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Flashcards in Microbiology: Gram Positive Cocci Deck (23):

GP Cocci (GPC)

-Appear as dark purple clusters (strep as chains)


Lab tests to differentiate GPC

-Catalase test: separates staph from strep and entero (only staph is catalase positive)
-Coagulase test: separates staph aureus from other staph (only staph aureus clots plasma)
-Hemolysis on blood agar: distinguishes various types of bacteria
-Alpha: partial hemolysis leaving green area (S penumoniae, Viridans)
-Beta: complete hemolysis leaving clear area (S pyogenes)
-Gamma: no hemolysis
-Lancefield grouping: group-specific cell wall Ags (groups A, B, D. Refers to polymorphic immunogen on well wall. Primarily beta/alpha hemolytic strep)
-Enterococci differ from strep in ability to grow in presence of high salt, bile, and hydrolyze esculin


Characteristics of Staphylococcus

-Non-motile, non-spore forming
-Facultative anaerobes, grow on non-selective media
-Have polysaccharide capsule can also made of fibrin (due to coagulase)
-Techoic acid binds to fibronectin to facilitate adhesion
-Peptidoglycan has endotoxin effects (not an actual endotoxin)


Characteristics of Streptococcus

-Facultative anaerobes
-Grow on 5% sheep blood or nutrient broths
-Secrete toxins


Characteristics of Enterococcus

-Group D lancefield Ag
-Hemolysis patter variable


3 most common disease causing GPC

-Staph Aureus
-Strep Pyogenes
-Enterococci (E faecalis, and E faecium)


Staph Aureus

-Found in nose, epithelial and mucosal surfaces
-Spreads to sterile sites via trauma, person contact, fomites
-Grows on 5% sheep blood agar, selective media is mannitol salt agar
-Changes the color of sheep blood from red to gold via hemolysis (Au=gold)


Virulence factors of Staph Aures

-Protein A: binds Fc component of Ig (prevents opsonization)
-Coagulase: builds insoluble fibrin capsule around bacteria (prevents immune cell access)
-Hemolysins (cytotoxins): directly toxic to hematopoietic cells
-Leukocidin: toxin specific to PMNs
-Catalase: prevents toxic action of PMN-derived hydrogen peroxide
-Penicillinase (B-lactamase): destroys B-lactam ring of penicillins and renders them inactive
-Capsule and techoic acid


Penetration of Staph Aureus

-Hyaluronidase: hydrolyzes hyaluronic acid in CT
-Fibrinolysin: dissolves fibrin clots
-Lipases: allows survival and spread in fat-containing areas


Secreted toxins of staph aureus

-Exfoliative toxins: causes scalded skin syndrome
-Toxic Shock Syndrome Toxins (TSST): super antigen that cross-links MHCII on APCs causing non-specific T cell response
-Cytotoxins (alpha, beta, delta, gamma): panton valentine leukocidin (PVL, gamma toxin) found in methicillin resistant staph aureus (MRSA). Causes lysis of leukocytes via pore formation, tissue necrosis (acquired virulence factor)


Medical syndromes of staph aureus

-Skin and soft tissue (impetigo, cellulitis, abscess, wounds)
-Bone and joint infections (osteomyelitis, septic arthritis)
-Pneumonia (infection of lung, empyema)
-Bacteremia and endocarditis (infection of blood, infection of heart valves, respectively)
-Food poisoning (enterotoxin B)
-Scalded skin syndrome (exfoliative toxin): blisters and peeling of skin
-TSS: localized growth of staph aureus w/ release of TSST into blood (fever, hypotension, rash, multi-organ failure)


Therapy to staph aureus

-Have resistance to penicillin due to B-lactamase
-Alteration of PBP (to PBP2) causes MRSA (methicillin resistance), coded by mecA gene
-B-lactamase resistant penicillins (anti-staph penicillins) are not effective against MRSA, but are against some staph aureus
-Can use 1st generation cephalosporins
-Vancomycin very effective (especially against MRSA)


Coagulase-negative staph

-Most common is S Epidermidis
-Colonizes surface of skin, mucous membranes
-Can spread during implantation of devices, form person contact
-Contains capsule
-Often resistant to B-lactamase penicillins, cephalosporins
-Sensitive to novobiocin
-Not very virulent, infect patients w/ indwelling medical devices and immunocompromised
-S Saprophyticus is 2nd most common cause of UTI (resistant to novobiocin, used bactrim or ciprofloxacin)


Streptococcus Pyogenes

-Group A strep
-Infects skin and upper respiratory tract
-Not normal flora but may be carried on mucous
-Spread by person contact w/ mucous or respiratory droplets
-Beta hemolysis on blood agar, lancefield A group
-Different from other beta hemolytic strep by: bacitracin sensitive, and positive PYR test (has nz that forms red product)
-Tx is penicillin


Virulence factors and toxins of strep pyogenes

-Lipotechoic acid, F proteins both bind to epithelial cells
-M proteins (used in epidemiological studies): antiphagocytic protein w/ over 100 serotypes
-Secretes many toxins: pyogenic (pus-forming) exotoxins, streptolysin S and O, streptokinase, hyaluronidase


Medical syndromes of strep pyogenes

-Skin, soft tissue infections: erysipelas (superficial), cellulitis (deeper), necrotizing fasciitis (deep subcutaneous necrosis w/ high mortality), wounds
-Streptococcal pharyngitis (strep throat): pain, swelling, fever, white exudate on tonsils. Can be complicated by rheumatic fever, post-streptococcal glomerulonephritis, scarlet fever
-Pneumonia, bacteremia
-Puerperal fever (post-partum endomyometritis)


Toxin complications of strep pyogenes

-Scarlet fever: pyogenes must be lysogenized by bacteriophage (stimulates to produce pyrogenic exotoxin or erythrogenic toxin). Both toxins are superantigens
-Is a complication of strep pharyngitis, onset of rash, fever, strawberry tongue. Tx w/ penicillin
-Streptococcal TSS


Non-suppurative (no pus) sequelae

-Acute rheumatic fever (ARF) follows strep throat: cross-rxn of Abs to strep (M1 and M3) w/ Ags in heart
-Causes acute inflammation of joints, heart, subcutaneous tissue, CNS, chronic damage of heart valved
-Acute Glomerulonephritis (AGN) follows strep throat or skin infection: acute inflammation of glomeruli due to Ab-Ag (M12, M49) complexes in basement membrane of glomerulus
-Results in hematuria, proteinuria, hypertension, edema
-Tx for both is penicillin


Streptococcus agalactiae (group B)

-Normal in female genital tract and lower GI, can colonize upper resp tract
-Mother to infant in utero transmission (10-30% of pregnant women asymptomatic)
-Looks same as group A strep under microscope and blood agar (both beta hemolysis), use CAMP test (extracellular protein acts synergistically w/ beta-lysin of S aureus to enhance hemolysis, found in GBS but not GAS)
-Causes UTI in pregnant women; neonatal septicemia, meningitis, penumonia; infections in immunocompromised
-PCR screening of pregnant women, with vaginal culture
-Tx is penicillin


Viridan streptococci

-Alpha hemolytic (thus green)
-All resistant to antibio opticin
-Normal in GI, female genital, transmission is getting access to sterile sites
-Causes localized infections (abscesses) and systematic infections (endocarditis)


Streptococcus Pneumoniae

-Nontypable, usually alpha hemolytic diplococci
-Identified by quellung rxn: adding anti-capsular Abs to cause swelling of capsule (also: optician sensitive; other viridans are resistant, and bile solubility test; bile lyses colonies)
-Colonizes nasopharynx, transmitted via respiratory secretions
-Virulence factors: capsule (what vaccines are directed against), pneumolysin (cholesterol dependent chymolysin (damages both alveolar epithelial and pulmonary endothelial cells, up regulate IL6)
-Diseases: penumonia, otitis media (ear), sinusitis, meningitis, bacteremia
-Tx: cephalosporin and vancomycin (resistant to penicillin)
-Prevention: adult vaccine w/ 23 capsular types, child one w/ 13



-Most common are E faecalis, E faecium (group D strep)
-E faecium more likely to be drug resistant
-Both normal flora of human GI tract and female genital tract
-Transmission: access to normally sterile sites, person contact, fomites
-Most diseases in immunocompromised, healthy people can develop UTI
-Possible for endocarditis, peritonitis (infection of lining of abdomen due to bowel perforation), bacteremia
-Tx: inherently resistant to many antibios. Can use ampicillin + gentamicin (aminoglycoside), or vancomycin (effective against any GP)


4 key bacteria w/ capsules

-S pneumo
-H influenzae
-N meningitidis
-Pseudomonas Aeruginosa
-Klebsiella pneumoniae
-All encapsulated bacteria have resistance to phagocytosis
-Removing spleen (asplenia) increases risk of infection to encapsulated bacteria