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lecture 5 greenberg

carbuncle lateral and deep extension of S. aureus; several coalesced furuncles with several openings to the surface with discharging pus
abscess central area of necrosis, infection with dead host cells and bacteria surrounded by reactive fibrosis
empyema infection of thoracic cavity external to lung
erysipelas infection of superficial skin with marked involvement of lymphatic vessels
exfoliatin EC product of S. aureus responsible for intradermal splitting and necrosis seen with scalded skin syndrome (SSS)
furuncle small abscess or boil; painful, indurated, erythematous and caused by S. aureus
impetigo infection of the superficial layers of skin - epidermis and outer dermis
leucocidin exotoxin of S. aureus that destroys PMN leukocytes (specifically Panton-Valentine leukocidin)
puerperal sepsis bacteremia in mother following childbirth
shock syndrome characterized by hypotension from systemic vasodilation
likely function of coagulase in S. aureus makes it an invasive organism; allows it to wall off infection and stop blood supply thus inhibiting leukocyte entry into wound
function of protein A in S. aureus bings IgG's Fc portion, allows bacteria to evade immune cells labeling it for phagocytosis
Name another Staphylococcus besides aureus that's resistant to methicillin up to 98% of S. epidermidis and other coag neg spp.
Staphylococcus saprophyticus the only coag neg Staphylococcus that is resistant to novobiocin disc on agar plates; causes 20-30% of symptomatic UTIs in young, sexually active females
L-pyrrolidonyl arylamidase (PYR) diagnostic enzyme for Group A beta hemolytic strep (S. pyogenes)
important diagnostic tool to distinguish beta hemolytic strep bacteria apart bacitracin resistance
M protein major virulence factor within Streptococcus pyogenes; is antiphagocytic and allows them to bind to epithelial cells & keratinocytes; ~ 100 diff serotypes identified by M protein DNA sequencing
hyaluronate capsule typical of group A beta hemolytic strep, barrier to complement components and binds CD44 on host tissues
methods of virulence for GABHS M protein, EC matrix binding protein, hyaluronic acid capsule, Ig-binding protein, C5a peptidase, streptolysins, DNAases acting on lysed cells in pus, streptokinase, superantigens
streptokinase GABHS - degrades clots by activating host plasminogens and allowing spread in tissues
name of GABHS proteases that degrade host and bacterial tissues SpeA, -B and -C proteases
2 important immune-mediated conditions caused by GABHS infection acute post-streptococcal glomerulonephritis acute rheumatic fever
tonsillopharyngitis/strep throat - mainly caused by this bacterial group GABHS (sometimes groups C or G)
differences btwn TSS by S. aureus and GABHS S. aureus - inapparent site of infection, lacks bacteremia and low fatality rate
description/mechanism of acute rheumatic fever occurs 7-21 days post-strep infection of the PHARYNX; thought to be a cross-rxn to antibodies initially produced against Strep, affects heart and other tissues
signs of acute rheumatic fever heart inflammation producing arrhythmias, polyarthritis, fever, skin abnormalities, choreiform movements
description/mechanism of acute poststreptococcal glomerulonephritis occurs 7-21 days post-strep infection of either skin or pharynx; immune complexes to Strep antigens are deposited in glomerular subepithelium
signs of acute poststreptococcal glomerulonephritis from simple proteinuria or microscopic hematuria to complete renal failure then death
mechanism of puerperal sepsis GABHS (or GBBHMS) travel up vagina, invades endometrium and uterine lymphatics to cause bacteremia
the major virulence factor associated with GBBHS type III capsule, allowing evasion of phagocytosis
abx of preference for treating GBBHS PCN or ampicillin
environmental niche of GBBHS vagina - causes many OB and neonatal infections
most prevalent causative agent of CAP Streptococcus pneumoniae
niche of Strep pneumo upper resp tract/oropharynx
2 main spots Strep pneumoniae has specific adhesion factors for NAG and 3-Gal disaccharides on epithelial cells; PAF in the plasma
phase variation - definition and example of bacteria that exhibits it ability to up or downregulate adhesion factors in the cell wall according to the site of attachment or infection; pneumococci
3 abx of choice for pneumococcal infection PCN G, vanc and Rocephin
features on would look for when Gram-staining sputum for pneumococcal infection GP, lancet or football-shaped diplococci, optochin-sensitive, alpha hemolytic
drug of choice to treat VRE ampicillin
special features typical for growing Enterococcus grow in presence of bile and 6.5% NaCl
niche of viridans Streptococci like species mutans, sanguis and salivarius mouth, on surface of teeth and gums
name diseases from toxins of Clostridia: difficile, tetani, botulinum, perfringens C-diff diarrhea (nosocomial usually) tetanus - spastic neurological dz perfringens - gas gangrene, necrotizing skin infections botulism - paralyzing neurological dz
name diseases from toxins of Bacillus genus: cereus and anthracis anthrax - non-hemolytic type food-borne diarrhea, is hemolytic
2 most medically important non spore-forming GP rods Corynebacterium and Listeria (both are non-filamentous also)
the most likely people to be affected by anthrax spores abbatoir or slaughterhouse workers who are exposed to the hides or meat of animals who were previously infected
3 clinical syndromes that could result from anthrax spore intoxication cutaneous - from open wounds, trauma GI - from eating contaminated meat inhalational - from inhaling aerosolized spores
3 virulence factors of Bacillus anthracis edema toxin, lethal toxin and protective antigen
B. anthracis virulence factors are A-B toxins protective antigen - B edema and lethal factor - A (EF = calmodulin-dependent adenylate cyclase = anti-inflammatory cytokines; LF = MAPK kinase that stops cell growth)
best abx to treat B. anthracis doxycycline and cipro (if naturally occuring, PCN hopefully)
pneumococcus vaccines 13-valent polysaccharide version for children 23-valent " " " adults
2 types of illneses produced from B. cereus intoxication emetic and diarrheal illness
Contrast the 2 syndromes from B. cereus intoxication emetic - from heat-stable endotoxin, improperly heated fried rice, sx within 1-6 hours diarrheal - heat-labile endotoxin, from ingesting spores in cream sauce, vegetative cells germinate in gut, sx in 12-24 hrs
Clostridium species/type associated with gas gangrene perfringens type A (a in both gas and gangrene)
Clostridium species/type associated with necrotizing enterocolitis perfringens type C (C in colitis)
How does C. perfringens gain access to soft tissues and skin? usually through trauma/dirty wounds where clostridia were in soil or feces and contacted wound
T/F Inflammatory cells are usually intermixed with C. perfringens when looking at gas gangrene tissue histologically. no, they release toxins to lyse WBCs = no inflammatory cells
method of contracting C. perfringens gastroenteritis/specific pathogenic substance ingesting meat that was stored at high temps allows spores to germinate and release heat-labile enterotoxin once in the body
mechanism of action of C. difficile toxins toxins A/B - combo of enterotoxin that causes massive fluid secretion and cytotoxin that causes death and sloughing of intestinal epithelium
possible deadly outcome of C. difficile diarrhea toxic megacolon
abx of choice to kill any remaining C. tetani bacteria at site of infection in tetanus pt metronidazole (NOT!! PCN)
functions of the two chain toxin of C. tetani heavy - specific binding to GABA-containing inhibitory nerves light - endopeptidase that cleaves synaptobrevin = no vesicle release
neurotoxin that causes tetanus tetanospasmin
mechanism of C. botulinum toxin has light chain endopeptidase that prevents ACh release from NMJ = flaccid paralysis
most typical circumstance in which person comes into contact with C. botulinum home canned products, eating food that wasn't cooked well enough and heat-labile toxin persists
why no raw honey to infants? infant botulism from possible clostridial spores in honey
tx for tetanus equine antitoxin
how C. diphtheriae become virulent by acquiring the diphtheria toxin from a lysogenic phage
niche of C. diphtheriae resp tract and skin
mechanism of A-B toxin of diphtheroids B binds cell surface, A ADP-ribosylates EF-2 (elongation-factor 2) effectively stopping eukaryotic protein synthesis
vaccines available? tetanus, botulism, diphtheria, C. difficile infection tetanus - yes botulism - no diphtheria - yes C. diff - no
cause of death from diphtheria toxin-induced cell death of throat epithelium, formation of pseudomembranes, obstruction of throat and resp failure from inability to get air or diaphragm paralysis
primary route of infection of Listeria fecal-contaminated foods like milk or queso fresco, even when properly refrigerated
abx of choice for Listeria ampicillin, possibly also Bactrim for some isolates
Listeria's preferred method for growing in host intracellularly, induces phagocytosis then escapes into cytoplasm to replicate
tests to differentiate btwn Listeria and Streptococci Listeria - catalase +, beta-hemolytic Streptococci - catalase -, all types of hemolysis
erysipelothrix caused by Erysipelothrix rhusiopathiae - erysipelas-like rash on hands of fisherman/abattoirs
causes severe acne Propionibacterium acnes
diseases caused by Listeria monocytogenes meningitis or bacteremia in immunocompromised and neonates, most typically though self-limited diarrheal illness
psychrophilic able to live in refrigerator temps
Created by: sirprakes



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