micro exam 2 Flashcards

Question

what are the virulence factors?

Answer 1

adherence (candida using mannoprotein-fibronectin) invasion - breaks in skin (sporothrix) - tiny spores (coccidioides immitis in W Mx and S America) - transformation into more invasive form (candida albicans) - proteases assist in dissemination injury - immunopath in most fungal infections - direct tissue damage in immunocomp - exotoxins are not produced IN VIVO mycotoxicoses (intoxication by ingesting fungus)

Answer 2

- claviceps purpurea (cereal grains) produces ALKALOIDS (toxic) that can cause vascular and neuro symps in ERGOTISM --> ergot alkaloids can be used to treat migraines due to vasoconstriction or neural bvs, its a serotonin analog that affects cholinergic n and bvs - aspergillus flavus (nuts and corn) produces ALFATOXINS that are associated with hepatocell carcinoma --> large doses can cause acute liver failure = jaundice, vomiting, RUQ pain, increased ALT/AST and bilirubin - amanita mushrooms produce potent hepatotoxins (amanitin and phalloidin) --> amatoxins interfere with TRANSCRIPTION (inhibit RNA pol 2) leading to fulminant hepatic failure (later renal), responsible for MOST of toxicity --> phallotoxins binds to ACTIN FILAMENTS and prevent DEPOLYMERIZATION and CYTOTOXICITY, cause early GI symps (ab pain, vomiting, severe and cholera like diarrhea)

Answer 3

neutrophils and Th1 cell responses

Answer 4

nikkomycin = inhibits chitin synthase (cell wall) amphotericin B (big gun) and nystatin (used topically = disrupts cell membrane (these are for serious infection and want to treat ASAP, last option, use amphotericin for a bit then downgrade to nystatin) azoles and terbinafine = inhibits cell membrane (ergosterol) echinocandins = inhibit cell wall synthesis (glucans) flucytosine = inhibits DNA synthesis

Answer 5

efflux pumps --> azoles (basically in resistant bacteria, azoles will be released extracellular via pumps) altered metabolism or transport mutations --> mutations in permease or other enzymes lead to FLUCYTOSINE resistance target altering mutations --> altered glucan synthase causes resistance to ECHINOCANDINS hydrolytic enzymes analogous to beta lactamses are generally not made by fungi

Answer 6

severe renal toxicity

Answer 7

topical tx like azole compounds or terbinafine (inhibit cell membrane synthesis)

Answer 8

makes arthroconidia which are inhaled and cause resp infection common in SW US and S America

Answer 9

Need to give something systemic, maybe not amphtericin B right away unless patient is very sick. Use systemic azoles or echinocandins

Answer 10

This patient can deteriorate very quickly, so use systemic amphotericin B; get pt started on it for maybe 2 weeks and then downgrade to azole

Answer 11

COVID, LRI, and TB

Answer 12

LRI, malaria, preterm birth comps, COVID, diarrheal diseases, TB, and HIV/AIDS

Answer 13

bacteria - carbapenem resistant enterbacteriaceae - drug resistant N gonorrhoeae - vancomycin resistant enterococcus - multi drug resistant pseudo aeruginosa - multi drug resistant acinetobacter viruses - HSV, HIV, HPV parasites - cysticercosis (tapeworm from undercooked pork and eggs in human feces) - rat lungworm (angiostrongylus)

Answer 14

transplacental = rubella during birth = strep agalactiae (group B strep) transmammary = CMV

Answer 15

direct contact = shigella airborne = influenza fecal oral = shigella sexual = HIV fomites = shigella vector = malaria animal bites = rabies skin injuries and mucous membranes = HIV

Answer 16

live, attenuated (best results) = contain live, but weakened microbes or microbial toxins that cannot produce disease (sabin polio vaccine) inactivated = contain killed microbes (salk polio vaccine) subunit vaccine = contain specific Ags that best stimulate immune system recombo subunit vaccines = obtained using recombo DNA technology (Hep B virus) toxoid = contain inactivated toxins that induce immune system to produce toxin-neutralizing Abs (tetanus) conjugate = made of carb moiety linked to a strongly immunogenic protein (H influenza type B) nucleic acid (DNA and RNA) = introduce genes that code for essential microbial Ags and employ host cells to make, secrete, and display these Ags recombo vector = use attenuated virus or bacterium to deliver the DNA of target microbe to human body

Answer 17

urinalysis --> pyuria, hematuria, and casts (pus and WBCs) culture - organisms and antibiotic sensitivity - urine is NORMALLY STERILE - most infections are caused by ONE organism - common etiologic agents differ between comp and uncomp infections ***nosocomial UTIs and UTIs in men are often complicated, order blood culture along with urine if you suspect upper UTI (pyelonephritis)

Answer 18

<10k CFU/mL = contaminant >3 org = contaminant 10k-<100k CFU/mL = depends on other factors >/= 100k CFU/mL = clinically SIGNIFICANT with symps ***send clean catch, midstream urine for culture and refrigerate once sample collected

Answer 19

on blood agar --> GP, GN, and yeast on MAC --> GNR, lactose and non lactose fermenters escherichia/citrobacter = butter like appearance klebsiella/enterobacter = mucoid, shiny appearance

Answer 20

oral cavity and upper resp tract

Answer 21

do a gram stain has to be no more than 10 squamous epi cells (low power field) --> indicates saliva in oral cavity presence of neutrophils is consistent with LRT sample

Answer 22

for nosocomial infections, particularly ventilator-associated pneumonia for community acquired pneumo is questionable

Answer 23

S. pneumo, H. influenza (doesn't grown on blood, fastidious and requires chocolate agar), and M. catarrhalis *** you do not get a count for sputum but you get semi-quantitative data (not easy to determine vol), some pathogens can be contaminants too

Answer 24

blood agar = GP cocci and GNR --> hemolysis pattern in strep is important chocolate agar = H. influenza MAC = GNR, differentiates lactose (pink) vs nonlactose fermenters aerobic ONLY

Answer 25

candida H. parainfluenza coagulase neg staph enterococci GPR other than nocardia and B. anthracis strep other than S. pneumo, S. pyogenes, S. agalactiae, and S. anginosus

Answer 26

pyelonephritis

Answer 27

primary infection = occur in absence of another predisposing infection or condition secondary infection = complicate predisposing infections or conditions (ex: influenza --> damage of the resp epi --> aspiration of staph auerus --> pneumo) conditions that result from an infection at a distant site

Answer 28

vesicles = VZV, smallpox, HSV 1 and 2, coxsackievirus A, molluscum contagiosum virus erysipelas = strep pyogenes bullae = staph aureus, strep pyogenes, clostridium perfringens, vibrio vulnificus cellulitis = strep pyogenes, staph aureus, pseudo aeruginosa, pasteurella multocida necrotizing fascitis = strep pyogenes, clostridium perfringens, vibrio vulnificus myositis = clostridium perfringens, staph aureus, trichinella spiralis, coxsackievirus B, dengue fever virus osteomyelitis = staph aureus, salmonella typhi, pasteurella multocida septic arthritis = N gonorrhoeae, staph aureus, H influenza

Answer 29

acute = vesicular chronic = red, scaly, or lichenified pruritus is present in both

Answer 30

staph saccharolyticus (strict anaerobe)

Answer 31

S. aureus (coag pos) --> skin and soft tissue, blood stream, pneumonia, osteomyelitis, TSS and SSSS, food poisoning S. lugdunensis (CoNs) --> tendency to be false pos, prosthetic and native valve endocarditis, skin and soft tissue, blood stream, osteomyelitis S. epi (CoNs) --> prosthetic and native valve endocarditis, blood stream, impants, IV catheters S. saprophyticus (CoNs) --> UTIs

Answer 32

medium size, white, creamy, or light gold BUTTERY looking complete hemolysis

Answer 33

fibronectin-binding proteins for initial attachment clumping factors --> binds to fibrinogen and converts to fibrin, similar to coagulation but instead brings bugs together so they can grow into abscesses, aid in walling off and protecting against phagocytes (bc of clumps, immune cells may not be able to engulf whole clump or penetrate into it = systemic antibiotic won't be able to reach) cytolytic toxins (cytotoxins or hemolysins) - ALPHA TOXIN most IMPORTANT --> PORE FORMING TOXIN, not produces by CoNs staph PVL (panton-valentine leukocidin) enterotoxins (food poisoning) --> heat stable, 18 types, causes diarrhea and vomiting, superags capable of activating aggressive T cell response TSST-1 --> cytotoxic to ENDO cells, absorbed SYSTEMICALLY thru vaginal mucosa/other, superag capable of activating aggressive T cell response exfoliatins (SSS) --> EPIDERMOLYTIC TOXIN that separates strata granulosum and corneum (desmogleins), causes superficial layer of epi to slough off sparing deeper layers protein A --> cell wall component, capable of binding and neutralizing IgG, blocks phagocytosis enzymes --> coagulase, protease, hyaluronidase (hydrolysis of hyaluronic acid in CT) lipase --> produced by coag pos and CoNS, degrades lipids secreted by sebaceous glands, facilitates spread into tissues

Answer 34

attachment biofilm increases resistance to antimicrobials and host defenses toxins are presumed absent or clinical significant has not been determined mission of staph = get into cell, penetrate tissues and form localized infections by COAGULATION other staph = formation of BIOFILM

Answer 35

fam = micrococceeae cat pos, resemble staph in gram stain some micrococci produce BRIGHT PIGMENTS (colonies will have color) micrococci are ox pos and bacitracin sensitive unlike staph which which is ox neg and bacitracin resistant ex: micrococcus luteus (yellow colonies) and micrococcus roseus) (pink colonies)

Answer 36

bacillota like staph aerotolerant anaerobes (dont require O2 but not affected if present) require enriched media A = strep pyogenes B = strep agalactiae C = strep dysgalactiae D = strep bovis (viridans) enterococcus spp. (D Ag) anginosus, mutans, mitis, salivarius groups (viridans) - skin colonization with GAS is transient - infection occurs at sites of insect bites or scratches (impetigo) - transmission by direct contact and fomites (impetigo, wound, and puerperal infections) - M PROTEINS of skin isolates differ from resp isolates (determines serovar --> when they infect a person, they develop immunity which is protective against that specific serovar but not other serovars, enables px to be infected many times with strep pyogenes) - skin and soft tissue infections are more common in SUMMER MONTHS (scratching or insect bites common in children) resp GAS epidemiology is diff (pharyngitis and scarlet fever more common in WINTER AND SPRING)

Answer 37

PYR POS (red on test) BACITRACIN SENSITIVE indicators of recent infection - ASOT (often false neg with skin infections) - anti-DNase test - anti-hyaluronidase for definitive id - biochem tests - molecular testing - MALDI-TOF mass spec

Answer 38

M protein = 80-100 diff serotypes (immune evasion), interferes with phagocytosis (immune evasion), adhesion to host cells by binding to FIBRONECTIN F protein and lipoteichoic acid = adhesion to host cells by binding to FIBRONECTIN hyaluronic acid capsule = interferes with opsonization and phagocytosis (immune evasion), masks surface ag (immune evasion) streptolysins O and S --> lyse RBCS, WBCS, and other cells, STREPTOLYSIN O is PORE FORMING TOXIN hyaluronidase --> helps spread of macromolecules and infection Spes --> T cell superag, Spe A,B,C,F, scarlet fever (***SpeB has ability to digest tissues and ECM)

Answer 39

impetigo = superficial, involves epi folliculitis = involves epi and dermis erysipelas = involves epi and dermis cellulitis = involves almost all layers (epi, dermis, subcutaneous fat) necrotizing fasciitis = involves all the layers above plus fascia and muscle

Answer 40

folliculitis = inflam of hair follicle that is restricted to epi (no intervention or symps) furuncle = painful, suppurative inflam of hair follicle that may extend into dermis or subcutaneous tissue carbuncle = multiple large, coalescing furuncles, may cause fever (no intervention) cutaneous abscesses = collection of pus within DERMIS and deeper skin tissues, painful, tender, fluctuant, and erythematous nodule (requires surgical intervention)

Answer 41

extensive, RECURRENT, folliculitis barbae, and non resolving should be treated with ANTIMICROBIALS, topical or systemic depending on case abscesses should be incised and drained, empiric antimicrobial tx and warm compresses are additional alternatives

Answer 42

exfoliative toxins

Answer 43

presence of violaceous color and bullae GN, motile, ox pos, SALT and BRACKISH WATER, GULF OF MX

Answer 44

petichiae --> purpura --> ecchymoses

Answer 45

endocarditis = blood (4) SSS = mainly nasopharynx (4), but some skin and blood (10 pneumonia = sputum (3), some blood (2) food poisoning = food (3), some feces (1) catheter infections = blood and catheter tip (4) TSS = vagina/wound (4), some blood (1) cutaneous infections (impetigo, folliculitis, furuncle, carbuncle) = skin (4), some blood (2) septic arthritis = synovial fluid (4), blood (3)

Answer 46

pos slide test shows clumping (dependent on clumping factor) --> can have false pos, esp with S. lugdunensis pos tube test shows clotting

Answer 47

cutaneous diphtheria skin and resp gram pos, coryneform (club shaped due to volutin granule which is phosphate storage that is useful for bugs), NON-SPORE FORMING, NON-MOTILE, catalase pos RODS both C. diphtheriae and C. ulcerans have been implicated in cutaneous infecitons other species include members of normal microbiota of phaynx, nasopharynx, distal urethra, and skin CHINESE LETTER APPEARANCE exotoxin is main virulence factors (resp infections) systemic dissemination of toxin is rare in cutaneous infections (no cardio or neuro symps) --> skin is infection is mainly localized so it develops slower and allows immune system to mount a response while in resp infections bacteria doesn't disseminate into bloodstream but the toxin does both toxigenic and non-toxigenic strains can cause disease skin lesions range from pustules to non-healing ulcers --> this develops DIRTY GREY PSEUDOMEMBRANE transmission by contact with exudates from skin lesions outbreaks among HOMELESS, IV DRUG ABUSERS, LACK OF VAX HX autoinfection not likely to cause pharyngeal infection due to robust humoral response associated with skin infections (vax targets toxin not bug) --> resp infection is characterized by rapid progress isolation in lab requires special media and longer incubation (notify lab if suspect corynebacterium) tx = erythromycin (penicillin) or antitoxin for systemic spread (passive immunization bc it is a premade Agm active toxoid)

Answer 48

cutaneous anthrax resp, GI, and cutanenous gram pos, SPORE FORMING, non-motile, NON-HEMOLYTIC, cat pos RODS *** most other bacillus spp. are motile and beta hemolytic (also resistant to penicillin) common disease in LIVE STOCK if vax not used animals are infected by ingestion of food contaminated with B. anthracis spores (when animal decomposes, before this pH will change in environment and surroudning so bugs will sense changes and form spores, decompose into soil and continue to spread) humans contract disease via occupational exposure to animals (WOOL SORTER'S DISEASE) or as a result of acts of bioterrorism AB toxin POLY D glutamic acid capsule provides resistance to phagocytosis cytotoxic exotoxin made of 3 proteins - protective ag (PA) is required for ATTACHMENT to host cells (vaccines contain Ab specific to PA) - edema factor (EF) is an adenylate cyclase - lethal factor (LF) is a protease (important signaling proteins) cutaneous anthrax is most common form of infection papule forms at site of inoculation, which spreads into RING OF VESICLES, then NECROSIS in central part of lesion leads to ULCER (eschar) formation with raised periphery that appears granulomatous eschar is PAINLESS, does NOT contain pus, and resolves in 1-2 wks infection may spread systemically causing fever, malaise, and HA may spread along lymph vessels causing lymphangitis BOX CAR SHAPED MORPHOLOGY or BAMBOO STICK if spores present and don't stain (large encapsulated, GP rods) dx should be confirmed by isolation of detection of microorg from clinical samples --> samples from cutaneous lesions should be submitted for culture and PCR large, grey colonies with IRREG EDGES (MEDUSA-HEAD and BEATEN WHITE EGGS APPEARANCE) tx = cutaneous anthrax not altered by antimicrobial tx but does prevent dissemination, current recs are CIPROFLOXACIN and DOXYCYCLINE

Answer 49

aeromonas spp edwardsiella tarda erysipelothrix rhusiopathiae vibrio vulnificus mycobacterium marinum common agents involved in infections of wounds inflected in AQUATIC environments or by aquatic creatures wounds may result from trauma associated with inanimate objects, fish spines, bites of aquatic animals, medicinal leeches, etc

Answer 50

most extraintestinal infections by VIBRIO vulnificus and AEROMONAS spp occur in MEN

Answer 51

underlying hepatic disease may predispose to life-threatening course infections present in various forms like cellulitis, abscess, wound infections, necrotizing fasciitis, or other

Answer 52

ox pos, GLUCOSE FERMENTING, GNR occur in aquatic habitats, esp during warmer and summer months (more people for swimming) A HYDROPHILIA is most common aeromonad isolated from wound infections

Answer 53

opportunistic non-lactose fermenting member of hafniaceae presentation varies and ranges from cellulitis to fulminant wound infection and bacteremia E tarda is related to enterobactericeae

Answer 54

erysipeloid non motile, non sporulating, pleomorphic org (GNR) that tends to form FILAMENTS colonizes many animals (mammals, birds, and fish), particularly SWINE and TURKEY, and can also be found in soil and contaminated ground water zoonotic disease with risk groups including butchers, meat and fish handlers, farmers, hunters and vets infects humans through cuts and scratches lesions are sharply defined, elevated, and PURPLISH-RED ZONES that spread as CENTRAL AREA FADES (want to take cultures from the edges) may be associated with low-grade fever, lymphangitis, lymphadenitis, and/or arthralgia can spread causing diffuse skin infection, septicemia, and endocarditis microscopic = may resemble corynebacterium or show gram-variable rxn (red and purple cells), shows ALPHA HEMOLYSIS culture = tissue biopsies or lesion aspirates in nutrient broth and subcultured on blood agar, culture takes about 48 hrs tx = PENICILLIN

Answer 55

GN, ox pos, non-spore forming, motile rods (curved) --> all vibrio are motile bc they have polar flagellum mostly restricted to injuries associated with SALT OR BRACKISH WATER exposure wound infection may progress to necrotizing fasciitis (can spread to bloodstream, secondary to septicemia or primary septicemia commonly due to oysters) and/or multiple organ system failure HEMORRHAGIC BULLAE grows on common culture media tx = DOXYCYCYLINE

Answer 56

strictly AEROBIC, rod shaped (slightly pleomorphic), non motile, non-spore-forming, ACID FAST BACTERIA (will be red, if not acid fast then it will be blue) CELL WALL IS SIMILAR TO GRAM POS BACTERIA cell wall contains MYCOLIC ACIDS (makes bacteria acid fast, in this bacteria acids are long chains unlike corynebac where it's short and nocardia where it's intermediate) and LAM (important for forming proteting Abs) --> these are hydrophobic components that interfere with gram staining most grow slowly on lab media while some do not grow in vitro (M leprae do not grow on anything) nonpath (non-tuberous) strains are widely distributed in environment (water, plants, soil) diseases causes by this bacteria have SLOW ONSET and CHRONIC NATURE path mycobact have HIGH INFECTIVITY and LOW VIRULENCE in hosts with norm immune systems (exposure is huge but ppl who show symps are small frac)

Answer 57

HANSEN DISEASE neuro manifestation but mainly skin and PNS ARMADILLOS and some PRIMATES may also be infected inhaled via resp droplets or from armadillos, goes to lung where there's robust response from alveolar macrophages, so doesn't cause pulm symps from lungs, seeds in blood and goes systemically hematogenous spread to skin causes disease, will affect n bc of low temp w/ severe n damage, ppl can lose touch sensation and can impair movement, leading to injuries tuberculoid leprosy (paucibacillary --> skin lesions DO NOT have bugs) - characterized by skin lesions and n involvement - CMI eradicates the disease in most pxs lepromatous leprosy (multibacillary, MORE SEVERE bc loss of sensation leading to injuries w/o knowing) - characterized by skin lesion and mucous membrane plaques and nodules, and progressive n damage - slowly progressive, malig disease that results in deformities and can be life-threatening - effective CMI does NOT DEVELOP (anergic) skin test is helpful in determining if px has response to exposure or not tx = combo therapy with RIFAMPIN

Answer 58

Th1 and CD4+ cells

Answer 59

can be fungus like bc of branching or actinomycetes chronic granulomatous infection of skin and subcutaneous tissue first described in Madurai so it's called MADURA FOOT infection acquired by traumatic inoculation by thorns or splinters contaminated with soil (like in barefoot farmers) mycotic mycetomas (eumycetomas) caused by FUNGI --> Madurella spp and Pseudallescheria boydii actinomycotic mycetomas (actinomycetomas) caused by ACTINMYCETES --> Nocardia brasiliensis (MOST COMMON), other Nocardia species, Actinomadura, and Streptomyces main lesion is formed by granulomatous inflam response in DEEP DERMIS and SUBCUTANEOUS TISSUE and may spread to bone lesion contains GRANULES formed by aggregates of etiologic agent and may form drainage sinuses (extend to skin and release exudates) PAINLESS lesions (allows it to grow slowly over the years) unless there is secondary bacterial infection or bone involvement

Answer 60

edematous skin lesion at initial presentation subcutaneous nodule develops in several years massive swelling, sinus tracts, and granules develop over severeal more years may result in disfigurement and disability, mortality is rare

Answer 61

tx is combination of antimicrobial therapy and surgery as needed eumycetomas require surgery while actinomycetomas respond to antibiotic tx alone TRIMETHOPRIM-SULFAMETHOXAZOLE in combo with AMIKACIN or STREPTOMYCIN

Answer 62

gram variable (with GP CELL WALL, filamentous), branched (TREE LIKE), BEADED (due to some portions stain red and others purple), partially acid fast (intermediate) commonly found in soil and plants multiple species in disease most common are N. ASTEROIDES and N. BRASILIENSIS lab dx - gram stained smears from exudates and SULFUR GRANULES (yellow) --> these granules are more commonly associated with actinomycetomas - colonies may resemble fungi and take 3-7 days to grow

Answer 63

catalase and superoxide dismutasae help resist oxidative killing by phagocytes survival in macrophages by preventing phagosome-lysosome fusion and inhibiting phagosome acidification iron-chelating compound nocobactin (E. coli have aerobactin)

Answer 64

chronic granulomatous infection characterized by formation of ABSCESSES and DRAINING SINUSES that discharge SULFUR GRANULES most commonly caused by ACTINOMYCES ISRAELII cervicofacial actinomycosis is common form due to presence of causative org in ORAL CAVITY part of normal flora through alimentary tract clinical dx is based on presentation, history of slowly progressing lesion, imaging, and lab results defining specific etiology may be complicated with paucity of microorgs in lesion and presence of other co-infecting agents (mostly GNRs)

Answer 65

aerobic, GN, NON-FERMENTING RODS, oxidase and catalase pos ubiquitous in the environment, particularly WATER UNCOMMON transient intestinal and oropharyngeal flora causes wound and burn site infections, ecthyma, gangrenosum, hot tub rash (folliculitis), nail infection, perichondritis, other infections are aggressive and hard to treat caused by opportunistic infections in the eye (CONTACT LENSES), wounds, urinary tract, and burns sometimes colonizes resp tract of pxs with CF by formation of a biofilm pigment production = PYOCYANIN when mixed with yellow tissue or media that normally produces green discoloration multiple pseudomonads produce PYOVERDIN but only P. aeruginosa produces PYOCYANIN ox and catalase pos and GLUCOSE OXIDIZER usually beta hemolytic, spreading colonies with FRUITY ODOR tx = piperacillin, ceftazidime, cefepime, fluoroquinolones (ciprofloxacin), carbapenems, aztreonam, gentamicin, tobramycin, polymyxin B and colistin

Answer 66

- pili and slime layer mediate attachment - endotoxin (GN, lipid A, causes fever) - exotoxin A inactivates EF-2 by ADP-ribosylation, blocking protein synthesis elastase degrades elastin (ecthyma gangrenosum) --> helpful for tissue invasion phospholipase C --> for tissue destruction and spreading resistance to multiple antimicrobial agents

Answer 67

GNR or coccobaccili with fastidious growth requirements found in many animal reservoirs and are transmitted to humans through direct animal contact or ARTHROPOD BITES (sandflies, lice, fleas) initial isolation on enriched blood agar in CO2 atmosphere takes 2-6 wks 3 common species - B. HENSELAE = cat scratch disease, transmitted by fleas - B. QUINTANA = trench fever, transmitted by body lice - B. BACILLIFORMIS = oroya fever and verruga peruana, transmitted by sandflies

Answer 68

Mycetomas: - Occur in the extremities, often the feet - Caused by traumatic innoculation of the bug (usually Nocardia) from the environment - Aerobic actinomycete (Nocardia) Actinomycosis: - Occurs usually in the face (lumpy jaw) - Caused by anaerobic actinomycetes that are present in the normal oral flora (A. israelii), that create burrowing abcesses into the tissue after minor trauma

Answer 69

- putrid drainage (DX) - polymicrobial infections (strict anaerobe and facultative anaerobe) - involving endogenous flora (like actinomyces) - abscess formation tx is empiric based on gram stain results and anatomical site involved (large GP bacteria = clostridia, GNR = bacteroides) culture and sensitivity is often not practical bc of multiple orgs, time consuming, labor intensive, often fails, and inadequate standardization most infections are treated with metronidazole (breaks DNA, common for anaerobes), carbapenem, beta-lactam-beta lactamase inhibitor (piperacillin + tazobactam aka zosyn)

Answer 70

large, RECTANGULAR, GP, ANAEROBIC RODS normal flora of colon primary specimen see absence/paucity of neutrophils spores rarely seen, pus cells are ABSENT in gram-stained smears all produce alpha toxin which is a LETHICINASE (SPHINGOMYELINASE) --> damages phospholipid bilayer of PM --> affect endo, blocking blood supply in small caps neutrophils recruited and attach to inner surfaces of bvs (L shift) growth is accompanied by production of HYDROGEN and CARBON DIOXIDE (gas gangrene and crepitus - crackling sound when) infection by traumatic inoculation of microorgs that might be present in environment or intestinal flora ex: px in a car accident has foreign object punctured into rectum, then symps of gas gangrene and crepitus dx is clinical, readily isolated in culture using routine methods tx = surgical excision of all devitalized tissues penicillin (for clostridia) in combo with CEPHALOSPORINS (for contaminants) antimicrobial therapy sufficient for cellulitits

Answer 71

produces multiple EXOTOXINS - alpha toxin (phosholipase C, sphingomyelinase, lecithinase) - alpha toxin disrupts cell membranes or erythrocytes, leukocytes, and myocytes via lecithinase and sphingomyelin hydrolysis - alpha toxin triggers platelet aggregation, cap occlusion, ischemia, and necrosis leading to tissue damage - alpha toxin absorbed systemically and can trigger shock - PERFRINGOLYSIN O*** (pore forming toxin) may also play role by compromising cap endo (edema) and attacking immune cells can cause spherocytosis due to the effects of RBC cell mem

Answer 72

anaerobic, GNR MOST COMMON ANAEROBIC PATHOGEN, isolated from soft tissues and blood part of ENDOGENOUS INTESTINAL FLORA patho - polysac capsule protects against phagocytosis and promotes adhesion and abscess formation - relative O2 tolerance --> advantage over other anaerobes bc they can cause infection in soft tissues that have O2

Answer 73

icosahedral, enveloped, linear dsDNA genome obligate intracell pathogen, goes into nucleus and use pol II TEGUMENT is unique (located btwn envelope and virion, contains transcription factors) latency, life long infections, recurrence characteristic use viral proteins for DNA synthesis, can infect proliferating and quiescent cells epidemiology - up to 90% of gen pop have HSV 1 Abs - HSV 1 seropositivity is higher in low socioeconomic groups - up to 30% of sexually active adults in W societies are HSV 2 seropositive (HSV 2 is less than 1) - HSV 2 is more common in WOMEN than men, in BLACK than whites - many infected subjects are unaware of infection, continue to shed virus, act as a reservoir - HSV 1 transmission thru SALIVA and VESICULAR SECRETIONS (papule--> vesicle --> pustule) - HSV 2 transmission thru DIRECT SEXUAL CONTACT of skin or mucous mem with secretions or mucosal surfaces of a person with ACTIVE INFECTION

Answer 74

alpha - rapid rep, latency in NEURONAL CELLS - HSV 1 (HHV 1) - HSV 2 (HHV 2) - VZV (HHV 3) beta - slow rep - CMV (HHV 5) gamma - rapid rep, infection in LYMPHOCYTES - EBV (HHV 4) - KSHV (HHV 8)

Answer 75

alpha herpesviruses primary infection targets EPI CELLS (rep at site of inoculation, cause prim infection after release of virions, follow n. endings and axons to DRG), latency in NEURONAL CELLS (DRG) then move back to epi upon reactivation --> virions travel in axons to estalish latency in sensory ganglia (trigem in facial and lumbar and sacral in genital) reactivation triggered by SUNLIGHT, FEVER, and STRESS HSV 1 infections = above waist (oral) HSV 2 infections = below waist (genital) viral rep - virions bind to surface receps - tegument and nucleocapsids are liberated into cytoplasm - genome and tegument transcription factors are released into nucleus after nucleocapsid docks onto a nuclear pore - immediate early gene expression produces proteins that regular early gene expression - early genes inclue viral DNA POL and THYMIDINE KINASE (DRUG TARGETS***) - DNA rep and late gene expression are followed by assembly in, and budding from, nucleus (takes part of host nuclear mem) - transcription is limited to LATENCY ASSOCIATED TRANSCRIPTS (LATS, reg RNA molecules), during latent infection tx controls symps but DOES NOT CURE infection, reduces shedding and transmission C section recommended for infected mothers circumcision reduces risk tx = ACYCLOVIR --> nucleoside analogue (deoxy-GTP) that requires viral THYMIDINE KINASE (monophosphate) and host enzymes to be converted into triphosphate form (active form) --> causes CHAIN TERMINATION once incorporated into replicating viral genomes VALACYCLOVIR has better bioavailability, but identical to acyclovir

Answer 76

- vesicles or blisters are filled with serous fluid containing infectious viruses - base of lesion contains multinucleated giant cells - incomplete immunity develops after infection, BOTH humoral and cell mediated immunity - some cross protection btwn HSV 1 and 2 but its incomplete

Answer 77

primary = blisters and infection inside oral cavity reactivation = perioral blisters

Answer 78

isolation in cell culture from vesicle fluids collected with syringe or swab (from lesions) CPE = intracell granulations, enlargement, intracell inclusions DFA, EIA, PCR, TZANCK SMEAR*** HSV 2 --> looked for MULTINUCLEATED GIANT CELLS IN TZANCK SMEAR, take specimen from base of lesion, tx with acyclovir

Answer 79

HHV 8, gamma herpesvirus may see angioproliferation found in 100% of kaposi sarcoma tumors id shortly after HIV was discovered in MSM with AIDS*** 100% association with primary effusion lymphoma (B CELL LYMPHOPROLIFERATIVE DISORDER or pleural, peritoneal, or pericardial spaces) 50% association with multicentric Castleman disease (B CELL LYMPHOPROLIFERATIVE DISORDER of lymph nodes) in AIDS pxs epidemiology 5% of US blood donors are seropositive - least common among HHV seroprevalence amoung US MSM is 25% (abt same among MSM-AIDS pxs had KS in pre-ART era aka antiretroviral therapy) seroprevalence in CENTRAL AFRICA*** is 50% transmitted by sexual contact among MSM or by saliva (ASHKENAZI JEWISH AND MEDITERRANEAN)

Answer 80

- infects primarily B cells - also infects endo cells, monocytes, epi cells, and sensory n cells - ENDO SPINDLE CELLS in KS tumors harbor virus - produces growth stim (IL-6 homologue) and antiapoptotic proteins (IL-6 and Bcl-2 homologues) - SUPPRESSES p53 and pRB***

Answer 81

manifestation - most common and aggressive form is AIDS related - affects skin, oral mucosa, lymph nodes, and visceral organs - lesions are macular, papular, nodular, or plaques; red, pink, brown, or violaceous - severity ranges from minimal cutaneous lesions to extensive involvement of visceral organs dx is based on clinical exams and histpath studies lab studies on CD4 counts and HIV viral load should be performed when applicable tx - lytic infection with FOSCARNET (pyrophos analogue) or GANCICLOVIR (nucleoside analogue) - no tx for latent infection - no vaccine - ART is useful in AIDS pxs

Answer 82

classic KS = indolent tumor or LEs, most common in OLDER MEN of MEDITERRANEAN or ASHKENAZI JEWISH descent endemic KS = more aggressive, LEs and ORAL CAVITY, mostly in CENTRAL AFRICA iatrogenic KS = transplant pxs, REVERSIBLE upon removal of immunosuppression epidemic (AIDS related) = MOST AGGRESSIVE, affects mouth, torso, or face, regresses on ART, can be lethal in absence of ART

Answer 83

alpha herpes primary infection leads to CHICKENPOX (varicella) reactivation leads to herpes zoster (SHINGLES) life long infection 90% acquire infection by adulthood in temperate regions 50% acquire infection by age 70 in tropical regions transmission - inhalation of aerosolized exudates from skin lesions or RESP DROPLETS - the MOST CONTAGIOUS HHV - communicability greatest 1-2 days before rash and continues 3-4 days after dx - clinical dx of rash - Tzanck smear findings not distinguishable from HSV infection - immunofluorescence or PCR may be used to distinguish VZV from HSV tx - expresses THYMIDINE KINASE and is response to ACYCLOVIR and similar drugs - antiviral therapy indicated in - ALL pxs with varicella 18 or > - immunocomp pxs with varicella or shingles - immunocompetent adults with shingles prevention - passive immunization in immunocomp pxs at risk (works BEFORE onset of skin lesions) varicella = live attenuated (childhood vaccine) shingles = recombo or live attenuated (ppl >/= 50 y/o)

Answer 84

- rep occurs during PRIMARY INFECTION in resp epithelia, tonsils, and local lymph nodes after initial infection - PRIMARY VIREMIA and infection of RETICULOENDO CELLS follows - SECONDARY VIREMIA mediated by T CELLS spreads the infection to SKIN - latency is established in sensory ganglia (trigem n) and reactivation results in rash in corresponding dermatome (herpes zoster) <--> lytic cycle in keratinocytes and alveolar macrophages - cell mediated immunity controls spread of infection - Abs prevent reinfection (ABS DO NOT ENTER CELL) - shingles occurrence often corresponds with a decline in cell immunity after 50 years of age - reactivation is more severe and more frequent in immunocomp pxs

Answer 85

small pox lesions are denser on face, extremities, and sometimes palms varicella lesions are denser on head, chest, trunk, and extremities

Answer 86

1. Transcription of immediate early genes --> a-proteins 2. a-proteins stimulate transcription of early genes --> B-proteins 3. B-proteins function in DNA replication, and late genes are transcribed --> y-proteins 4. y-proteins participate in virion assembly *spikes are made by ribosomes on RER

Answer 87

icosahedral, circular dsDNA, NON-enveloped (better at living on surfaces than enveloped) expresses early genes (E1-8) required for rep and late (L1-2) structural genes virus infects the BASAL LAYER of STRATIFIED SQUAMOUS EPI most common STD in US infection causes genital warts and PREDISPOSES to CERVICAL CANCER (women) and other genital cancer) (vulvar, vaginal, penile, anal, and oropharyngeal) sexually transmitted - one exposure = 60% chance of infection HUMANS ARE THE ONLY RESERVOIR OF HPV oncogenic --> HPV 16 and 18 genital warts --> HPV 6 and 11 patho don't infect surface of skin but instead the SB due to penetration thru lesions/abrasions - infect epi SQUAMOUS-COLUMNAR JXNS (anus and cervix) - association with cancers has been demonstrated, but underlying mechs not clear tx = medical (cytotoxic or immune modulatory) or surgical - cryotherapy with liquid nitrogen, electrocautery, laser surgery - aims to clear warts - no permanent cure/complete clearance of viral infection - recurrence is common

Answer 88

- entry and uncoating followed by delivery of viral DNA to nucleus - viral early genes transcribed by HOST RNA pol - early genes (E6,7) encode proteins that abrogate cell cycle suppression naturally provided by host tumor suppressors (p53, pRB) causing abnorm prolif --> genome integration = E6/7 overexpressed = cancer --> extrachromosomal genome = E6/7 not overexpressed = benign growth (genital warts) - genes that reg viral transcription and rep are expressed - viral DNA is rep using HOST DNA pol at different levels of epidermis - late genes (L1,2) encoding structural proteins are expressed as cells differentiate into keratinocytes (do not divide above basale) - viral assembly occurs in NUCLEUS and virions are released by cell lysis (not in malig transformation) - latent infection is established by viral DNA (integrated or extrachromosomal) that remains in the basal layer

Answer 89

achieved on PEs KOLIOCYTOSIS (perinuclear vacuolation and nuclear enlargement) may be detected in PAP SMEARS or BIOPSIES viral Ags can be detected in cervical swabs or tissue biopsies using immunoassays also molecular methods (PCR) NOT POSSIBLE TO GROW HPV IN CELL CULTURE pap smear findings = multinucleate cells and cells with PERINUCLEAR HALOS colposcopy should be performed to follow up on abnorm pap smear findings

Answer 90

condensed nucleus (looks like RAISIN) and large perinuclear cytoplasmic vacuole

Answer 91

gardasil 9 is a 9-valent (HPV 6, 11, 16, 18...) for males and females 9-26 y/o --> give to infected person to prevent infection by another genotype + serovar reduces risk of acquiring infection DOES NOT TREAT EXISTING INFECTIONS

Answer 92

LARGEST viruses enveloped linear dsDNA DNA dependent RNA pol in virion genome rep occurs in CYTOPLASM use viral DNA.RNA pol, it's coded for by genes on genome of virus not host on microscopy, can see BRICK cells,*** some with lateral bodies (collection of protein) and core dumbbell viral rep - viral entry via fusion with PM - transcription of early genes is mediated by VIRAL transcriptase within core (3 waves = immediate early, early, late) - core uncoating followed by translation and expression of late genes and genome rep - virions are assembled into MATURE VIRIONS (MV) --> non-enveloped, interacts with target - MVs are released by cell lysis or budding as EXTRACELL ENVELOPED VIRIONS (comes from golgi, PM, endosome) 11111

Answer 93

smallpox virus (VARV) --> smallpox (variola major and minor) Mpox virus (MPXV) --> monkey pox vaccinia virus (VAVC) --> vaccine related infections molluscum contagiosum virus (MCV) --> molluscum contagiosum

Answer 94

caused by MPXV zoonotic disease transmitted to humans from RODENTS (main reservoir) Central and W Africa (Congo and Democratic of Congo) transmission from animals by direct contact with infected animals or bodily fluids, biting, scratching, consumption of infected meat, and fomites human to human transmission via resp droplets, close skin and sexual contact, fomites most cases in 2022 outbreak were in men and MSM patho - rep at stie of entry (resp tract, skin, mucous mem) - spread to draining lymph nodes - primary viremia and spread or organs - secondary viremia and spread to skin causing skin lesions (intense constitutional symps)

Answer 95

chickenpox = CROPS, umbilicated, in chest, shoulders, and face HSV = vesicles, oral and genital, reactivation --> perioral smallpox = papular, vesicular pustular lesions denser on FACE, extend to PALMS and SOLES, all at same stage, umbilicated molluscum contagiosum = single or several umbilicated papules, could be genital but usually not, more common in CHILDREN

Answer 96

superficial --> stratum corneum, hair, and nails subcutaneous --> dermis and subcutaneous tissue deep or systemic --> hematogenous disseminaton of microorgs

Answer 97

dermatophytes pityriasis (tinea) versicolor tinea nigra piedra

Answer 98

sources of infection = humans, animals, and soil (more from carpets like ppl walking barefoot, wrestling) infection is initiated when fungal elements in skin scales or hair make contact with new host's skin fungal growth in skin is aided by proteases course of infection shaped by - etiologic agent GROWTH RATE (faster growth will have an edge) - level of MOISTURE (athlete's foot aka tinea pedis) - nature of AFFECTED AREA - host IMMUNE RESPONSES (Th1, NK cells, innate immunity) - rate of DESQUAMATION (impede infection) innate and cell-mediated immunity control most infections dx lesion's appearance is HIGHLY SUGGESTIVE confirmation with direct microscopic exam is highly recommended dx aided by KOH exam to reveal SEPTATE HYPHAE in skin scrapings from the advancing margins and hair can be isolated in lab in a few days to wks ALL HAVE SEPTATE HYPHAE and MACROCONIDIA, some have microconidia (pear shaped) differentiation is based on morphology of macroconidia tx TOPICAL antifungal drugs used in superficial and non-extensive infections --> miconazole (not administered systemically due to toxicity), tolnaftate, or terbinafine (inhibits cell mem synthesis) Majocchi's granuloma, tinea capitis and barbae, and extensive or deep infections are treated with ORAL antifungal drugs --> itraconazole or terbinafine if fungi treated with topical but didn't work, then give in combo with any of the oral drugs some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?

Answer 99

superficial skin infections tinea corporis tinea manuum tinea cruis tinea pedis (athlete's foot) tinea faciei tinea barbae (bearded area) tinea capitis deep skin infections MAJOCCHI's GRANULOMA hair infections tinea capitis and barbae nail infections tinea unguinum - onychomycosis

Answer 100

has scales and small fissures strong ODOR (due to secondary bacterial infections) can get bacteremia

Answer 101

microconidia

Answer 102

TrichoSPORON cutaneum do NOT confuse with trichophytonsome types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?some types of tinea infections, you get hyperkeratinization --> provide space for fungus to grow away from bloodstream when you give something systemic, is it going to penetrate into hyperkeratinized area or once it's stopped, does it come back?

Answer 103

Piedraia hortae

Answer 104

SABOURAUD agar

Answer 105

intertriginous dermatitis = moist, erythematous, pruritic plaque with SATELLITE lesions w/o purulence that could be malodorous dermatophyte infections = will be annular, usually no pustules, fungus is found in the scrapings erythrasma = not raised, looks like wrinkled, striped skin, has a fine scale and no pustules

Answer 106

sporotrichosis chromoblastomycosis mycetoma (maduromycosis) phaeohyphomycosis rhinosporidiosis

Answer 107

introduced by traumatic inoculation typically limited to subcutaneous tissues, lymphatic vessels, and contiguous tissues sporotrichosis and rhinosporidiosis are each caused by ONE AGENT chromoblastomycosis, mycetoma, and phaeohyphomycosis are caused by MULTIPLE orgs

Answer 108

asteroid bodies and daisy petal arrangement splendore-hoeppli substance

Answer 109

delayed type hypersensitivity to fungal infection where the allergic reaction occurs in a different part of the body than the primary fungal infection site symp of rxn typically appear 1-2 weeks after the primary fungal infection and may include: Itchy, red rash Bumps or vesicles Pustules Erythema nodosum (raised, painful lumps) Eczema-like patches

Answer 110

chronic fungal infection of scalp caused by Trichophyton Schoenleinii yellow cup shaped crusts that group together like HONEYCOMB

micro exam 2 Flashcards

(138 cards)