Staphylococcus

usually < 5 yrs, extreme tenderness, Nikolsky’s sign (involved and uninvolved skin), usu. spares oral mucosa, recovery without scarring, differentiate from TEN

exfoliative toxins A and B, cultures negative, superficial split in granular layer

Toxic Shock Syndrome (TSS) [pic] [pic]

300 cases/yr / ½ from females/tampons / can also be caused by Group A strep

Micro: superantigen, IL-1,2 / TSST 1 similar to enterotoxin B and C (occurs in 20% of S. aureus)

Presentation: fever, vomiting, diarrhea, diffuse erythroderma with desquamation (7-10 d), non-purulent conjunctivitis, hyperemia of mucosal surfaces, myalgia

Rash: almost always seen within first 24 hrs, purpural lesions can even look like RMSF, meningococcemia, cleavage pattern of lesions differentiates from ?strep SS and other causes

Complications: abnormalities of 3 or more organ systems including rhabdomyolysis, encephalopathy, azotemia, elevated ALT/AST, thrombocytopenia

Ddx: TSS from Group A (rarely B) Strep, RMSF, meningococcemia, EM, others

Treatment: anti-staph B-lactams (nafcillin or possible vancomycin until negative nasal swab for MRSA is obtained) and clindamycin for “eagle effect” (large number of organisms reach a slowed growth curve and this lack of cell division necessitates use of anti-anabolic agent such as clindamycin

Supportive: IV fluids and management of sepsis / ?vancomycin for MRSA strains?

Surgical debridement/drainage of any obvious source

Pneumonia

recovery 3-6 wks / CXR resolution by 3-6 months

Food poisoning

preformed toxin, 2 hrs / Pappasito’s Mexican restaurant

Bacteremia

must treat 4-6 wks (with positive cultures) unless you have an obvious source that is quickly removed (see Harrison’s) – otherwise the infection may recur later as endocarditis et al.

Osteomyelitis (see other)

Endocarditis (see other)

Arthritis

MRSA (methicillin resistant Staph aureus)

Current thinking is that nasal carriage predicts MRSA infection / A nasal swab can help

determine whether a person is colonized with MRSA, and guide empiric abx coverage for

presumed or culture-negative S. aureus infection (i.e. if nasal swab is positive, you need to use vancomycin) / it follows that contact precautions may not be all that useful to prevent transmission

Treatment: vancomycin, linezolid, synercid, (sometimes, if sensitive, rifampin, bactrim) / quinolones and carbapenems not effective on MRSA

Note: you can usu. trust sensitivities (e.g. if it says bactrim sensitive, you can use bactrim)

S. epidermidis

catalase +

protective slime / adherent slime / line or device related

S. saprophyticus

catalase +

UTI in young women / more resistant

S. hemolyticus

more resistant

Streptococcus

GP diplococci

Strep pyogenes (Group A)

Micro: catalase negative, B-hemolysis, bacitracin (A disc) / M protein for attachment (anti-M is protective) / anti-phagocytic

Diseases: impetigo, cellulitis (erysipelas), pharyngitis, tonsillitis, purpural sepsis, TSS (exotoxin), necrotizing fasciitis/myositis, scalded skin, septic joint (via transient bacteremia, culture from blood and joint only ~66% sensitive), pyoderma, bacteremia

Reactive: scarlet fever (erythrogenic superAg), rheumatic fever (anti-ASO, streptolysin O), glomerulonephritis, reactive arthritis (not necessarily rheumatic fever)

Clinical: the lymphadenopathy of Staph and Strep infections usu. produces warn, red, tender nodes, but can be cold when the purulence is deep within the node

Treatment: Penicillins (and other)

S. agalactiae (Group B Strep)

CAMP +, B-hemolysis

mother to child via vaginal delivery / pneumonia, neonatal bacteremia, meningitis (esp. neonates), UTI

Treatment: ampicillin

Group C Strep

pharyngitis / bacteremia / endocarditis / (animals)

Treatment: same as Group A Strep

Enterococcus (Group D Strep)

Micro: g-hemolytic (non) / bile esculin / PYR positive / 6.5 NaCl (not other group D)

Diseases:

· Urinary

· Biliary

· Wound

· Bacteremia

· Endocarditis (for PCN allergic patients, some say linezolid not enough,)

Transmission: VRE is generally a nosocomial infection that is selected by prior antibiotic treatment (with vancomycin as well as other agents) and is not a community-acquired infection (people do get colonized by fecal matter contamination)

E. faecium

more commonly resistant to amp and vanc / also has endogenous anti-AG enzyme

E. faecalis

Treatment:

VRE à linezolid and synercid / chloramphenicol, doxycycline may have

some efficacy /evernimycin and daptomycin also in clinical trials?

Non VRE à ampicillin for simple infection / amp + gentamicin for severe infection

· Aminoglycoside resistance

both sp. / high level resistance to gentamicin predicts resistance to all others (except not necessarily streptomycin) / sometimes, Enterococci can have an enzyme that chews up all AG’s except gentamicin

· B-lactamase

only E. faecalis (and but one strain of E. faecium)

· Penicillin resistance

altered/over-production of PBP’s – both sp. / note: if resistant to one B-lactam via altered PBP’s, then it’s usually resistant to all of them