Gram-positive cocci (Staphylococci and Streptococci) 2/2

alpha

Viridans, Pneumococci, and Enterococci are this hemolytic status

anginosis, bovis, mitis, mutans, salivarius

5 subgroups of Viridans streptococci

normal oral or bowel flora

Viridans streptococci is normally here

dental caries

S. mutans causes —

abscesses

S. anginosis tend to form —

colon cancer

S. gallolyticus (aka bovis): bacteremia highly associated with —

endocarditis

Viridans streptococci are major agents of “subacute” infective —

fever, weight loss, new heart murmur, anemia, emboli (months)

Symptoms of infective endocarditis

•Organism introduced into blood stream by:

•tooth brushing, bowel movement

•Intravenous Drug Use (IDU)

•VS express adhesins; attachment to heart valves

•Risk factors: abnormal or damaged valves

•Congenital (bicuspid aortic valve)

•Rheumatic Fever

•Prior IE, prosthetic valves

Pathogenesis of subacute infective endocarditis

“vegetation” of host and bacterial products

Viridans streptococci: bacteria encased in —

low, slowly

Viridans streptococci have — density and grow —

Bacteremia is intermittent and low-grade

Why Viridans streptococci may need 4-6 blood cultures for diagnosis

penicillin sensitive: ceftriaxone; relatively penicillin resistant: vancomycin; or penicillin + aminoglycoside

Viridans streptococci treatment

In those with valvular heart disease, prophylactic antibiotic are given before dental extractions or urological or GI procedures

Prevention of Viridans streptococci

•Normal bowel / urogenital flora

•short chains / pairs; a or y hemolytic; bile acid tolerant

Enterococcus faecalis and E. faecium: what are they and how do they look

vancomycin

Has evolved alternative biosynthetic pathways for peptidoglycan amino acid side chains

30-50% of E. faecium are now — resistant

UTIs or abdominal abscesses

Enterococcus faecalis and E. faecium: local infections are usually —

Bacteremia can occur, hospital acquisition is usually catheter related

community acquisition often leads to endocarditis

Enterococcus faecalis and E. faecium: hospital vs community acquired manifestations

For penicillin or vancomycin susceptible:

•Not endocarditis: 1 drug (10-14 days)

  ampicillin, piperacillin, or vancomycin

•Endocarditis:  2 drugs needed for bactericidal activity (6 wk.);

  ampicillin, piperacillin, or vancomycin + gentamicin or ceftriaxone;   ID consult

Resistant: •lipopeptide (daptomycin), oxazolidinone (linezolid)

  Not endocarditis: 1 drug

  Endocarditis: 2 drugs; ID consult 

Enterococcus faecalis and E. faecium treatment (dependent on endocarditis)

coagulase positive

Staph aureus coagulase status

“grapes of staph,” B-hemolytic, catalase positive (bubbles form on plate when hydrogen peroxide is added)

Identification of Staphylococci

•S. aureus:

–coagulase-positive

–colonies are yellow, “aureus”

–highly pathogenic

•Coagulase-negative staphylococci (CONS):

–usually not speciated by clinical laboratories

–less pathogenic (opportunistic)

How coagulase status is associated with pathogenicity

fibrinogen to fibrin  

S. aureus is coagulase positive and therefore converts — to —

penicillinase

Staph was penicillin sensitive but acquired — in the 40s

•Penicillinase stable β-lactams (methicillin, 1950s):

–Methicillin Sensitive  S. aureus (MSSA)

– most effective drugs are nafcillin, cefazolin

•Methicillin-Resistant S. aureus (MRSA; 1970s)

–Altered penicillin binding protein (PBP2A) fails to bind methicillin and all β-lactams

MSSA vs MRSA

HA: debilitated patients with antibiotic pressure, wounds, implanted devices got it, often involves IV-line related bacteremia, urinary catheter-related infeection, ventilator associated penumonia, only susceptible to vancomycin

CA: normal hosts, commonly presents with furuncles and carbuncles and rarely with necrotizing pneumonia. Vancomycin, Tmp-Smx, doxycycline, clindamycin used.

Hospital vs community acquired MRSA: who got it, symptoms, and antibiotics used

•anterior nares or skin (axilla, perineum)

–infants (60%), adults (25-35%)

–wounds promote colonization

S. aureus commonly colonizes —

MSSA or CA-MRSA

Community acquired S. aureus infections are usually — or —

skin, soft tissue

Community acquired S. aureus infections usually occur in what body part?

endocarditis

Community acquired S. aureus infections can lead to bacteremia and associated —

suppurative (pus forming) or toxin mediated

Two groups of S. aureus diseases

endocarditis

Bacteremia in S. aureus infection is a marker of — unless proven otherwise

Suppurative: Folliculitis, furuncles, carbuncles, impetigo, burn infections, pneumonia

Toxin-mediated: •Food poisoning (common)

•Scalded skin syndrome (rare)

•Toxic Shock Syndrome (TSS; really rare)

examples of suppurative and toxin-mediated S. aureus infections

•binds to the Fc region of IgG_1,2,4

–inhibits C3b deposition and phagocytosis

S. aureus virulence factors: Protein A —

–Microbial surface components reacting with adherence matrix molecules (MSCRAMM): > 20 family members; bind fibrinogen, collagen, fibronectin, cytokeratins

-Teichoic acid: binds epithelial cells

S. aureus virulence factors: Adhesins —

provokes cytokine release

S. aureus virulence factors: lipoteichoic acid, peptidoglycan

antiphagocytic

S. aureus virulence factors: capsule

•hyaluronidase, fibrinolysin (staphylokinase), lipases, nucleases (spread through tissues)

S. aureus extracellular products: examples of enzymes

dermonecrotic

S. aureus extracellular products: a-hemolysin does this

It is a sphingomyelinase

S. aureus extracellular products: B-hemolysin does this

it is a leukocidin

S. aureus extracellular products: y-hemolysin does this

It is a leukocidin and hemolysin

S. aureus extracellular products: d-hemolysin does this

Panton-Valentine Toxin

Leukocidin associated with most CA-MRSA strains

suppurative (pus)

S. aureus: the primary cause of — skin infections

S. aureus

Most common cause of impetigo

S. aureus and S. pyogenes

Co-infections of — and — are present in 20% of impetigo cases

pustule within a hair follicle

example of suppurative skin infection: folliculitis

•pustule spreads into the subcutaneous tissues. They are hot, tender, and the patient may have a fever

What is a furuncle?

carbuncle

can be HUGE

If furuncles interconnect, they become a —

bacteremia

•CA-MRSA / MSSA; usually not associated with —

•local antiseptics (chlorhexidine) or first generation cephalosporin

Treatment of folliculitis and impetigo:

• incision, drainage + oral antibiotics

–CA-MRSA: Tmp-Sx, doxycycline, clindamycin

–MSSA: above agents or b-lactam

Treatment of furuncles/carbuncles:

pneumonia (often post-flu in extremes of age)

Besides skin infections, other S. aureus suppurative infections include

–Septic arthritis (large joints; rheumatoid arthritis, diabetes)

–Osteomyelitis (growth plates of long bones in children; vertebral bodies in adults)

–Pyomyositis (muscle)

–Endocarditis (heart valves)

•S. aureus translocates from the nose or skin into the bloodstream and seeds joints, bone, muscle, or heart, causing:

–incision and drainage (if abscess / infected fluid  present)

– 4-6 weeks of IV antibiotics

Treatment of disseminated S. aureus (like in septic arthritis, for example)

there is no device or obvious source of infection

S. aureus bacteria is classified as community acquired when —

IV drug users

Community acquired S. aureus is common in —

endocarditis

Community acquired S. aureus bacteremia usually represents —

•Positive blood cultures, vegetations  on transesophageal echocardiography (TEE)

Diagnosis of S. aureus bacteremia

4-6 weeks of IV abx

Treatment of S. aureus bacteremia

IV catheter (so device should be promptly removed)

Health care associated S. aureus bacteremia is usually associated with —

•prosthetic devices (valves, pacemakers)

•sustained bacteremia (+ blood cultures 72 h after antibiotics and catheter removal)

•slow response to treatment (fever > 72 h)

•renal failure

–Risk factors for endocarditis (TEE indicated):

•shorter courses of IV therapy or substituting oral antibiotics are inappropriate: relapse with endocarditis / osteomyelitis

Health care associated S. aureus: oral antibiotics, IV abx <2 weeks?

proteolysis, heating

Staph enterotoxins resist — and —

food poisoning

Toxin mediated Staph is most common cause of — in US

mast cells to release inflammatory mediators

Staph enterotoxins stimulate —

Staphylococcal scalded skin syndrome

Exfoliative toxins made by Staph, distributed systemically, cause —

–Mucosal or skin colonization; umbilicus in infants (outbreaks in nurseries)

–Disrupts desmosomes in the granular layer of the epidermis: intraepidermal separation

–Nikolsky sign (rub off the epidermis)

–Heals without scarring

–Distinguish from Toxic Epidermal Necrolysis (epidermis separates from dermis; drug induced)

Features of Staph scalded skin syndrome

variant of scalded skin syndrome that is localized due to some immunity to toxin; rupture yields crusted lesions

Bullous impetigo:

Toxic shock syndrome toxin-1

Menstrual TSS: associated with —

absorbed across mucosa; activates T cells; cytokine storm causes capillary leakage, hypovolemia, shock

•TSST-1, Staph enterotoxin B, SEC are superantigens and have these effects

•Fever, BP < 90

•Generalized rash followed by desquamation of skin and mucus membranes and hair and nail loss

•Multiple organ systems involved (shock)

•Treatment: incision and drainage if abscess present, vancomycin / nafcillin + circulatory support; 5% mortality

Features of toxic shock syndrome

skin, biofilms on devices

Coagulase-negative Staphylococci are ubiquitous inhabiters of the — and have a propensity to form —

vancomycin

Coagulase-negative Staph is typically only sensitive to —

UTI

Staphylococcus saprophyticus is coagulase-negative bacteria that is 2nd most common cause of — in young women

bacteremia (and associated endocarditis)

S. aureus and CONS species: uropathogens only in the setting of a Foley catheter or foreign body; otherwise bacteruria likely reflects —