micro exam 3 Flashcards

Question

what is the most common REPORTABLE STI?

Answer 1

chlamydia also most common bacterial STI

Answer 2

prevalence = estimated number of infections, NEW OR EXISTING, in given time incidence = estimated number of NEW infections, diagnosed or undiagnosed

Answer 3

HPV, HSV-2, and HIV all of these have high prevalence, HPV the most

Answer 4

chlamydia, HIV (high prevalence), gonorrhea, and syphilis

Answer 5

- annual chlamydia and gonorrhea screening for at-risk sexually active WOMEN (<25 y/o, new of multiple sex partners, and residing in communities with high disease burden) - annual chlamydia, gonorrhea, syphilis, and HIV screening for sexually active MSM - early during preg screening for PREG AT RISK women for chlamydia, gonorrhea, syphilis, HIV, and hep B

Answer 6

mostly sexually transmitted but can be species of ureaplasma, mycoplasma, trichomonas, and virus (HSV and adenovirus)

Answer 7

chlamydia - most commonly reported STI in US - caused by serovars **D-K** of CHLAMYDIA TRACHOMATIS, serovars A,B, C of TRACHOMA gen in Africa, and serovars L of lymphogranuloma venereum (LGV) gonorrhea - SECOND MOST COMMON reported STI in US - caused by NEISSERIA GONORRHEAE

Answer 8

with = STI without = can be confused with cystitis (UTI)

Answer 9

gonococcal (N. gonorrhea) - binds specifically to COLUMNAR EPI CELLS of GU tract, anal canal, pharynx, and conjunctiva - 95% or more of males experience urethral discharge, women often have NO SYMPS but can have urethritis accompanied by cervicitis - discharge is THICK and PURULENT or mucopurulent non-gonococcal urethritis (chlamydia trachomatis and other) - more likely to be ASYMP or LACK urethral DISCHARGE - discharge is WATERY and NON-PURULENT

Answer 10

pneumonia or inclusion conjunctivitis

Answer 11

sepsis or ophthalmia neonatorum

Answer 12

males - most infections resolve without treatment - small numbers develop prostatitis, epididymitis, or urethral stricture females - most infections are ASYMP (50-70%) - few undiagnosed infections develop ascending infections - **PID** (endometritis, salpingitis, abscesses, and ab pain) is main SERIOUS COMP - 0.5-3% may develop disseminated infection if left untreated

Answer 13

urethral discharge - micro exam shows 2 OR MORE WBC/oil immersion filed in gram-stained smear or urethral exudate - gram stain of male urethral exudate = WBC with gram neg INTRACEL DIPLOCOCCI is considered DX for N. gonorrheae in symp males first void urine - pos leukocyte esterase test - micro exam = more than 10 WBC/hpf of sediment NAAT

Answer 14

gonorrhea = ceftriaxone (single dose, IM) chlamydia = doxycycline unless lab testing rules out one or the other, current tx is USING BOTH DRUGS ex: man with discharge --> do gram stain, shows gonorrhea morphotype what are you going to do with px? tx? no bc it wasn't mentioned if women then do culture or PCR basically question wants to dx not treat so perform Gram stain (if male) or PCR/culture (if female)

Answer 15

cervicitis

Answer 16

infectious C. trachomatis and N. gonorrheae less common mycoplasma and ureaplasma noninfectious mechanical or chemical irritation

Answer 17

many times asymp --> risk for comps (like PID which is inflam of soft tissues in pevlis that can affect tubes and endomtrium --> infertility, ectopic preg, and chronic ab pain most common presentation = vaginal discharge that may be GRAYISH or YELLOW, possibly with odor may also manifest as - abnorm bleeding, itching, irritation of external genitalia - pain during intercourse, bleeding or spotting after intercourse - dysuria - lower back or ab pain dx is mainly clinical, but lab results also important

Answer 18

direct exam - MORE THAN 10 WBC/hpf of exudate (associated with chlamydial and gonococcal infection of cervix) px are often assessed for signs of PID and tested for C. trachomatis and N. gonorrheae may also be tested for BACTERIAL VAGINOSIS (BV) and trichomoniasis tx is same as urethritis N. gon = ceftriaxone C. tra = doxycycline mainly use combo of both

Answer 19

vaginal infection in women of CHILDBEARING AGE

Answer 20

symp vaginitis usually caused by infection with yeast C. albicans risk factors for both vulvovaginitis and BV - sexual activity at early age - having numerous, anonymous, or freq changes of sexual partners - having female sex partners - ethnicity (AA and mex-americans at high risk) - frequent douching (disturbing norm biota) - use of broad-spec antibiotics - diabetes mellitus and immunosuppression

Answer 21

bacteria - Gardnerella vaginalis yeast = candida albicans and other candida species protozoan parasites = trichomonas vaginalis mechanical or chemical irritations - contraceptives, feminine hygiene products, soaps, and some clothing

Answer 22

vaginal lactobacilli are DEPLETED, causing increase in vaginal pH allows for overgrowth of Gardnerella vaginalis, mycoplasma, ureplasma, and other anaerobic orgs like prevotella, prophyromonas, peptostrep, and mobiluncus causes ABNORM (MILK, THIN), VAGINAL DISCHARGE and distinct unpleasant odor like ROTTING FISH trichomoniasis = itching, burning, dysuria, lower ab pain, genital redness or soreness, and a smelly vaginal discharge that can be clear, white, yellowish, or greenish cervix is punctate and papilliform in appearance --> STRAWBERRY CERVIX males present with symps of non-gonococcal urethritis (watery, non-purulent discharge) strawberry cervix caused by trichomonas vaginalis

Answer 23

vaginal thrush or moniliasis genital itching or burning, with an abnorm vaginal discharge - slightly watery, white discharge to a thick, COTTAGE CHEESE curd like discharge men present with itchy rash or burning at tip of penis

Answer 24

saline wet mount = **CLUE CELLS** (vaginal squamous epi cells coated with G. vaginalis), Trichomonas vaginalis, candida, and pus cells (will show moving T. vaginalis) gram-stained slides = CLUE CELLS, T. vaginalis, candida, pus cells KOH prep = candida amine test (whiff test) = add one or 2 drops of 10% KOH to vaginal discharge and detection of FISHY ODOR - culture of G. vaginalis or DNA detection

Answer 25

vulvo - trichomoniasis = visualization of MOTILE trichomonads in saline prep of vaginal fluid, pouch inoculation, oligonucleotide probe test or Ag test - candidiasis = budding yeast cells observed in gram-stained smears and wet mounts (NON-MOTILE) BV = presence of 3 Amsel criteria*** - milky homogenous, thin discharge - CLUE CELLS - pos amine test (whiff test) - pH >4.5

Answer 26

BV = metronidazole and clindamycin cream applied intravaginally trichomoniasis = metronidazole candiasis = OTC meds or prescription antifungal agents --> azole antifunal agents that inhibit ergosterol production (important fungal PM)

Answer 27

- genital herpes (HSV-2) - most common - syphilis (treponema pallidum) - chancroid (haemophilus ducreyi) - lymphogranuloma venereum (chlamydia trachomatis) - donovanosis (klebsiella granulomatis)

Answer 28

outer mem of GN bacteria

Answer 29

borrelia burgdorferi (can be seen with LM and bright/giemsa stain) treponema pallidum leptospira interrogans these 2 are too thing to be seen by LM, use phase contrast or dark field microscopy OR conventional LM if impregnated with silver + fluorescent microscopy

Answer 30

genital ulcer disease transmitted through intimate contact where infectious orgs are present in lesions of skin or mucous mem can be transmitted vertically to unborn fetus or via blood transfusion more common in males, esp MSM treponema pallidum is sensitive to desiccation, disinfectants, and high temps which is why it can't survive outside the host it's a slow growing org which leads to prolonged tx lacks OM LPS and has few proteins, allowing it to hide in host, persisting for long time CANNOT be isolated in culture media or cell culture

Answer 31

- spirochetes proliferate slowly at site of infection without triggering inflam response - endothelium of BVs affected leading to necrotic lesions - granulomatous tissue rich in lymphocytes, macrophages, and plasma cells forms - CHANCRE is an UNPAINFUL ulcer that develops during PRIMARY INFECTION*** - bacteria spread thru blood and lymph to multiple organs - DTH rxn may play role in pathogenesis - partially protective Abs develop - no specific toxins or other virulence factors are known lab testing for dx = rising titer (tells you it's early phase bc it will plateau later on) or seroconversion (new infection)

Answer 32

primary - incubation abt 3 wks - papule develops into INITIAL CHANCRE***, usually external genitalia or cervix - inguinal lymphadenopathy may develop - chancre HEALS SPONTANEOUSLY in 4-6 wks (heal but bacteria might not be cleared) secondary - mucocutaneous maculopapular RASH*** (does NOT spare hands or soles of feet) - lymphadenopathy - systemic symps - CONDYLOMATA LATA*** develop in genital and perennial area in 1/3 of pxs - lesions heal spontaneously, but 2/3 enter latency

Answer 33

latent infection (0-few years after initial inoculation) - early latent ( 12 months) infection is ASYMPTOMATIC with PARTIAL IMMUNE PROTECTION - transmission to others is possible during early latent, particulary 1st 6 months - 1/3 of untreated pxs enter tertiary stage tertiary (15-20 years after initial infection) - immune sequelae of primary or secondary syphilis - neuro symps, cardiovasc effects, GUMMAS*** (do not contain bugs) --> neurosyphilis, aortic aneurysm and rupture, destructive gummas of SKIN, BONE, joints, or other organs congenital - deformities, rash, jaundice, meningitis, deformed bones, deafness, blindness - anemia, thrombocytopenia, and liver failure in terminal cases

Answer 34

dark field microscopy (material from lesion) and DFA - primary and secondary syphilis ONLY nontreponemal (nonspecific) Ab tests --> good for SCREENING and follow up - RPR - VDRL rise during primary syphilis and reach peak in secondary syphilis, slowly decline with advancing age, w/ tx wil lrevert to normal over a few wks which is why it's good for follow up treponemal (specific) Ab tests --> remains elevated even after successful tx, confirms syphilis - FTA-ABS - MHA-TP follows the same course as nontreponemal but REMAIN ELEVATED even after successful tx

Answer 35

benzathine benzylpenicillin (IM bc causes cardiac arrest via IV) for early (primary, secondary, and early latent) and late (late latent and tertiary) syphilis in ABSENCE of neurosyphilis and ocular disease penicillin G (IV) for neurosyphilis and ocular disease doxycycline no vaccine atm JARISCH-HERXHEIMER rxn may occur 24 hrs after the start of tx and manifest as fever, chills, rash, and other symps (hypotension, worsening liver and renal fxn, seizures) --> rxn occurs bc lots of bugs are dying, active immune cells to ingest them and produce cytokines

Answer 36

STD caused by more virulent and invasive serovars (L) of C. trachomatis most occur in tropical and subtropical regions of Africa, Central and S America, and Asia strictly HUMAN PATHOGEN with no known animal reservoir - epi cells, monocytes, and macrophages are main targets of infection - systemic spread is caused by monocytes and macrophages that become infected in local lymph nodes - 1st step in infection is binding to susceptible cells via MOMP and inducing own phagocytosis - lysosome fusion is inhibited, allowing intracell survival - host cell apoptosis regulated by chlamydia to prevent cells from undergoing apoptotic cell death during RBs rep and allow it after enough EBs are produced - main injury is due to release of proinflam cytokines from infected cells and elimination of infected cells by immune response - left untreated or due to failure of containment by immune system, necrosis and fibrosis cause scarring at site of infection

Answer 37

contains OM, IM, and dense core (cell wall similar to GN but doesn't gram stain) LPS is WEAK ENDOTOXIN MOMP --> determines host range and tissue tropism, binds to heparan sulfate OMP2 is cysteine rich and responsible for rigidity of EBs --> enables EBs to be environmentally resilient (outside cell or host) reticulate bodes are fragile due to lack of cysteine rich proteins (REPRODUCTIVE FORM, only inside cell and if they go outside they will die)

Answer 38

- elementary bodies (EBs) bind susceptible cells via MOMP interaction with heparan sulfate - EBs induce their own phagocytosis - EBs then inhibit phagolysosome formation - EBs are transformed into reticulate bodies (RBs) and rapidly replicate - RBs become EBs - host cell ruptures releasing infectious EBs - RBs may give rise to persistent bodies (PBs) leading to chronic disease

Answer 39

cytoplasmic inclusion bodies consisting of EBs

Answer 40

primary - small genital or rectal lesion that ulcerates and possible rectal inflam (hemorrhagic ulcerative proctitis), NOT PAINFUL similar to syphilis secondary - spreads to regional lymph nodes, causing PAINFUL lymphadenopathy and potentially BUBOES tertiary - can lead to chronic inflam and destruction of affected tissues

Answer 41

comps - urethral or rectal strictures - perirectal abscesses and fistulas lab dx - clinical presentation, epidemiologic info, and exclusion of other etiologies of fenital or rectal ulcers, inguinal lymphadenopathy, and/or proctitis - bubo aspirates --> test with tissue culture, DFA, EIA, and NAAT tx = doxycycline

Answer 42

aka soft chancre known to result in BUBO FORMATION (other conditions include LGV, plague, and bartonella) major cause of genital ulcerative disease in africa, SE asia, caribbean, and latin america caused by Haemophilus ducreyi Haemophilus is member of family Pasteruellaceae --> GN, nonsporulating, non-motile, facultative anaerobic, coccobacillary to bacillary, oxidase pos org

Answer 43

- initial lesion is erythematous, tender papule (PAINFUL) that turns into pustule in few days - pustule ruptures, forming ulcer - PAINFUL GENITAL ULCERATION, INFLAM INGUINAL ADENOPATHY, AND BUBO FORMATION (CHARACTERISTIC) - soft chancre are characterized by ragged or uneven soft edges and a grey to yellow purulent exudate - lesions are spontaneously resolved after wks or months - lesions may rarely form outside genitals

Answer 44

culture of ulcer exudates or aspirated bubo material to isolate causative agent - prompt delivery to lab is crucial - GC agar suppmented H. ducreyi are pleomorphic, GN coccobacilli that occasionally occur in chains or SCHOOL OF FISH*** under development or validated in-house --> PCR and immunoassays

Answer 45

antibiotic therapy resolves clinical symps, prevents transmission to others, and cures the disease single dose of oral AZITHROMYCIN penicillinase production is common so penicillins are not used

Answer 46

genital ulcerative disease caused by klebsiella granulomatis (xtremely fastidious) rare in the US, mainly from immigrants and travel to endemic areas like india, central australia, brazil, and S africa most common in UNCIRCUMCISED MEN WITH POOR HYGIENE transmission thru sexual and non-sexual contact

Answer 47

spread by direct contact with lesions during sexual activity - produce FIRM PAPULE or subcutaneous nodule that ulcerates at primary site of inoculation, usually in genital region 4 types - ulcerogranulomatous (MOST COMMON) = PAINLESS, beefy red, nontender, nonindurated ulcers that bleed on touch - hypertrophic (verrucous) = ulcer with raised irreg edges - necrotic = ulcers with sig tissue destruction and offensive smell - sclerotic or cicatricial = ulcers with fibrotic tissue and scarring comps = disseminated infections - most commonly spreads to liver and bone - women more likely to develop dissemination during pregnancy untreated infections may result in extensive tissue destruction and spread to extragenital sites via autoinoculation

Answer 48

determined clinically based on detailed hx and PE findings of ulcerative lesions on a px with sexual contact in endemic region giemsa or wright's staining of tissue --> id intracell DONOVAN BODIES in macrophages culture using eggs, PBMC, or cel lines tx = doxycycline

Answer 49

painful = Mpox, HSV, chancroid painless = syphilis, LGV, donovanosis

Answer 50

genus lentivirus family retroviridae subfam lentivirinae 2 species = HIV-1 (worldwide, chimps) and HIV-2 (W africa, monkeys)

Answer 51

STD that targets immune cells and causing loss of immune function, making pxs susceptible to opportunitistin infections and specific types of cancers final stage is AIDS which to lead to the same things most cases, progression to AIDS occurs in 2-15 years in absence of ART rapid progressors (<10 years), conventional progressors, and long-term non-progressors exist (>10 years) high prevalence in Sub-Saharan Africa transmitted by - sexual intercourse (anal - most effective -, vaginal, oral) - direct contact with infected body fluids/tissue (blood, semen, vaginal secretions, breast milk, saliva) via broken skin or mucous mem - injection, accidental needle stick, or contaminated medical devices - mother to child transmission (transmammary, transplacental, and birth) - can splatter into eye, nose, or mouth - no cases of airborne, foodborne, waterborne, or vector-borne infection - virus NOT transmitted by casual contact or sharing food or water likelihood of transmission is affected by viral loads, pxs are most infectious during acute infection and late after progression to AIDS ART reduced viral loads, decreases chance of transmission

Answer 52

retrovirus - RNA dependent DNA pol (RT enzyme) no curative tx or vaccine AIDS is terminal stage almost norm life expectancy with HAART (high active antiretroviral therapy) better outcome with early tx

Answer 53

enveloped RNA virus with 2 copies of SS, + sense RNA genome envelop carries gp160 that is cleaved into gp120 (binding host cell) and gp41 (fusion) virions composed of core, phospholipid envelope of host-cell origin, and matrix (p17) btwn 2 core composed of CAPSID (p24)***(DIAGNOSTIC BC 1st AG DETECTED IN PX) that surrounds 2 nucleocapsid molecules and 3 enzymes these 3 enzymes are encoded by POL GENE = RT, integrase (integrate viral genome into host), and protease matrix protein p17 and capsid protein p24 encode by GAG GENE gp120 and gp41 encoded by ENV GENE

Answer 54

- viral entry occurs after binding of gp120 to CD4 molecule and co-recep (CCR5 and/or CXCR4) - binding co-recep brings virion closer to PM facilitating entry - viral genome is reverse transcribed into cDNA, later integrated into host genome (use RNA identical to mRNA, which is heteroduplex, to make copy DNA --> use same RT, it will degrade RNA using RNase H --> this RT will make another copy of DNA aka DNA dependent DNA pol, after this integrase will integrate provirus into host genome) - after assembly, virions emerge by budding from surface of host cells - viral RT reverse transcribes ssRNA into ssDNA - RT then acts as RNaseH and degrades genomic RNA, then synthesizes second strand to produce ds cDNA (provirus) - ds DNA is translocated to nucleus and integrated into host genome by integrase - cell transcription machinery transcribes provirus resulting in viral mRNA and new viral genomes - viral RNA molecules are transported to cytoplasm, where translation and later packaging occurs - polyproteins are cleaved by viral and cellular protease - virions depart host cell by budding from surface, process by which virion acquire portion of host cell mem and now becomes viral envelope - virions mature outside host after budding

Answer 55

entry inhibitors = CCR5 binding blockers and fusion blockers RT inhibitors = NRTIs and NNRTis integrase inhibitors protease inhibitors

Answer 56

- integration of provirus requires cell prolif --> most viral cDNA molecules exist as unintegrated molecules, circular or linear - transcription of provirus is dependent on transcription factors that are only present in activated cells - cytokines produced in response to other infections may promote viral rep by activating HIV-infected cells and promoting provirus transcription

Answer 57

15-45% rate of transmission w/o intervention tx of both mother and children = almost complete prevention tx is given during preg, labor, and post-natal

Answer 58

- infection causes destruction of immune system mainly CD4 T cells causing them to malfxn and leads to their depletion fro mGALT and periphery - CD8 CTL kill infected CD4 and are main contributors to initial control of viral infection - CD4 death caused by virus-induced cytolysis, attack by CD8 CTL and induction of apoptosis - initial non-specific activation of B cells result in hypergammaglobulinemia - with depletion of CD4 cells, CD8 cells gradually decline in peripheral blood, GOOD INDICATOR OF PROGRESSION TO AIDS - later during chronic phase, B cell exhaustion ensues leading to dysfxnal B cells

Answer 59

- freq muts causing alts of Ags, most notable gp120 - glycosylation of gp120 and protection of co-recep binding site - crippling immune response by depleting CD4 cells - direct cell-to-cell transmission to avoid Ab neutralization - establishing latent infection in macrophages, DCs, and memory CD4 cells (makes px pos for life) - mass stim of B cells lead to massive production of Abs that are NOT useful in fighting infection

Answer 60

acute infection - 2-4 wks from initial infection (incubation period) - asymp or flu like symps - lasts for abt 2 wks clinical latency - 3- >/= 10 years - massive lost and gradual decline in CD4 cells accompanied by opportunistic infections, pxs during this phase a relatively healthy but viral rep is aggressive (this says CLINICAL, not viral latency, so there is still active viral replication with subclinical symps) AIDS - drop of CD4 count BELOW 200/mm^3 and emergence of severe opportunistic infections and particular cancers ex: thrush is opportunistic infection that can occur in clinical latency, in pharynx and not esophagus but if it goes into esophagus and causes esophageal candiasis then it's AIDS defining condition

Answer 61

recurrent bacterial pneumo MAC pneumo extrapulm crytococcosis (fungal infection) chronic cryptosporidiosis (parasite) kaposi's sarcoma toxoplasmosis of brain wasting syndrome

Answer 62

dx - Ab detection in serum = anti-p24 test (presumptive), western blot (definitive), does NOT turn pos during acute/early infection - PCR - sensitive test to detect integrated viral DNA in cells or RNA in plasma - plasma viral loads and CD4 cell counts are used for monitoring disease progression - tropism testing = needed before initiation of CCR5 blocker therapy - drug resistance testing if the Ab differentiation immunoassay have neg or indeterminate results then do PCR to see if there's + or - RNA, + RNA means acute HIV-1 infection --> if px has exposure that's abt 1 wk long then do PCR bc it shows positivity within 1 wk exposure while Ag takes 3-4 wks or later to develop tx - ART = restoration of immune fxn, reduction of viral load (slows destruction of CD4 cells and reduces chances of transmission), reduction of chronic immune activation and inflam want to begin ART ASAP regardless of CD4 counts and DO NOT STOP (once started, tx should continue indefinitely)

Answer 63

upper UTIs - renal parenchyma = pyelonephritis - ureters = ureteritis lower UTIs - bladder = cystitis - urethra = urethritis (STD) - prostate = prostatitis uncomp UTIs - occur in anatomically and fxnally norm urinary tract comp UTIs - occur in presence of anatomical, fxnal, or pathogen-related factors that promote establishment of infection - anatomical or fxnal abnorm - immune deficiencies - multi-drug resistance

Answer 64

0-3 months = most occur in UNCIRCUMCISED BOYS, then girls, then circumcised boys influence of circumcision decreases over time during 1st year to end 3-6 months = more girls than boys 12-24 months = more girls than boys basically after 3 months, it will always have a higher prevalence in girls than boys 65 or > = more common in men due to enlarged prostate UTIs in neonates are associated with BACTEREMIA and CONGENITAL ANOMALIES affecting urinary tract UTIs are rare during the first few days of life even in bacteremic neonates prevalence is higher among uncircumcised boys, esp first 3 months of life higher in white children than black higher in girls than circumcised boys

Answer 65

most UTIs (beyond neonatal period) are ascending infections (urethra --> bladder, causing cystitis which is either eliminated here or progresses to the kidneys) reduced urine flow - obstruction, urethral stricture, prostatic hyperplasia/carcinoma - neurogenic bladder (spinal cord injuries) --> spasmodic or flaccid (unable to completely empty bladder) - vesicourethral reflux (urine reflux back into urethra) enhanced inoculation/colonization - sexual activity - spermicidal contraceptives (may change microbiota) - antimicrobial therapy (may change microbiota) - residual urine due to incomplete emptying - catheterization - urinary or fecal incontinence (E. coli pass thru stool but some can colonize and ascend) urine is not source of bacteria that's going to inoculate, GI is but if there's liquid there + incontinence then there's moisture all the time causing colonization

Answer 66

mostly bacterial infections community acquired - E COLI IS MOST COMMON - entercoccus - staphylococcus saprophyticus nosocomial - E. coli - CoNS - klebsiella - candida other GNRs --> klebsiella, proteus, citrobacter, enterobacter, acinetobacter, pseudomonas other bacteria like staph aureus, M. tb, strep agalactiae viral infections possible but limited to lower UTIs fungal infections in immunocomp pxs parasitic ova (schistosoma haematobium) --> this is a trematode parasitic worm, its eggs will pass in the urine, going into fine capillaries of the bladder, due to movement and compression of organs the spines on will puncture the capillaries and come thru

Answer 67

defenses - normal flora of the periurethral region and distal urethra (lactobacilli, CoNS, diphtheroids, and streptococci) - urine's high osmolality, low pH, low nutrients, and high urea - mechanical removal of bacteria (desquamation and flow) - bladder epi (TLRs, adaptive immunity, exfoliation) establishment of infections requires (E. coli) - entry = ascending (most common) or hematogenous (immunocomp and neonates) - attachment --> type I pili are associated with cystitis (present in all E. coli, will bind to bladder but will be removed, more important effective BEFORE ENTRY) --> P pili are associated with pyelonephritis (bind to epi of bladder, C. coli with this are uropathogens) - tissue damage (cytolysins which are hemolysins) - aerobactin - intermittent expression of pili - P pili don't bind PMNs, because they are not seen by PMNs, when the bacteria are inside the bladder they will switch from type I to P pili to avoid phagocytosis and removal

Answer 68

foreskin mucosa is more likely to bind uropathogens than the skin of the penis and there's also slight urine retention, esp during 1st year of life tight foreskin, which is rarely seen after one year of age, may partially block urethral meatus

Answer 69

- bacteruria can be asymp - cystitis = dysuria, frequency, urgency, hematuria, pyruia, and suprapubic pain (shared with urethritis and prostatitis) - pyelonephritis = cystitis symps with fever, chills, nausea, vomiting, and flank pain pyelonephritis in males, elderly, children, or in presence of symps for >7 days should be consider complicated until proven otherwise can see emphysematous pyelonephritis in pxs with DM due to acid and gas production from glucose fermentation by bugs, will be seen as hairy or raised like shadows on xray classical symps are often absent in children, particularly neonates and infants neonates and other children under 2 with pyelonephritis present with - failure to thrive - poor feeding - fever - vomiting

Answer 70

upper UTIs may lead to comps like renal scarring, HTN, ESRD comps are more likely in children and neonates

Answer 71

urinalysis --> PYURIA, nitrite (some bugs convert nitrate into nitrite), hematuria, casts, and BACTERIA culture - orgs and antibiotic sensitivity - urine is norm sterile - most infections are caused by one org - common etiologic agents differ btwn comp and uncomp infections use sheep blood agar, MAC agar, and CLED agar (designed for urine and candida) incubate in 35 celsius w/o CO2 for 24 hrs (no anaerobic incubation) specimen types = URINE, urethral swabs, and prostatic secretions sample collection for urinalysis and urine culture = voided midstream, urethral catheterization, cystoscopic collection, suprapubic aspiration unacceptable or suboptimal specimens = foley catheter tips and bagged urine from neonates and infants dipstick test --> leukocyte esterase is indicative of PYURIA, nitrite is indicative of GN infection microscopy - >10 WBC/microliter by hemocytometry (very accurate) and > 10 WBC/hpf on spun samples

Answer 72

> 3 orgs = contaminants <10k CFU in asymp px = contaminant >/= 100k CFU = UTI or asymp bacteruria <100k but >/= 100 CFU in symp women = UTI <100k but >/= 10k CFU = dependents (treat symp men, on antimicrobials, other than E. coli and proteus)

Answer 73

these are proteins that fall out solution inside kidney's tissues, inside tubules --> either become casts or precipitate formed in lumen or renal tubules some are dx of renal disease made of TAMM-HORSFALL PROTEIN - hyaline (usually colorless, can indicate concentrated uribe due to dehydration of hypoperfusion) - granular (common finding in prerenal azotemia - increased urea and creatinine- and acute tubular necrosis) - blood (common finding in pyelonephritis) - pus/WBC (common finding in glomerulonephritis)

Answer 74

uncomp cystitis = nitrofurantoin or TMP/SMX comp UTI or pyelonephritis = ciprofloxacin or levofloxacin treat asymp bacteriuria (>/= 10^5 CFU/mL) - preg (due to changes in hormones and chances of reflux increase bc ureters become more laxed) - renal transplant (if there's rejection, bacteria at site might trigger inflam) - urologic surgery treat symp bacteriuria (>/= 10^5 CFU/mL) consider treating symp with pyuria <10^5 CFU/mL - women down to >/= 100 CFU/mL - men - pxs on antimicrobials - org is no E. coli or proteus adjust tx according to culture results surgical intervention or corrective action as appropriate

Answer 75

75-80% of all morbidities in the US 80% are viral most uncomp viral URIs is 5-10 days and pxs are afebrile if fever is present, it occurs on first 2 days with constitutional symps as fever and constitutional symps resolve, respiratory symps become more prominent and peak 3-6 days respiratory symps may continue to persist to day 10 (longer than fever)

Answer 76

rhinoviruses, coronaviruses, adenoviruses, and enteroviruses

Answer 77

strep pneumo, H. influenzae, and M. catarrhalis viruses = RSV, corona, and rhino ear pain and pressure, often associated with URI decreased hearing and fever possible erythematous, bulging tympanic membrane, with loss of light reflex membrane may rupture releasing exudates tx = amoxicillin/clavulanate, nasal decongestant

Answer 78

infection of norm sterile sinuses by spread from nasal cavity or rarely by systemic spread impaired mucociliary action (causes swelling that leads to blockage and allows inoculation) or ostium obstruction and stasis cause bacterial overgrowth spread from nasal mucosa can be enhanced by forceful nose blowing (pressure when blowing nose will inoculate sinuses and cause bigger problems) MAXILLARY SINUS involvement is common due to clearance against gravity rhino, influenza, parainfluenza, s. pneumo, h. influenzae, and m. catarrhalis, less commonly strep pneumo aspergillus or mucor in immunocomp and uncontrolled diabetes

Answer 79

purulent nasal discharge, sinus/facial pain, nasal congestion, decreased sense of smell, and fever preseptal cellulitis, orbital cellulitis, retro-orbital cellulitis, osteomyelitis, meningitis, intracranial abscesses, cavernous sinus thrombosis culture of nasal secretions and swabs are of no use in clinical dx tx = nasal decongestant and corticosteroids if more than 10 days then amoxicillin or amoxicillin and clavulanate for bacterial and amphotericin B for fungal

Answer 80

viral - complete resolution or improvement in 7-10 days - fever is typically ABSENT or observed in 1st few days - secretions are CLEAR, turning PURULENT, then CLEAR AGAIN bacterial - persists MORE THAN 10 DAYS - more SEVERE SIGNS and SYMPS (high fever, obstruction, facial pain) - PURULENT secretion early on in infection - often occurs after typical viral infection

Answer 81

adenoviruses, influenza viruses, parainfluenza virus, coronavirus, rhinovirus, EBV, HSV GAS, group C and G strep, chlamydia pneumo, mycoplasma pneumo, arcanobacterium haemolyticum, corynebacterium diphtheriae s pneumo and h influenzae are frequent colonizers of oropharynx but don't cause pharyngitis gonococcal and syphilitic pharyngitis due to sexual behavior, sign of SEXUAL ABUSE when found in children

Answer 82

viral pharyngitis in adults - sore throat, cervical lymphadenitis, cough, hoarseness - less commonly fever, HA, malaise, fatigue, coryza influenza - abrupt onset of fever, HA, myalgia, malaise - can involve sore throat, nasal congestion, nonproductive cough - CLUE = SEASON infectious mononucleosis (EBV) - early = malaise, fever, HA - late = pharyngitis, tonsillitis (+/- exudate), cervical lymphadenopathy, high fever, splenomegaly, and SKIN RASH - CLUE = FEVER LONGER THAN EXPECTED HSV-1 - pharyngeal edema, oral ulcers, and exudative tonsillitis acute HIV infection resembles infectious mononucleosis strep pharyngitis - exudative tonsillitis, fever, tender cervical lymphadenopathy, typically WITHOUT COUGH, and rhinorrhea - CLUE = PRESENCE OF PETECHIAE arcanobacterium haemolyticum - mimics strep infections - clue = adolescent/young adult with SCARLATINIFORM RASH (associated with scarlett fever, rash with numerous small papules that feel like sandpaper and are blanchable) PROLONGED FEVER, and NEG CULTURE (bc it can be easily masked by growth of other orgs) diphtheria - gray pseudomem that may cover entire pharyngeal opening causing suffocation - CLUE = TRAVEL HX and PRESENCE OF MEMBRANE

Answer 83

suppurative comps secondary to GAS infections - sinusitis - peritonsillar abscess - retropharyngeal abscess non-suppurative comps secondary to GAS - acute rheumatic fever - acute glomerulonephritis - scarlet fever secondary to influenza infections - pneumo - pericarditis - elevated liver enzymes secondary to other viral pharyngitis - bacterial infections (sinusitis, otitis media, pneumonia) - pericarditis (echovirus, coxsackievirus, HIV, and many others)

Answer 84

pxs with modified centor score of >/= 3 are tested for strep RADT --> antibiotics if pos pxs with modified centor score of <3 or >3 with neg RADT are not treated with antibiotics pxs with worsening or persisting symps after 5-7 days should be re-evaluated GAS is most important treatable etiologic agent mere presence of etiologic agent does not prove causation coinfection with viral and bacterial agents are possible awareness of seasonality is often important GAS - RADT is 70-90% sensitive 90-100% specific - DNA probe is 95% sensitive 100% specific - culture - gold standard influenza - rapid influenza dx tests (RIDT) - RT PCR most sensitive and specific

Answer 85

inflam of the larynx, trachea, and large bronchi parainfluenza virus most common INSPIRATORY STRIDOR is key finding hoarseness and barking cough steeple sign on xray --> subglottic tracheal narrowing results in an inverted V shape tx corticosteroid therapy, w/ or w/o epinephrine no antimicrobial therapy

Answer 86

inflam of vocal cords of larynx parainfluenza viruses and rhinoviruses most common S. pyogenes, H. influenzae, M. catarrhalis and viruses other than above hoarseness and aphonia may be accompanied or preceded by URI hydration and voice rest, no antimicrobial therapy needed

Answer 87

inflam of epiglottis EMERGENCY due to obstruction of airway H. influenzae type B most common other = H. influenza, S. pneumo, S. pyogenes, S. aureus rapidly worsening sore throat with pain and difficulty in swallowing tx = ceftriaxone (IV) and adequate airway maintenance prevention = immunization against Hib and S. pneumo

Answer 88

inflam of the bronchi caused by influenza virus, parainfluenza, RSV, and coronavirus smoking and other causes of impaired mucociliary action are predisposing factors stims coughing to clear increased amt of mucus from inflam response cough and chest main are most prominent symps URI symps include sore throat, nasal congestion, fever EXPIRATORY WHEEZES dx made clinically, culture not typically done, RIDT for influenza tx = supportive, antiviral therapy if influenza is dx prevention = influenza vaccine and resp precautions

Answer 89

inflam of bronchioles RSV most common and other resp viruses damage to epi lining of terminal bronchioles leading to inflam and obstruction initial symps of URI that worsen and may lead to RESP FAILURE in children dx is clinical and chest radiographs (STREAKY PERIHILAR OPACITIES) tx = supportive prevention = resp precautions

Answer 90

infection of lung affecting alveoli - more common at extremes of age - copd, cf (impairs mucociliary action), unconsciousness (aspiration of bugs), DM (decreased immunity and possibility of coma), mechanical vents (bugs growing on tubes) are risk factors - exposure to water aerosol increases risk of Legionella infection (like water sports) community acquired - s pneumo (MOST COMMON) - k. pneumo and h. influenzae (common) - staph aureus (destructive), influenza A and B (treatable), MERS-CoV, SARS-CoV, Legionella - bioterrorism agents - pneumocytis jirovecii in AIDS pxs hospital acquired - staph aureus, strep, GNRs - viral - fungal in immunocomp normally sterile lower resp disease occurs when - particularly virulent org --> bugs 5 micrometers or small can get into lungs and be phagocytosed by alveolar macrophages and survive - large inoculum (ex: fungus is present in air and we occasionally inhale it but when we go into the attic where black fungus is growing then we can get sick) - weakened immune defenses productive or nonproductive cough, fever, chills, chest pain, SOB, tachypnea, and abnorm lung sounds RUSTY SPUTUM in pneumococcal pneumo CURRANT JELLY in k. pneumo pneumonia comps - bacteremia - plural effusion or empyema - lung abscess - necrotizing pneumonia dx - infiltrate on chest radiography (GOLD STANDARD) - sputum gram-stain and culture, blood culture for hospitalized pxs - LEUKOCYTOSIS and NEUTROPHILIA in pneumo caused by encapsulated bacteria - pneumococcal polysac and legionella urine Ag test

Answer 91

outpx - empiric levofloxacin, doxycycline - antiviral therapy if influenza is prevalent in community inpx - empiric broad spec antibiotics - pathogen directed therapy - drainage of pleural effusion or empyema when applicable prevention - influenza vaccine - pneumococcal vaccine (>65, smokers, cormorbidities) - HiB vaccine - smoking cessation and alc therapy

Answer 92

due to aspiration of oropharyngeal bacteria or hematogenous spread may be preceded by pneumonitis and pneumonia risk factors = alc, drug abuse, seizures, and surgery POOR ORAL HYGIENE is predisposing factor (decreases amt of biofilms in oral cavity) anaerobes or mix of aerobes and anaerobes of oral cavity presentation mimics that of pneumo with productive cough foul smelling sputum indicative of anaerobic infection

Answer 93

- chlamydophila pneumo (obligate intracell path) - mycoplasma pneumo (take long to grow and not competitive) - legionella pneumoniae (requires special and long incubation) - mycobacterium spp (" ") - viruses

Answer 94

molecular testing (PCR) order specialized culture

Answer 95

- polysac capsule is essential for virulence - IgA protease - amidase (autolysin) hydrolyzes bacterial cell wall (gives colony its shape, PENNY APPEARANCE) - pneumolysin (pore-forming cytotoxin) lyses epi cells and phagocytes - cell wall components and pneumolysin activate complement and lead to inflam MOPS

Answer 96

sputum gram stain --> GP lancet shaped diplococci culture of sputum, blood, CSF, or other - alpha hemolytic on blood agar - susceptible to optochin - dissolved in bile or deoxycholate quelLUNG test --> use Abs against capsule, so get a little of colony then mix with Ab, if test pos then you will see visible capsule swelling and clumping of colonies urine testing for PNEUMOCOCCAL C-POLYSACCHARIDE PCR assays tx = penicillin G (severe) or V (mild), vancomycin for resistant isolates prevention = 13 valent pneumo vaccine and 23 valent unconjugated vaccine

Answer 97

GP club shaped bacilli that has CHINESE LETTER APPEARANCE DT induces ADP ribosylation of EF and shuts down translation toxin goes systemic and finds recep expressed in heart muscle, attacks heart, leads to immune cell infiltration and loss of tone of muscle --> enlarged heart silhouette DT encoded by beta phage transmitted thru resp droplets malaise, fever, pseudomem pharyngitis, cervical lymphadenopathy (BULL'S NECK), myocarditis, and arrhythmias bacteria do not invade by DT is absorbed and spread hematogenously will see shredded cardiac muscle which causes weak contraction with necrosis and inflam on histo anti-toxin Abs form during natural infection and are protective fatalities often result from HF or suffocation (due to pseudomem) initial dx is clinical

Answer 98

heart and nerves

Answer 99

microscopic appearance - GP, pleomorphic bacilli forming acute angles with each other (resemble chinese letters) - stains irregularly and displays METACHROMATIC AREAS (BABES-ERNST GRANULES) culture - CYSTINE TELLURITE blood agar and TINSDALE AGAR are selective and differential media (BLACK COLONIES WITH BROWN HALOS) toxigenicity testing - media with growth rate-limiting concentrations of iron - Elek test, ELISA, PCR amp of tox gene (detect AG) tx = administration of anti-toxin, erythromycin or other antibiotics prevention = toxoid vaccine (childhood and boost eat 10 years)

Answer 100

GN, fastidious bacillary or coccobacillary HiB most virulent pili and adhesions cell wall components damage resp epi secretory IgA protease polyribitol phosphate capsule no know toxin nontypeable strains most common in MUCOSAL infections encapsulated strains most common in INVASIVE infections haEMOPhilus Epiglottitis (cherry red endoscopy and thumb in xray) Meningitis Otitis media Pneumonia

Answer 101

dx fastidious bugs require X factor (hemin) and V factor (NAD) specimens collected from blood, resp, CSF, and conjuctiva tx = ceftriaxone (severe) and amoxicillin-clavulanate (mild) prevention = conjugated and unconjugated vaccines

Answer 102

aerobic, pleomorphic, GNR or filamentous bacteria often associated with FRESHWATER environments 1st recognized species and most common in US successful survival in various environments - facultative intracell parasite in lung macrophages and free living protozoans - tolerates wide range of temps - adherence to various surfaces and incorporation into biofilms - RESISTANCE TO CHLORINE transmission by inhalation of contaminated aersol person-to-person not common patho alveolar macrophage is 1st victim pathogen is internalized in LCV type IV injection secretion system enables delivery of many proteins from LCV into cytoplasm to orchestrate bug's agenda - phagosome-lysosome fusion inhibited - ribosomes, mt decorate vacuole - multiplication to large number - production of pore-forming toxin facilitates lysis of host cell and liberates pathogen progeny - tissue necrosis and systemic toxicity result from inflam response - LPS is less toxic than most GN bacteria - LPS is prime target of innate immunity (TLR on macrophage and DCs) - Th1 responses lead to macrophage activation and killing of invading pathogen - Abs are of dx value but don't seem to play protective role

Answer 103

clinical aspects - asymp, mild resp infections (pontiac fever), pneumonia (legionnaire's disease) - legionnaire's disease = pneumonic legionellosis characterized fever, HA, cough, myalgia, blood or purulent sputum, dyspnea, and chills often u/l or unilobar infiltrates infection may spread to distant organs and result in organ failure and/or neuro symps - pontiac fever = non-pneumonic legionellosis characterized by self-limited illness composed of fever, HA, cough, and myalgia dx aerobic, pleomorphic, faintly stained GNR in and outside phagocytes -- silver stain and fluorescence for better visualization DFA test is species-specific (CONFIRMATORY TEST) --> use Abs against legionella Ags conjugated with fluorescein culture of BAL, lung aspirates, or biopsies on buffered charcoal year extract (BYCE) with L-CYSTEINE and IRON urine Ag detection test PCR on resp samples colonies exhibit GROUND GLASS APPEARANCE and grow on BYCE after 5 days tx = azithromycin preventino - precautions to disinfection of water in hot-water tanks, cooling towers, humidifiers, and mist-generating devices - avoidance of aerosol inhalation, esp if immunocomp - taking proper action to end outbreaks, including hyperchlorination, heating, or other appropriate measures

Answer 104

aerobic, GN bacillary or coccobacillary org B. pertussis is cause of whooping cough B. parapertussis is milder disease similar to pertussis B. bronchiseptica causes resp infections in BIRDS and MAMMALS and is considered an opportunistic human pathogen causing resp and wound infections transmission thru resp droplets HIGHLY CONTAGIOUS humans are only reservoir primarily affects CHILDREN effective vaccine available, part of childhood vaccine - filamentous hemagglutinin, pili, pertactin facilitate attachment to host cells - PT is an AB toxin that mediates ADP ribosylation of G protein (Gi) --> increase AC, cAMP, and EDEMA - disruption of chemokine recep signaling, lymphocyte entry into lymphoid tissues, and LYMPHOCYTOSIS - HYPERSINSULINEMIA, hypoglycemia - hypersensitization to HISTAMINE - tracheal cytotoxin kills ciliated cells in resp mucosa (persistent and whooping cough) - no invasion or spread to lower parts of resp tract (NO PNEUMONIA) - Ab produced during natural infection but not long lasting or completely protective

Answer 105

- catarrhal phase = profuse mucoid rhinorrhea and non-specific symps including sneezing, coughing, conjunctivitis, etc, disease is HIGHLY CONTAGIOUS - paroxsymal phase = severe, repeated coughing spells often followed by whoop, vomiting may follow, LYMPHOCYTOSIS PEAKS (up to 40k) - convalescent phase = gradual fading of symps dx best confirmed by isolation of agent dx - culture of nasopharyngeal secretions, NOT PHARYNX - fastidious org, not like other species - charcoal blood agar with antibiotic selective agent (DROPS OF MERCURY) - grows in 5 days - DFA and PCR tests available tx erythromycin BEFORE paroxsymal phase supportive therapy if no tx has been started before paroxysmal attacks prevention = vaccination

Answer 106

results from inhalation of infectious spores which invade ALVEOLAR MACROPHAGES, but don't germinate until they reach the MEDIASTINAL LYMPH NODES innate immunity inhibited by toxins and capsule bacteria rapidly spread to blood stream and CNS (meningitis and hemorrhagic brain infection) ET and LT injure almost all cell types, esp CARDIAC and SMOOTH MUSCLE MASSIVE EDEMA and HEMORRHAGE are hallmarks of anthrax mediastinitis and meningitis person to person doesn't occur initial presentation nonspecific, followed by resp distress and cyanosis fatal if not treated dx confirmed by lab anthrax can be see in gram stains of sputum, blood, CSF, and pleural effusion culture of these samples on blood agar LOOKS LIKE RECTANGULAR RODS/BAMBOO dx = PE, imaging studies, blood culture and PCR, CSF culture with gram stain and PCR, pleural fluid culture with gram stain and PCR tx - IV ciprofloxacin + clindamycin or linezolid antibiotic regimen should include a protein synthesis inhibitor with good CNS penetration (linezolid) passive immunization to neutralize toxin aggressive management of pleural effusion

Answer 107

GN short rods of enterobacteriales, bipolar staining, grows on common media, non-motible causes PLAGUE zoonotic infection of RODENTS reservoir - urban plague = rats and their fleas - sylvatic plague = wild rodents (prairie dogs, squirrels, field rats, deer, mice) and their fleas vector = rat fleas many route of infection and clinical presentation - bubonic = flea bites - pneumonic = hematogenous or inhalation (contagious) - septicemic = secondary to bubonic or pneumonic most cases in Madagascar and west coast of US LPS endotoxin causes fever and septic shock LPS variant in host is not recognized by TLR4 resistance to phagocytosis - type III secretion system enables bacterium to inject effector proteins into phagocytic cell - protein capsule (F1) interferes with phagocytosis - plasminogen activator protease degrades complement components C3b (opsonization) and C5a (phagocyte migration, chemotactic factor, anaphylotoxin) spread = plasminogen activator protease cleaves plasminogen into plasmin which degrades fibrin clots

Answer 108

natural infection confers lasting immunity anti-F1 Abs cell mediated immunity

Answer 109

bubonic - flea bite - 2-7 days incubation - 50-90% mortality untreated, 10-20% treated will see marked lymphadenopathy in axilla and inguinal LNs pneumonic - primary - inhalation - secondary - hematogenous seeding - 1-3 days incubation for primary - 100% mortality uncreated, 50% treated septicemic - flea bite or hematogenous spread from pneumonic or bubonic - 100% mortality untreated fever, bubo, hx of contact with rodents/fleas compatible morphology in gram stain - bubo, blood, or sputum isolation of agent from bubo, blood, or sputum immunofluorescence microscopy, molecular, MALDI-TOF tx = gentamicin-doxycycline combo therapy, timely tx critical to decreased mortality of bubonic by 10% prevention rodent and insect control avoidance of reservoir animals in natural habitats pet flee control vaccine NO LONGER AVAILABLE

Answer 110

agent of zoonotic disease tularemia (RABBIT FEVER) aerobic, non-motile, coccobacillary or bacillary, GN, facultative intracell pathogens tularemia has multiple forms like pneumonic disease contracted by ingestion, inhalation, arthropd bites, percutaneous via contact with infected tissues, occupational exposure reported in all states except Hawaii most virulent strains in N America lipid-rich capsule in virulent strains LPS not recognized by TLRs (in Y. pestis it is recognized in cold blooded vector but not warm blooded bc they switch) multiplication occurs in alveolar macrophages and epi cells (can occur in other cells) hematogenous spread occurs if not treated, lesions may form in multiple organs LPS stimulates protective Abs

Answer 111

pneumonic disease after inhalation of bug or secondary to untreated extrapulm disease typical pneumonia presentation making it difficult to dx also just hard in general bc it's like other conditions, sometimes missed due to growth requirements hx of TICK OR DEER FLY BITES or exposure to dead or wild animals are clues for dx lab should be notified bc proper media with cysteine should be used, prolonged incubation, and proper precautions for protection of lab personnel lab dx - most grow on choclate and GC medium producing smooth gray-white colonies - specialized med w/ added cysteine is optimal - serologic and molecular dx testing often used to avoid risks associated w/ culture tx = gentamicin prevetion - avoid arthropod bites - PPE when handling animals - live attenuated vaccine for occupational exposure

Answer 112

causes highly contagious Q FEVER small GN coccobacilli that may cause pneumonia upon inhalation cattle, sheep, GOATS are primary reservoires shed in urine, feces, milk, AMNIOTIC FLUID of reservoir animals (vets and farmers) inhalation of aersolized birthing material or excreta is most common route transmission by tick bites, ingestion of unpasteurized milk person to person possible but rare spore like form is stable for long time in environment primary target is alveolar macrophage reps in phagolysosomes where it resists digestive enzymes and low pH

Answer 113

symps = high fever, HA, myalgia, and arthralgia (fever, lung, liver) patchy interstitial pneumo may or may not be present hepatosplenomegaly and elevated liver enzymes lab dx by direct immunofluorescence assays of infected tissues or PCR tx = doxycycline

Answer 114

tier 1 - B anthracis - F tularensis - botulinum neurotoxin - botulinum neurotoxin producing clostridia - Y. pestis other - C. burnetii - staph aureus enterotoxins

Answer 115

n asteroides most common acquired thru inhalation of aerosolized orgs mostly affects immunocomp pxs with underlying disease or receiving immunosuppressive therapy inflam, suppurative, and destructive lesions result in confluent bronchopneumo w/ cavities and extension to pleura may spread to brain, invovlement with concurrent or recent pneuo suggestive of nocardia infection high mortality slow growing, isolation is facilitated by many orgs and distribution of lesions prolonged tx due to slow growth beaded appearance on histo, acid fast staining (Ziehl-Neelsen)

Answer 116

a israelii most common part of endogenous flora of GI thoracic infections are are, resulting from traumatic intro of infectious agents often polymicrobial like other anaerobic infections lesions spread across anatomical barriers, contain few microcolonies (SULFUR GRANULES) and form draining sinuses slow growing org, require prolong antibmicrobial therapy

Answer 117

LACK CELL WALL very small looks like FRIED EGG requires CHOLESTEROL in culture resp infections - mycoplasma pneumo urogenital infections - mycoplasma hominis - mycoplasma genitalium - ureaplasma urealyticum ***sensitive to heat and drying should be inoculated at beside or promptly transported can't gram stain, no cell wall METHYLENE BLUE can stain colonies ACRIDINE ORANGE stain cells lab dx using PCR and serology (should be collected during ACUTE and CONVALESCENT stages for rising titer)

Answer 118

humans are only reservoir transmitted by resp droplents causes damage and necrosis in resp epi (H2O2) inhibits ciliary action does NOT invade mucosa or deeper tissues autoAbs, including COLD AGGLUTININS, produced clinical feats atypical pneumo and bronchitis tx azithromycin or doxycycline

Answer 119

aerobic, nonmotile, ACID FAST BACILLI with GP cell wall structure but do not gram stain high lipid content in cell wall - long chain mycolic acids and LAM - resistance to antimicrobials, survival in environment, and acid fastness lots of nonpath strains in environment infection = slow onset, chronicity, and granulomatous lesions high infectivity and low to mod virulence in immunocompetent

Answer 120

- m tb = human, cause tb, common transmission - m africanum = human, cause tb, common transmission - m bovis = animal, cause tb, rare transmission - baccilus calmette guerin (BCG) = artificial culture, cause local lesions, very rare transmission all m tb complex

Answer 121

most common form is chronic pneumo but extrapulm does occur caused by one of the m tb complex orgs tend to aggregate in SERPIGINOUS CORD-LIKE arrangement --> rough colonies and increased persistence in macrophages, in both patho and nonpatho mycobacteria human pathogen transmitted by inhalation of resp droplets but can also be ingestion and skin inoculation TB causes 25% of deaths among AIDS pxs

Answer 122

pathogen inhaled in resp droplets some reach alveolar spaces in MIDDLE and LOWER zones of lung tubercle bacilli are recognized by complement receps and other surface molecules on the surface of alveolar macrophages they are then phagocytosed and survive in phagosomes inside naive macrophage stage 1 = m tb rep in NON-ACTIVATED MACROPHAGE - urease keeps pH up, inhibiting digestive enzymes - antioxidants counter ROS - cord factor inhibits phagosome lysosome fusion stage 1 = m tb are killed in ACTIVATED MACROPHAGES - fate determining event - phagosome forms, acidification occurs this leads to either - complete clearance - incomplete clearance --> primary infection or reactivation of latent infection causes scars, tubercles, caseating necrosis, and cavitary lesions - infected macrophages secrete cytokines that attract other immune cells --> new macrophages arrive and more infection and rep occur, T cells arrive and Th1 response is initiated - Th1 CD4 cells mediated CMI, macrophage activation, and DTH --> large number ot T cells and macrophages accumulate creating GHON FOCUS/LESION option 1 = containment, resolution, fibrosis, and calcification option 2 = lesion enlargement, dissemination, and necrosis - necrosis startes in CENTER of tubercule due to ations of TNF-alpha, ROS, perforin and granzymes eventually leading to necrosis and cavities - further liquefaction of necrotic lesion results in cavitation - erosion into airways results in bloody sputum and coughing up of infectious bacteria in all cases, INVOLVEMENT OF LOCAL LNs is lightly

Answer 123

mycobacteria will infect macrophages --> causes release of IL-12 which binds to T cell/NK cell receptors and activate them --> leads to release of IL-2 and IFN-gamma which activates macrophage to release TNF-a and IL-12 and kill the intracell pathogens

Answer 124

primary - tubercle bacilli spread from site of infection to hilar and mediastinal LNs --> see lymphadenopathy on CXR - adaptive immunity (Th1) and DTH develop - Ghon focus and lymphadenopathy on SAME SIDE = Ghon complex - primary progressive lung disease in form of tb pneumonia latent - containment of infection by CMI/activated macrophages reactivation from distant sites may occur later on BLUE CHEESE looking caseous necrosis

Answer 125

inhalation of tubercle bacilli in resp droplets small enough to reach alveoli leads to - complete clearance with no comps - primary infection (10%) - latent infection (90%) --> no reactivation --> reactivation after period of latent infection host factors associated w/ high risk of poor outcome - HIV/AIDS, chronic renal failure, uncontrolled DM, immunosuppressive drugs, young children, older adults, smoking

Answer 126

pxs may have pulm, extrapulm, or both extrapulm in 10-40% of pxs pulm tb is primary or reactivation primary tb - fever, pleuritic or retrosternal chest pain, pleural effusion - rare symps = fatigure, cought, arthralgia, and pharyngitis - ghon focus/compex in middle and lower zones - CXR often norm or hilar/mediastinal lymphadenopathy, pleural effusion, and infiltrates - initial lesions may resolve or progress to cavitation - enlarged node may compress bronchi or rupture into them (pneumonia) - hematogenous spread common = foci of infection that may or may not reactivate later, extrapulm disease like tb meningitis, disseminated tb (miliary) secondary tb - FEVER, COUGH, WEIGHT LOSS, malaise, hemoptysis, anorexia, and chest pain - less common = pleural disease, dyspnea, RDS - affects apical and pos of upper lobes - small infiltrates to cavitary lesions - massive coalescing lesions lead to caseating pneumo - untreated pxs may --> succumb to severe pul disease, recover, or suffer chronic disease and remain infectious

Answer 127

tuberculin induces DTH which is tested for in tuberculin skin test PPD of tuberculin injected intraderm and results in 2-3 days induration of 10 mm or MORE*** = pos rxn pxs who were immunized with BCG or infected w/ other mycobacteria may show pos rxn immunosuppressed may show neg due to anergy

Answer 128

cough >2-3 wks, lymphadenopathy, fever, night sweats, weight loss previous disease, travel to endemic areas norm to alveolar infiltrates, cavities on radio definitive dx based on isolation of agent DETECTION OF AFB in SPUTUM smears or by NAA tests is CONFIRMATORY tuberculin test (PPD) doesn't distinguish btwn mycobateria tho rough, buff, and tough colonies on enriched media in 3-6 wks common media = LOWENSTEIN JENSEN demonstration of AFB in acid fast smears using ziehl-neelsen or AURAMINE RHODAMINE IFN gamma release assays - T spot TB test - quantiFERON test - specific to TB including LTBI these do NOT distinguish between active or latent

Answer 129

quantiFERON blood sampled mixed with Ag, send to lab, incubate, T cells interact with Ag (blood mixed with Ag on the spot) look for production of cytokine in supernatural not common w/ BCG vaccine and does NOT cross react, much lower freq of cross-reactivity w/ environmental mycobacteria TSPOT take blood and add anticoag, send to lab expose to various Ags, put in machine that produces a color to be able to see it then count spots where cell has been producing cytokine basically purify peripheral blood MN cells ib blood before adding AG in both see if px has T cells specific for TB or not, look for release of IFN gamma in response to exposure to TB Ag, Ags here are diff from PPB of tuberculin test

Answer 130

TB disease - initial (bactericidal) phase = 2 months of isoniazid, rifampin, pyrazinamide, and ethambutol PLUS continuation phase = 4 months of isoniazid and rifampin LBTI - 3 months of isoniazid and rifampin OR - 9 months isoniazid prevention - BCG vaccine - diagnose, isolate, and treat - treat both TB and LTBI

Answer 131

aka atypical mycobacteria, environmental mycobacteria, and mycobacteria other than tb species of mycobacterium other than m tb complex and m leprae in environment (soil and water) - reservoir exposure universal but disease is rare in immunocompetent most disease in indvs with comp immunity, malignancies, or chronic pulm disease case to case transmission rare, only in CF pxs more resistant to antibiotics used against M tb

Answer 132

I (photochromogens) - slow, pig in light, M kansasii and marinum II (scotochromogens) - slow, pig in light and dark, m scrofulaceum III (nochromogens) - slow, no pig, m avium and intracellulare IV - rapid, no pig, m fortuitum and chelonae

Answer 133

photochromogen m kansasii - cause pulm infections that resemble tb - unknown natural habitat m marinum - causes SWIMMING POOL GRANULOMA or FISH TANK GRANULOMA - found in fresh and salt water

Answer 134

scrotochromogen m scrofulaceum - causes granulomatous CERVICAL LYMPHADENITIS (scrofula) in YOUNG CHILDREN - found in aquatic environments and human oropharynx

Answer 135

m avrium and intercellulare - cause pulm infections identical to tb mainly in immunocomp pxs - widespread in environment - ANTIMICROBIAL RESISTANCE most common

Answer 136

- attachment to target cell receps (sialic acid) is mediated by HA - nucleocapsid release and translocation to nucleus (for pol II) - viral transcriptase functions --> RNA dependent RNA pol transcription of mRNA from infecting genome and newly synthesized copies, transcription of genomic -ssRNA via +ssRNA intermediate (use this to make copies of progeny) --> endonuclease cap snatching = goes into nucleus, interacts w/ host pol II to find mRNA (5' end) and split it to make primer (for it to be translated, it needs to be capped) --> transcription - translation producing viral transcriptase, HA, and NA - HA and NA are synthesized by ribosomes of RER and are targeted to PM - nucleocapsids assembled in nucleus are translocated to regions of PM that have been decorated by viral glycoprotein spikes - packaging and budding results in a newly-formed progeny that reminds attach to the host cell's sialic acid - NA cleaves sialic acid and liberates virions allowing then to infect new cells

Answer 137

M2 protein aids in uncoating and is targeted by AMANTIDINE and RIMANTADINE NA is targeted by ZANAMIVIR and OSELTAMIVIR anti-HA are neutralizing Abs because it prevents binding of bug anti-NA Abs inhibit spread of infection but preventing cleavage of sialic acid and release of virion

Answer 138

human viruses are not stable in environment while avian infectivity last for weeks, enhancing potential for epidemics

Answer 139

drift = mutations (gradual accum of mutations, viral pol lacks proof reading) shift = reassortment in cell co-infected with 1 or more strains of virus

Answer 140

- HA determines species susceptibility and tissue tropism --> human HA binds sialic acid alpha 2,6 galactose on epi cells of nasal cavity, paranasal sinuses, pharynx, trachea, and bronchi --> avian HA binds sialic acid alpha 2,3 galactose in bronchiolar epi cells (more likely to cause pneumo because they travel deeper) - NA liberates newly-formed virions and interferes with mucs entrapement - infection of ciliated epi cells leads to fxnal and structural abnorms and disruption of mucociliary action - viral infection results in a shutdown of macromolecule synthesis followed by desquamation of goblet and ciliated cells - restoration of damage takes 2 to many wks - mononuclear leukocyte infiltrates and local inflam occur as a result of tissue damage - impaired mucociliary actions makes host susceptible to secondary bacterial infections - containment of infection ends acute phase when interferon and NK cells are produced, followed by CTL and Ab responses - protection against future infection appears to rely on Ab levels ad affinity to structures of infecting virus, which decrease over time anti HA are most protective, prevent infection anti NA are protective, limit spread

Answer 141

NA inhibitors (A and B) - oseltamivir and zanamivir within first 48 hrs influenza endonuclease inhibitor (A and B) - BALOXAVIR is most effective when given in first 48 hrs M2 protein inhibitors (A only) - amantidine and rimantidine useful in first 24 hrs

Answer 142

genome not seg HA and NA are NOT on SAME spike separate fusion protein rep in cytoplasm no sig antigenic shifts or drifts

Answer 143

- measles = fever, rash, coryza, cough, and KOPLIK SPOTS (white spots in mouth) - mumps = fever, myalgia, and PAROTITIS (orchitis) - parainfluenza = CROUP, URI, and LRI

Answer 144

infections mostly affect infants and young children parainfluenza 1 (fall) = major cause of acute croup in infants and young children and URI and tracheobronchitis in all ages parainfluenza 3 (all year) = major cause of croup, bronchitis, bronchiolitis, and pneumonia in infants and young children and URI and tracheobronchitis in older children and adults

Answer 145

for HA or NA, but instead G (surface attachment protein) and F (fusion) proteins

Answer 146

by PCR or Ag detection methods and isolation from resp specimens aggressive use of steroids and bronchodilators (due to asthma misdx) may lead to poor prognosis or even death tx supportive ribavirin, IVIG, monoclonal ABs in immunocomp pxs vaccine and passive immunization are recommended for prevention control measures like handwashing, isolation

Answer 147

- F protein important for syncytia formation and cell death - infection confined to epi cells and patho similar to influenza (proinflam cytokine damage, necrosis, mononuclear infiltrates, early CTL control) - Th1 response = better outcome - Th2 = neutrophil/eosinophil infiltration and diminishes CD8 CTL responses - immunity brief and incomplete so reinfections occur initial illness manifests in form of upper resp symps bronchiolitis and penumo follow in infants disease severity decrease in older children

Answer 148

enveloped, +ssRNA alpha (better), beta (bad), gamma, and deltacoronaviruses beta is divided into A, B (SARS-CoV 1 and 2), C (MERS-CoV), and D spikes bind to host cell receps (ACE2 for SARS-CoV and DPP4/CD26 for MERS-CoV) neutralizing Abs raised against spike protein rep in cytoplasm unlike influenza which is in the nucleus viral envelop from host ER and golgi

Answer 149

asymp or severe upper resp symps that may progress to pneumo, resp failure, septic shock, and multi organ failure typicalyl severely ill px with an adult w/ severe pneumo and RDS, sometimes with renal injury

Answer 150

incubation 2-14 days (4-5 DAYS MOST COMMON) abt 33% asymp cough, fever, myalgia, HA, dyspnea, sore throat, diarrhea, n/v, other pxs may develop pneumo, sepsis, ARDS leading to death

Answer 151

clinical presentation and lab for both SARS - serology - RT-PCR on resp specimens, stool, serum, plasma covid - RT-PCR in resp secretions - Ag detection in resp secretions - lymphopenia - elevated liver enzymes, LDH, and inflam markers - coagulation abnroms MERS - serology - RT-PCR best done on LOWER RESP specimens with upper resp as alt tx covid - dexamethasone (steroid, initial tx) - paxlovid (viral protease inhibitor, initial tx) - IL-6 recep inhibitors (give later in course, immunomod) - JAK inhibitors - remdesivir prevention = vaccines, PPE, isolation, social distancing

Answer 152

non-enveloped, icosahedral, linear dsDNA capsid fibers are antigenically variable responsible for type specificity, cell tropism, and recep binding cause resp infections, conjunctivitis, gastroenteritis, cystitis infection persists for a few days or years, symp or asymp transmission thru resp droplets, fecal-oral, or direct inoculation outbreaks among military personnel and children less than half result in symp disease specific types associated with specific presentation survive for long time on surfaces and are RESISTANT TO DISINFECTANTS virus shedding persists for long periods causes fever, rhinitis, pharyngitis, cough, conjunctivitis, and diarrhea common causes of non-strep exudative pharyngitis in children also laryngitis, croup, bronchiolitis, and pneumo PHARYNGOCONJUNCTIVAL FEVER gastroenteritis and hemorrhagic cystitis

Answer 153

- bind cell surface recep by fibers - entry by viropexis - uncoating and translocation of genome to nucleus - viral rep in nucleus --> transcription using host RNA pol and DNA rep using viral DNA pol - virions assembled in nucleus - released by lysing host cell which is mediated by adenovirus cell death protein

Answer 154

- infect epi cells of mucosal surfaces in affected organs - penton fibers are TOXIC to cells and may cause tissue damage - acute infection cause tissue necrosis and mononuclear inflam response - latent infection is asymp and often affects TONSILS and ADENOIDS - viremia may occur causing spread to liver, kidneys, bladder, lymphoid tissues, or CNS - spread to distant sites may result in inflam - asymp stress reactivation may occur for several months (not lifetime like HSV) - integration into host genome may result in years of latency - SMUDGY INTRANUCLEAR INCLUSIONS seen in some infected cells - neutralizing Ab responses protective, lifelong, and type-specific

Answer 155

genome amp (PCR), Ag detection, isolation, and serology virus isolation from oropharynx or feces may not be related to disease - asymp shedding tx = no specific tx prevention = ORAL LIVE VACCINE

Answer 156

adeno has lack of cytoplasmic inclusions unlike CMV

Answer 157

beta herpesvirus primary infection followed by latency (lifelong infection) detected in monocytes, macrophages, DCs, megakaryocytes, and myeloid progenitor cells causes CYTOMEGALY in infected cells viral rep similar to other herpesvirus except slower than alpha many or most ppl have Abs isolated from saliva, nasopharyngeal secretions, genital secretions, urine, breast milk, blood, and WBCs shedding for months or years after primary infection transmission by close direct contact like sexual transmission among DAYCARE CHILDREN then their parents transmission by blood transfusion and organ transplant occurs but not common

Answer 158

- infects vascular endo cells leading to NUCLEAR INCLUSIONS (OWL'S EYE CELLS), perinuclear inclusions, and cell enlargement - pathogen effects = direct and immune mediated tissue damage - most tissue damage in pneumo results from killing of infected cells by CTL and cytokine damage

Answer 159

- primary infection can be symp or asymp, while reactivation is ALWAYS ASYMP in IMMUNOCOMPETENT - primary and reactivation is more likely to be SYMP in IMMUNOCOMPROMISED - mononucleosis like illness may develop in healthy individuals with primary infection - intrapartum and postpartum transmission common but not important - in utero transmission often detrimental to fetus, esp when primary infection occurs in early preg - congenital infection --> most common congenital viral infection --> results from primary infection or reactivation during preg --> adverse outcome in primary due to absence of maternal Abs and high viremia --> damage more likely during 1st trimester --> symp and asymp infections may lead to DEAFNESS or COGNITIVE IMPAIRMENT --> symp infections present with hepatoplenomegaly, jaundice, anemia, microcephaly, chorioretinitis - seroneg preg moms should avoid sources of infection like child in daycare can be severe or lethal in immunocomp pxs like transplant recipients and HIV/AIDS pxs - gastroenteritis - retinitis - pneumo

Answer 160

dx - detection of NA, Ag, or CPE in infected tissues - detection of Ag or NA in body fluids - isolation in culture - serology (rising titer) tx - ganciclovir - cause bone marrow suppression - foscarnet - cause nephrotoxicity - immune globulin - no tx for healthy pcs prevention - safe blood transfusion and organ transplant - safe sexual practices

Answer 161

ganciclovir for CMV (works for the other viruses too) acyclovir for HSV, EBV, and VZV no acyclovir for CMV because it has a thymidine kinase that can't phosphorylate acyclovir

Answer 162

gamma herpesvirus infects epi cells and B cells (bind to CD21 or CR2) main agent of - INFECTIOUS MONONUCLEOSIS - african burkitt's, hodgkin and non hodgkin lymphomas - nasopharyngeal carcinoma and hairy oral leukoplakia (malig) also associated with other B cell lymphomas small number of infected B cells are immortalized (causes persistent viral stimulation that results in activating cytokines) integration in host genome is RARE only few genes are expressed during latency (allows it to survive) transmission thru SALIVA but not efficient so little exposure will not transmit, requires more intimate contact 90% of all humans are seropos (mainly college age) intermittent shedding by pxs abt 50% develop infectious mononucleosis when acquiring infection in teen and later in life (ex: ME will develop by age 5 and spread infection by direct contact w/ saliva) infection requires repeated exposure (low contagiousness) genital and transfusion transmission rare

Answer 163

- receps are CD21 (CR2) - initial infection in OROPHARYNGEAL epi, then naive tonsillar B cells, followed by viremia and spread to B cells at remote sites - infection results in --> lytic infection in epi cells or B cells (primary or reactivation) --> latent infection in memory B cells (repeat exposure) --> stim and immortalization of B cells (hyperprolif that can lead to leukemia or lyphoma) - benign polyclonal B cell activation - B cell prolife and EBV Ags activate T cell responses, resulting in ATYPICAL LYMPHOCYTES (DOWNEY CELLS) - productively infected B cells eliminated by cell immune responses in infectious mononucleosis - small numbers of latently-infected B cells remain for life and EBV activation and shedding may occur upon B cell activation by cognate Ag - fail to contain infection = lymphoproliferative disease - C-MYC*** translocation in Ig have and light chain occurs in BURKITT'S LYMPHOMA - malaria has role in C-myc translocation and development of burtkitt's lymphoma - specific and unrelated (HETEROPHILE) Abs induced

Answer 164

- subclinical or mild infection, esp in children - infectious mononucleosis malaise, lymphadenopathy, exudative pharyngitis, hepatosplenomegaly (AVOID CONTACT SPORTS) POS CERVICAL NODES more often involved than ant, generalized lymphadenopathy may occur palatal petechiae with streaky hemorrhages may be seen PENICILLIN and AMOXICILLIN administration associated with MACULOPAPULAR RASH lymphoproliferative syndrome - in pxs with immunodeficiency - persistent fever, lymphoadenopathy, and hepatosplenomegaly

Answer 165

dx infectious mononucleosis young adult w/ fever, pharyngitis, fatigue, lymphadenopathy palatal petechiae, splenomegaly, and pos cervical adenopathy is HIGHLY SUGGESTIVE lab dx infectious mononucleosis - lymphocytosis (>4500 or 50%) - atypical lymphocytes - HETEROPHILE AB TESTING - anti-viral capsid Ag, IgM (primary infection), and IgG (previously been exposed) - ANTI-EARLY AG IgG appears in acute phase then disappears - anti-EBV nuclear Ag, appears later (months or lasts for life) - elevated liver enzymes ddx - strep pharyngitis - no splenomegaly or elevated liver enzymes - CMV, HIV, toxoplasmosis requires lab test - CMV = MILDER or ABSENT PHARYNGITIS, but elevated liver enzymes and hematology resembles EBV - HIV = presence of mucocutaneous ulceration or rash - toxoplasmosis = pharyngitis and elevated liver enzymes rare, hematologic abnorms not seen - lymphoma, drug-induced syndrome tx - supportive - acyclovir for hairy leukoplakia in AIDS pxs prevention = limiting saliva transmission, no vaccine

Answer 166

paramyxoviridae structure and rep resemble parainfluenza virus - HN and fusion envelope glycoproteins - uses sialic acid on host cell surface as recep - rep in cytoplasm and budding thru PM transmission thru resp droplets, direct contact, fomites highly contagious among susceptible ppl 1/3 show no symps 5-15 y/os most affected communicability from 7 days BEFORE and 9 days AFTER

Answer 167

- initial rep in resp epi and local LNs (px not contagious yet) - viremia spreads infection to distant organs (PAROTID GLANDS, CNS, kidneys, etc) - tissue necrosis and inflam w/ mononuclear infiltrates - humoral and cell immunity contain and eliminate infection - protective Abs (IgG) persists for life

Answer 168

- 15-20% asymp, more likely in adults than in children - adults are more likely to experience severe course than children when symp - u/l or b/l PAROTITIS, fever, fatigue, HA, anorexia - symps last for 7-10 days - virus shed in saliva during infectious stage - VIRURIA remains for few wks after resolution of symps comps - mumps ORCHITIS in POSTPUBERTAL MALES - mumps oophoritis in postpubertal females - neuro comps - pancreatitis, myocarditis, arthritis

Answer 169

dx - should be suspected in pxs with parotitis and relevant environmental exposure even if vaccinated - virus can be detected or isolated from saliva, serum, CSF, urine - RT PCR for rapid detection - serological testing (IgM and IgG rising titers) - neutralization testing to eval immune protection tx = supportive prevention - mmr vaccine

Answer 170

phylum = basidiomycota C. neoformans*** and C. gatti are important Yeast forms under environmental and physiologic conditions POLYSAC CAPSULE (GXM) produced in tissues when grown in lab (inhibits phagocytosis) teleomorphs produced under special lab conditions, not seen in nature stain C. neoforms with INDIA ink --> see budding yeast cells and thick polysac capsule

Answer 171

associated with soil, decaying plants, BIRD (PIGEON) DROPPINGS can affect immunocompetent ppl, but invasive disease is more likely in immunocomp pxs (expect CNS symps) acquired by INHALATION of yeast forms or BASIDIOSPORES no human to human transmission stained red by PAS stain --> capsule not stained but there's clear halo around orgs patho - production of capsule critical for virulence - GXM has multiple local and systemic immune suppressive effects - titan cells are produced, too large to be phagocytosed - LACCASE enables production of MELANIN, protects phagocytosed orgs against killing - paucity of immune cells in various forms of infection is typical main infection is MENINGOENCEPHALITIS due to - crossing BBB in macrophages - high affinity to CNS - conversion of catecholamines to melanin by laccase

Answer 172

meningitis/meningoencephalitis = most common form of infection pneumo often asymp or mild C. gatti more likely to cause pneumo invasive disease more commonly affects SKIN or BONE skin lesions often LACK INFLAM

Answer 173

dx - CNS infection should be suspected in --> immunocomp, fever, HA, and other CNS signs/symps --> immunocompetent w/ subacute or chronic meningoencephalitis - imaging for CNS and pneumo - CSF and other specimens = neg staining, PCR, Ag detection, and culture - imaging xray and MRI (SOAP BUBBLE lesions in brain) tx - most pulm infections resolve w/o tx in immunocompetent - observation only for pxs with small, stable or improving pulm lesions and no disseminated infection - mild/mod = FLUCONAZOLE (6-12 months) - severe --> induction therapy (2 wks) = amphotericin B + flucytosine --> consolidation therapy (up to 1 year) = fluconazole, lifelong tx in AIDS pxs

Answer 174

coccidioidomycosis is only in the AMERICAS (SW US) blastomycosis and histoplasmosis are not restricted to the Americas but can be found along Ohio and Mississippi river

Answer 175

dimorphic fungus - mold (environment) - spherules/endospores (tissue) causes VALLEY FEVER life cycle occurs in deserts, esp rainy seasons which allows mold to form in soil, dry up with arthroconidia, wind blows and spreads soil which can cause inhalation into lungs found in alkaline soils of semiarid, hot deserts arthroconidia are spread by wind and infect humans by inhalation person to person rare S and central America, SW US living in endemic areas is risk factor cultured arthroconidia are HIGHLY INFECTIOUS

Answer 176

- arthroconidia bypass ciliary clearance and other mechanical entrapment mechs of resp tract due to their SMALL SIZE - arthroconidia have ANTI-PHAGOCYTIC properties enabling some to survive and turn into spherules - spherules are RESISTANT to phagocytosis due to large size and ECM - endospores are released surrounded by matrix that may play role in their survival - proteases and spherule outer wall may be linked to virulence - infection results in lifelong immunity - CMI critical in limiting progression of disease - AIDS pxs and pxs with impaired cell immunity are at high risk for progressive disease humoral immunity not useful

Answer 177

- primary infections are asymp or manifest as VALLEY FEVER valley fever = fever, malaise, chest pain, dry cough, and arthralgia - small numbers of pxs progress to invasive pulm disease - rare extra pulm disseminated infections may affect bone, joints, or meninges

Answer 178

- spherules clearly visible in wet mounts and stained sections - easy to isolate org in culture, but strict precautions to prevent spread of arthroconidia - ANTIBODY TITERS useful indicator of disease progression - those who develop pos skin test remain pos for life tx no tx for primary and pxs who shwo no risk for progression ITRACONAZOLE for severe for progressive infections

Answer 179

dimorphic fungus - mold (environment, 25 degrees C) - yeast (tissue and 37 degrees C) yeast forms reproduce by budding (blastoconidia) mold forms produce MICRO and MACROCONIDIA found in moist soil and in association with BAT and BIRD DROPPINGS growth of mold form is enhanced by humid weather inhalation of microconidia is believed to be most common route of infection no person to person endemic areas are present in all continents OHIO and MISSISSIPPI rivers

Answer 180

- infection acquired by inhalation of microconidia - conidia are transformed into yeast form in host - invading yeast cells are phagocytosed by PMN cells and macrophages - org survives inside phagocytes and is disseminated to LN, spleen, and bone marrow - withstand oxidative burst, modulate phagolysosome pH, and inhibit phagosome-lysosome fusion = key survival mechs - infections produce granulomatous lesions and leaves behind a calcified nodule, viable orgs can establish latent infection - infection results in long-lived immunity and pos skin test - CMI main protection

Answer 181

- most infections are asymp or show fever and cough for a few days - severe = fever, malaise, chest pain, extensive pulm infiltrates, mediastinal lymphadenopathy know to resolve - progressive pulm disease resembles tb - dissemination may occur, mainly in immunocomp which involves reticuloendo system or CNS - orgs can be detected in macrophages in biopsies, bone marrow, and peripheral blood

Answer 182

dx smallest yeast - direct demonstration of yeast forms - culture demonstrating MACROCONIDIA - molecular probes tx - primary infections localized to lung resolve w/o tx - itraconazole for mild lung infections - amphotericin B, followed by itraconazole for severe and disseminated infections

Answer 183

dimorphic fungus - mold (environment, 25) - yeast (tissue, 35) yeast forms produce blastoconidia with broad base, double wall that are mostly extracell and larger than histoplasma mold form produces MICROCONIDA, no macro on histo there is narrow connection btwn daughter and mother yeast cells US distribution overlaps with histoplasma NOT ASSOCIATED w/ bird or bad droppings inhalation of microconidia patho - infection stims inflam response in lung, w/ neutrophil infiltration or granuloma formation - yeast forms remain extracell, unlike histoplasma

Answer 184

- productive cough, chest pain, fever are seen in pulm infections - disseminated infections most commonly affect SKIN - osteomyelitis and urogenital infections common

Answer 185

dx - direct exam demonstrating yeast forms - culture demonstrate thermal dimorphism - molecular probes, important to confirm culture tx - primary infections localized to lung resolve w/o tx - itraconazole for mild lung infections - amphotericin B, followed by itraconazole for severe and disseminated infections

Answer 186

dimorphic fungus - mold (environment) - yeast (tissue) - SHIP CAPTAIN'S WHEEL causes paracoccidioidomycosis (S. american blastomycosis) restricted to Mx and central and S. america associated w/ soil typical px is male farmer, 30-60 y/o

Answer 187

- infection transmitted by inhalation of conidia - asymp disease is common, esp in women - symp disease may be --> chronic (90%) w/ lymphadenopathy and skin lesions in lung, upper resp mucous mem, and/or skin (granulomatous ulcers with MULBERRY BASE) --> acute/subacute (10%) w/ lymphadenopathy, hepatosplenomegaly, and/or bone marrow dysfxn

Answer 188

clinical dx - probable infection based on presentation and hx - confirmed by lab findings lab dx - culture on blood agar at 37c - id of yeast cells in exudates and tissues --> thick walled cells (round/pyriform or elongated) w/ multiple buds, each w/ narrow base (SHIP CAPTAIN'S WHEEL) - DNA sequencing tx itraconazole (localized) and amphotericin B (disseminated)

Answer 189

adult worms live in small intestine of DOGS, wolves, etc. (definitive hosts) human, sheep, cattle become infected when they ingest eggs (intermediate hosts) HYDATID cyst develops in organs of intermediate host pastoral more common than sylvatic using dogs by shepherds, poor hand hygiene, and feeding raw viscera to dogs propagate pastoral cycle moose, caribou, and wolves maintain sylvatic cycle in Alaska and Canada

Answer 190

- hydatid cysts cause mechanical damage to surrounding tissues, which may take few to many years - ruptured cysts may cause fever, utricarial, anaphylactic shock, dissemination of infection

Answer 191

- imaging - microscopic eexam of cyst fluid or sputum may show hydatid sand, protoscolices, hooks - serological testing is more useful in HEPATIC than pulm cysts tx percutaneous ultrasonically guided drainage and infusion of hypertonic saline (PAIR) surgical exicision prolonged course of ALBENDAZOLE (antiparasitic to prevent recurrence) after surgery or PAIR

Answer 192

found in artic and subartic regions adults words found in foxes, dogs, etc intermediate hosts are wild rodents, and sometimes humans life cycle similar to E. granulosus E. multilocularis cysts bud EXTERNALLY, causing progressive damage to surround tissues

Answer 193

trematode widely distributed in E asia LUNG FLUKE adults are found in capsules in LUNG of definitive hosts (humans) parasites may spread to other organs, including brain lung infection characterized by EOSINOPHILIC inflam rxn and capsules containing one or more parasites caused by ingestion of seafood, esp freshwater seafood ruptured cysts may cause chest pain and pleural effusion chronic bronchitis may develop due to secondary bacterial infection dx - demonstration of eggs in sputum or stool - imaging studies tx = praziquantel

Answer 194

infectious = metacercariae dx = unembryonated eggs

micro exam 3 Flashcards

(219 cards)