staphylococci

Question 1

describe staphylococcus

Answer 1

aerobic, gram positive cocci in pairs/groups. Catalase positive. All will show up as Sheep blood agar positive, MacConkey Agar neg, and catalase positive

Question 2

1. Describe how Staphylococci are distinguished from other gram positive cocci like streptococci.

Answer 2

staph are catalase positive micococci. Strep are catalase negative.

Question 3

Staph and coagulase

Answer 3

Staph aureus is coagulase positive and is hemolytic (appear golden). Most of the other staph species are coagulase negative and non-hemolytic (appear white)

Question 4

What is coagulase

Answer 4

A cell wall protein that binds to fibrinogen and converts it to fibrin cuasing clumping and protection from phagocytosis.

Question 5

What is protein A

Answer 5

Protein produced by Staph aureus that binds to Fc receptor of IgG and activates complement. This prevents antibody mediated phagocytosis.

Question 6

S. aureus capsule

Answer 6

virulence factor that inhibits phagocytosis and enhances attachment.

Question 7

S aureus lipotechoic acid

Answer 7

Virulence factor that binds to epithelial cells.

Question 8

S aureus hemolysins

Answer 8

Virulence factor that can cause RBC lysis (beta hemolysis) and tissue damage

Question 9

S aureus Panton-Valentine Leucocidin

Answer 9

Virulence factor that causes WBC lysis, protects from phagocytosis, invasive skin dz

Question 10

S aureus Exfoliatin A and B

Answer 10

virulence factors- toxins which bind to GM4 glycolipids (infants) and cause separation at granular-cell layer (desmosomes)

Question 11

S. aureus enterotoxins

Answer 11

Virulence factors- heat and acid stable. Preformed toxin in contaminated food causes vomiting and diarrhea (mediated by cytokine release). Enterotoxins B and C are associated with TSS due to focal infection

Question 12

Mechanism of toxic shock

Answer 12

toxic-shock syndrome toxin activates monocytes which and T cells, which produce IL-1, IL-2, gamm IFN and TNF resulting in shock

Question 13

Features which increase toxin production by S. Aureus

Answer 13

low pH, high protein, high pO2, High pCO2

Question 14

Staph normal flora locations

Answer 14

S. Aureus- mainly in nose, skin, throat and vagina. Coag-negative staph- mainly in skin, throat and some nose

Question 15

common mechanisms of antibiotic resistance

Answer 15

altered metabolism (ie. trimethoprim or sulfamethoxazole resistance), altered cell wall permeability, antibiotic altering enzymes, altered target

Question 16

Staph recombination

Answer 16

Transduction by bacteriophage is main mechanism

Question 17

What is MRSA

Answer 17

MRSA carries the MecA gene which codes for altered penicillin binding protein PB2A. This decreases Beta-lactam binding and provides the primary mechanism for methicillin resistance

Question 18

What is VISA and VRSA

Answer 18

Vancomycin inhibits D-alanine cross polymerization in peptidoglycan layer. VISA: Vanco intermediate Staph Aureus has MIC of 4-8ug/ml and increased numbers of peptidoglycan layers. VRSA: vanco resistant staph aureus has MIC of >16ug/ml and has the van A gene from enterococcus

Question 19

MSSA antimicrobial susceptibility

Answer 19

Resistant to penicillin, but sensitive to methicillin, cephalosporins, vanco, aminoglycosides, rifampin, etc.

Question 20

MRSA antimicrobial susceptibility

Answer 20

Resistant to penicillin, methicillin and cephalosporins. Sensitive to all others

Question 21

VISA/ VRSA antimicrobial susceptibilty

Answer 21

resistant to penicillins, methicillins, cephalosporins, vancomycin

Question 22

Coagulase-negative staph antimicrobial susceptibility

Answer 22

resistant to penicillin. Sensitivie to methicillin, cephalosporins, vanco (+++), rifampin (+++)

Question 23

Staph high vs low inoculum

Answer 23

With high inoculum, infection occurs. With low inoculum infection only occurs if capsule is present

Question 24

List infections caused by staph aureus

Answer 24

Furuncles (boils), cellulitis, lymphadenitis, osteomyelitis, uncommon cause of otitis, sinusitis and pneumonia (cystic fibrosis), septicemia, endocarditis

Question 25

Major host defense against staph aureus

Answer 25

phagocytosis- impeded by protein A, Panton-valentine leukocidin, and clumping factor and coagulase

Question 26

Chronic granulomatous disease

Answer 26

sex linked recessive neutrophil defect results in impaired hydrogen peroxide mediated intracellular killing. Increased susceptibility to staph infections

Question 27

Jobs syndrome

Answer 27

Increased IgE, poor neutrophil chemotaxis, cold staph abscess

Question 28

Scalded skin syndrome

Answer 28

Staph aureus infection of skin in infants with production of systemic toxin results in peeling that looks like it has been scalded

Question 29

Bullous impetigo

Answer 29

Staph aureus infection of skin in young infants with production of local toxins

Question 30

Staph scarlet fever

Answer 30

Staph aureus infection in older children. Does not cause the strawberry tongue

Question 31

Staph toxic shock syndrome Sx and cause

Answer 31

Acute fever, erythroderma desquamation, hypotension, multi-organ involvement of at least 3 of following: mucus membranes, renal, hepatic, GI, hematologic, CNS, muscular. Caused by infection with TSST-1 producing S. aureus.

Question 32

risk factors for staph toxic shock syndrome

Answer 32

exposure to TSST-1 S aureus strain, growth under conditions promoting toxin production, no pre-existing antibody to toxins, genetically predisposed

Question 33

Staph aureus virulence factors and the resulting diseases: Coagulase/ clumping factor/Protein A, exfoliatin, TSST-1 and enterotoxins

Answer 33

Coagulase/ clumping factor/Protein A: disseminatd infection or deep localized infection. Exfoliatin: scalded skin syndrome or scarlet fever. TSST-1: Toxic shock syndrome or scarlet fever. Enterotoxins: food poisoning or TSS

Question 34

compare Sx and treatment of mild vs severe strep and staph skin infections

Answer 34

Mild: Sx include impetigo, abscess, early cellulitis, mild scarlet fever. Treated with cephalexin PO and drain. Severe: Sx include necrotizing fasciitis, deep cellulitis/abscess, TSS. Treated with Nafcillin/cephalexin, vancomycin and clindamycin

Question 35

List coagulase negative staph sepcies

Answer 35

s. epidermidis (foreign bodies), S. saphrophyticus (UTIs), s. haemolyticus (vancomycin resistant), and s. lugdunensis (pyoderma and foreign bodies)