IR-7 Immu
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formula6ap on October 13, 2011
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Terms | Definitions |
|---|---|
 TORCH means? | TOxoplasma gondii Rubella CMV (cytomegalovirus) Herpes **acronym for grp of infectious diseases that can cause illness in "pregnant woman" and may cause "birth defects in newborns." |
| Toxoplasma gondii | - sporozoan - tissue coccidia (invades tissue) - widespread in humans, domestic/wild animals (i.e. cats) - asymptomatic or mild infection - serious congenital (existing from birth) and ocular (eye) infections - severe infections in immunocompromised patiens (HIV, Bone Marrow Transplant, elderly, etc) - ***PARASITIC INFECTION (only one of TORCH organisms) |
| Toxoplasmosis (defn) | infection with the parasite Toxoplasma gondii, transmitted to humans by consumption of insufficiently cooked meat containing the parasite or by contact with contaminated cats or their feces: the illness produced is usually mild, but in pregnant women may damage the fetus. |
| Toxoplasmosis (life cycle) | life cycle: 1. sexual stage in intestinal epithelium of cats/feline hosts 2. immature oocysts (eggs) passed in feces (pregnant women should not clean litter boxes!) 3. mature to infective stage in the environment in 2-21 days -- ingestion of these sporocysts may lead to infection--the trophozoites (tachyzoites) infect nucleated cells. |
| Toxoplasmosis (cont.) | - most infections asymptomatic - may be fever and lymphadenopathy (chronic swollen lymph nodes) - resempling Inf Mono - **most signif. infection = Congenital (existing from birth)w/ variable symptoms (depends on time during preg.) - Immunosuppressed = CNS symptoms, affect any organs, immunosupp. due to reactivation of a latent infec. |
| Congenital Toxoplasmosis | - causes blindness, psychomotor retardation, convulsive disorders - 1st half: intrauterine death, microcephaly (small head), or hydrocephaly (water in the brain) - 2nd half: asymptomatic at birth, ppossibly fever, hepatosplenomegaly (enlarged liver & spleen), jaundice at birth, chorioretinistis (inf. in back of eye) or CNS manifestation |
| Lab Testing (Direct examination) | - exam tissue via H&E stain (hematoxylin and eosin) - smear & imprints via Giemsa stain - immunoflorescence w/ anti-P30 monoclonal Ab (P30=Ag) - smears: tachyzoites--spindle to oval shape 3x7 um; Cysts - 30 um |
| Lab Testing (Serology) | - "most common" way to estab. diag. (ELISA/EIA) - Ab appear in 1-2 weeks - titer peaks @ 6-8 weeks - IFA or EIA "detect IgM" = congenital & accute infecions ***IgM used to diag. acute, primary infections - EIA elev. for 4-8 mnths - IFA fall by 2-4 mnths ***LOW TITERS not significant, since asymptomatic infect. are common. |
| Rubella - aka "Three day measles" or "German Measles" (3 names) | - first described in Germany, called Rotheln - 30s viral agent transmitted to man and monkeys - virus isolated in 1962 ***single-stranded RNA virus ***member of Togaviridae - highly contagious - transmitted via respiratory secretion - causes severe Congenital abnormalities if inf. in 1st tri |
| Rubella Epidemiology | - epidemics in school-aged child until attenuated vaccine (proof of immu thru "Positive" Sero. screening test) - now "more common" in older child & adolescents - college/univ camp. susceptible to rubella inf. - transmitted via inhalation of inf. droplets - highly communicable - incubation: 2-3 weeks - contagious period: week before to week after onset of rash - congental birth defects varies w/ time of maternal inf. - risk of fetal malformations: 1st month of preg. = 50-80% 2nd month = 25% 3rd month = 17% Note: cong. inf. infants declines w/ age but can still excrete virus up to 3yrs = reservoirs of inf. |
| Rubella (clinical aspects) | **Children - mild generalized lymphadenophathy (ch.swollen lymph nodes), followed by macular rash (usu. last 3 days) **Older individuals - malaise (body weak/discomfort), headache, fever - few complicatoin include post-inf. encephalitits (inflam. subst. of brain), thrombocytopenia, arthritis, arthralgia (sev. joint pain) **Congenital rubella (aka "Rubella Syndrome") - ton of problems. Not a good thing!! |
| Important Rubella Lab Diag notes | ***IgM found in fetus = Congenial rubella syndorome ***for current infection, paired sample is needed to observe IgM and IgG ***virus found in oropharynx and feces provides a reservoir for infection of others. |
| Lab Diag (Rubella) | Postnatally acq infection - incubation: 10-21 days - inf. peeps contagious for 12-15 days (5-7 days prior to rash) Virus isolated from feces, urine, placental/fetal tissue of abortuses Virus grown in rat kidney, rabbit cornea, and green monkey kidney cell line---microfoci of CPE ***remember Rubella virus produces microfoci CPE (cytopathic effect), so if CPE is absent in inoculated tube, virus possibly present. ***CPE virus will cause cells to change or die. |
| Lab Diag (Rubella) cont. | - absolute id req. "neutralization" of interference w/ rubella anti-serum - Rubella titer of 8 or greater = immune - titer of 16, 64, 512 or greater = acute and past infection - Paired sera should always be examined simultaneously - presence of titer in absence of disease = prev. infect. & hence immunity to re-infection - re-exposure = rise in Ab titer, w/o viremia - fetus little risk |
| Hemagglutination inhibition test | principle: virus agglut. ckn RBCs. - Patient sera comb. w/ Rubella Ag, if pt has Ab to rubella Ag then Ag-Ab forms not allowing the Ag to agglut. the "indicator" ckn RBCs. --Note: NO Agglutination = + |
| Rubella Vaccine | - Live, attenuated rubella vacc - Give alone @ 12 mnths old or @ 15 mnths old in MMR vacc |
| CMV (cytomegalovirus) | - ubiquitous (everywhere) human viral pathogen - member of "herpes" family virus - large enveloped "DNA" virus - spread from cell to cell, via intracellular bridges, in presence of Abin extracellular phase ***not a problem for someone healthy. - cell appearance of an "owl's eye" or alien - replication found in WBCs - long incubation period; slow replicative cycle in tissue - local or systemic infectoins either active or latent |
| CMV epidemiology | - endemic worldwide - high prevalence in "young children" living in under developed, crowded, intimate conditions - most often acq. peri- or postnatally; may be congenital - transmitted via organ transplants or transufsion of blood; req. intimate contact of secretion or excretions - nearly 100% of adults have Ab by age 35 |
| CMV (Congenital infection) | ***most common cause of congenital infections in humans. - transmission from mother to fetus poorly defined - maternal CMV infections subject to recurrence; genital tract - asymptomatic or mild hepatomegaly (enlarge liver) - symptoms vary - Congenitally infected infants excrete extreme high titer |
| CMV (acq. infection or reactivation) | - same or diff strain excrete titers as high as 10^6 - infect others via oral, sexual, or parenterally by organ or blood trans. - clinical manifestations: liver, spleen, heatopoitic syst, kidney, lungs - can cause negative mono. like syndrom w/ fever - CMV neg. blood = donors test neg for Ab to CMV |
| CMV (lab diag) | - culture method of choice - often recovered from urine (during active phase) - treatment = Ganciclovir |
| Herpes | ***most common manifestation = common cold sore, or fever blister. - 2 types: 1. HSV-1 (herpes simplex virus type 1) 2. HSV-2 (type 2) |
| 5 distinct herpes virus | 1. HSV-1 2. HSV-2 3. Varicella-zoster virus (aka Chicken Pox) 4. Epstein Barr virus 5. Cytomegalovirus |
| Herpes epidemiology | - widespread, **man only!! host - incubation: 2-12 days - Serologic evidence: by age 25 = 70-80% of individuals, by age 45 = nearly 100% in some populations - transmission by close contact: hand to mouth, kissing, sexual - **most common manifest. of HSV-1 is "gingivostomatitis" = sores on the mouth and gums - Adult: acute upper resp. illness pharyngitis and tonsillitis - Neonatal: thru infected birth canal; asymptomatic mothers; organs affected--lungs, liver, adrenals, brain, retina, skin |
| Herpes (lab diag) | - isolated from vesicular fluid, ulcer scraping, throat swap, saliva, cervical secretions, CSF, etc. - **virus grows rapidly in vitrow/ CPE - often in 24hrs (human diploid fibroblast and primary rabbit kidney tissue culture syst of choice) - **HSV produce specific pattern of CPE - "balloon" cells - Direct detection of Ag - prep by IF or EIA - IF or Immunoperoxidase methods to type HSV isolates - Serology: tool for determining prevalenc of exposure to HSV - EIA - determine "Ig" class of Ab responce |
| Syphilis | caused by Treponema pallidum destroyed by heat, cold, and drying out transmission: sexual contact, kissing open lesions, rarely blood incubation: usually 3 weeks; ranges 10-90 days congenital infections occur after 18th week of preg. |
| primary stage of syphilis | painless chancre appears 2-3 weeks after infection persist for 1-5 weeks & spont. heal (disappear but you still have it) one week after chancre appear, lymph nodes enlarge Ab are produced 1-4 weeks after chancre appears Dark-field analysis of lesion demos spirochetes T. pallidum once entered in circulatory syst is then carried to every organ in body |
| secondary stage of syphilis | 1-2 mnths after chancres (more severe) dissemination of organism (travels thru blood stream); involves CNS, eyes, bones, or liver develop flat lesions resembling warts in moist areas resolves w/i 2-6 weeks w/o treatment |
| Latent stage of syphilis | lack of clinical symptoms noninfectious stage (Ab present; not Ag) both nontrep and trep test are + diagnosis can only be made serologically at this stage |
| tertiary syphilis | occurs 2-40yrs after primary infection gummas (syphillic lesions) appear in areas of bones, skin, or subq tissue 10% untreated = cardio probs 8% untreated = CNS probs |
| Congenital syphillis | caused by maternal spirochetemia if mother recvs treatment (PCN or Doxy) during first 4 mnths of preg, ocngenital syphilis can be avoided |
| Hutchinsonian triad | associated w/ Congenital syphilis - short notched incisor teeth - interstitial keratitis (blindness) - nerve deafness |
| Syphalis (lab diag) | organism cannot be cultured long intervals of manifestation T cells and macrophage moderatley increase Ab destroy organism via damaging cell membraine enhances phagocytosis |
| nontreponemal sero tests | "think screening test" nonspecif Ab are called "reagin ab"--produced by infected patient against comp of their own or other mamm cells. Ab found in cardiolipin--cholesterol and lecithin i.e. tests = VDRL (veneral disease research lab) and RPR (rapid plasma reagin) |
| treponemal sero tests | ***don't do these unless onntrep sero tests are + specific for spoirochetes or T. pallidum (syphalis) - TPI, FTA-ABS (fluorescent), Hemaagglutination: MHA-TP (TP-PA) Note: used to "confirm" RPR & VDRL results TPI: obsolete TP-PA has replaced MHA-TP but folow the same princip. |
| VDRL and RPR (nontreponemal) | - Flocculation tests: soluble Ag particl coalesce to form large particles as clumps when aggregated by Ab - Results reported as reactiv or nonreacti or weak reactive (why not + or - ? b/c these are "screening" tests) |
| VDRL (nontrep) | used to monitor adequacy of treatment (quart. for 1yr) - Ag = buffer salin susp of cardiolipin (lecithin-cholesterol) - patient serum or CSF - rotate 4 min - read microscopically for agglut - inactivate via heating to avoid activating compliment |
| RPR (nontrep) | Ag = modified VDRL Ag containing choline & charcoal (to help see it) unheated serum (not CSF) added to RPR Ag rotate for 8 min **ART - automated reagin test (to test units of blood) + show flocc. of charcoal particles more sensitive than VDRL |
| FTA-ABS (trep) | Ag killed susp of T. pallidum (syphalis) Treponemes fixed on glass slide fluorescent Ab tagging! Test is specific! |
| MHA-TP (trep) | SRBCs coated w/ Treponemal Ag (+) forms flat, smooth mat accross bottom of well (-) compact button formed by the settling of nonagglutinated cells |
| TP-PA (trep) | Treponema pallidum - particle agglutination uses gelatin particle coated w/ treponemal Ag instead of sRBCs allows longer storage and stability of test cross reacting Ab's are elimin. |
| Syphalis (lab results) | greatest elevation of IgG in secondary syphilis higher titers indicative of active disease low titers < 8 suggest latent infection, prev treatment, or late syphilis treatment: long acting inj of PCN |
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