivax ●Recurs through Hypnozonites
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Plasmodium - Life Cycle (Mammalian Host)
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●When female anopheles mosquito bites, transfers Sporozites ●Carried to Liver, invade parenchymal cells ●Exoerythrocytic Phase: Binary fission, form Merozoites ●Erthyrocytic Phase: Merozites invade RBC, lie in parasitophorous vacuole ●Intracellular parasite rapidly nuclear divides (Schizogony) Merozites when overfill, get dunmped into circulation ●Some merozites enter RBC, DO NOT divide and become macro or micro gamete
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Plasmodium - Life Cycle (Mosquito Host)
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●During blood meal, gamete in RBC taken into gut ●Released from RBC ●Microgamtes divides by Exflagellation. ●Fusion of gametes ●Zygote penetrates btwn Columnar Epithelium of gut ●After series of divison, mature oocyst relased into Hemocoel ●Sporozites migrate to Salivary gland
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Paroxysms in Malaria
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●Due to dumping of Merozites into blood stream. ●Eventually synchronoy between merozited infecting RBC, and Merozites being dumped into bloodstream
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Malaria - Pathology
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●Normochromic, Normocytic Anemia : Hemolysis, Deppresion of erythropoissis, Increasd phagocytosis ●Headache, Myalgia, Irritability, Chills, Nausea, Vomitting & Diarrhea ●Late symptoms: Fever upto 40 C, Chills+Fever+Sweating on regular basis ●P.falciprum can make RBC sticky, thus block capillary beds
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Malaria - Epidemiology
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●Tropical and Subtropical ●Threat for non-immune people travelling to endemic regions ●P. falciparum has drug resitant varities
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Malaria - Diagnosis
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●Medical Emergency ●Febrile illness w/ travelling history, blood transfusions, drug addicts ●Definitive Dx by Microscopic examination of both Thick and Thin blood films
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Amebiasis
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| Entamoeba histolytica | Protozoa - Often harmless in Intestine
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Ambebiasis - Clinical Signs
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●Cyst in feces - $ trophozites - Attack to mucosal cells ●Can treavel to Liver - Form Abcess ●Incubation 3-4wks ●Generally asymptomatic ●Lesion inf intestines are "Flask Shaped"
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Amebiasis - Epidemiology
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●Humans are ONLY host, and Resovior ●Cyst viable only for a few days
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Amebiasis - Diagnosis
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●Parasites in stool - trophozites during severe diarrhea
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Amebiasis - Treatment
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●Paromomycin &/or Iodoquinol for ASYMPTOMATIC ●Metronidazole / Tinidazole for Diarrhea dysentry, Extra intestinal infection
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Trematodes
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●Non-Segmented worms ●All have Snails at intermediate hosts ●Surrounded by Tegument ●Eggs can be Embryoated or Unembryoated ●Larva encysts or directly penetrate human host to compelte life cycle
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Schistosomiasis
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●Separate Male and Female adults.●Man becomes infected directly through hair follicle
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Schistosomiais - Clinical
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●Asymptomatic ●Acute disease: Febrile, flu-like, fatigue, night sweats ●SELF-LIMITING ●Chronic: Intestinal infection, often asymptomatic but can be insidious
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Schistosomiasis - Prognosis
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●Usually excellent w/o Treatment
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Schistosomiasis - Treatment
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●New drugs, higher cure rates ●Praziquantal: acts on tegument of worm ●Oxamniquine
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Schistosomiasis - Prevention
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●Molluscacides ●Water sanitation engineering ●Public education
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Faccioloasis
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●Liver fluke ●Hemaphrodites ●Eggs produced and hatch in aqatic env, and taken up by host ●Attach to aquatic vegetation
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Faccioloasis - Clinical
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●Acute phase: Transient dyspepsia, and Abrupt High grade fever ●Chronic: Bile ducts, become obstructive there
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Faccioloasis - Treatment
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●Praziquantal ●Bithionol / Triclabendazole
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Paragonimiasis
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| Paragonimus westemani | ●Liver Fluke ●Raw, uncooked meat , seafood
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Ideal Bioterrorism Weapon Properties
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●Human pathogen with Short incubation time ●Effective at low dose ●Easilt transmissible ●Economical to produce and adapt as weapon
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Bioterrorism agents - Toxins
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Botulinum Toxin ●Most potentn biological toxin ●Ideal for food and water
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Bioterrorism agents - Microbes
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●Smallpox ●Plague ●Anthrax ●Tularemia ●Hemmorhagic fever viruses (Ebola, Lassa, Marburg, Yellow fevers)
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Anthrax
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B. anthracis ●Aerobic Gram + Rod ●Spore ●Zoonotic disease ●Cutaneous infection - Malignant pustule ●Pneumonia → Sepsis → Death
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Chronic Meningitis
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●10% Cyrtococcal ●1-5% CNS Toxoplasmosis ●5% Pulmonary TB, TB Meningitis
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CNS Findings Meningitis
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{Viral : ●Pressure Norm ●Type/# cells:Mononuclear ●Protein: ↑ ●Sugar: Normal } {Bacterial: ●Pressure: Normal or ↑ ●Type/# cells: Polys >100 ●Protein: ↑↑ Sugar:↓↓↓} {Subacute: ●Pressure:Norm ●Type/# cells: Monos ●Protein: ↑↑ ●Sugar: Normal or ↓}
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CNS Findings in Brain Abcess
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●Normal Pressure ●Poly cell ●Increased protein ●Normal sugar
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CNS Finding in Encephalitis
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●Inceased pressure ●Mononuclear cells ●Increased protein ●Normal sugar
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