Micro: Cross Flashcards
Tx of septic arthritis
- gram pos. cocci
- GNR
- neg. gram stain
- vancomycin
- cephalosporin or zosyn (piperacillin-tazobactam)
- vancomycin plus cephalosporin
most common organism for septic arthritis
S. aureus
next: streptococcus (GAS, GCS, GGS; GBS in neonates, DM, malignancies; GBS can be polyarticular; S. pneumoniae (less common))
other: coag. negative staph
Risk factors for septic arthritis
most common: PREEXISTING ABNORMAL JOINT ARCHITECTURE (gout, RA, osteoarthritis, etc) 1. advanced age 2. DM 3. previous joint surgery 4. IVDU 5. endocarditis 6. immunosuppression 1/4 don't have identifiable risk factor
Most common source of infection in septic arthritis
HEMATOGENOUSLY
other: direct inoculation (trauma, Sx, bite, percutaneous), spread from soft tissue
gram neg. bacilli for septic arthritis
- IVDU, iatrogenic (SURGERY or INTRA-ARTICULAR injection)
- young adults, late complement deficiency
- sickle cell and SLE
- cat or dog bite
- unpasteurized
- RA
at risk: elderly, immunocompromised, neonates, IVDU
- P. aeruginosa (staph aureus also common in IVDU)
- Neisseria gonorrhea, Neisseria meningitidis
- Salmonella
- Pasteurella multocida
- Brucella
- staph aureus most common
septic arthritis: N. gonorrhoeae
young sexually active adults (women more common, lower SE status, non-white, MSM, multiple partners, illicit drug use)
C5-C8 DEFICIENCY; splenectomy
dysuria, abnormal vaginal discharge
DERMATITIS: nonpuritic SKIN lesions, TENOSYNOVITIS, polyarthralgia
risk: menstruation, pregnancy, postpartum, C5-8 deficiency, ALE
alpha toxin (lecithinase)
C. perfringens traumatized tissue (especially muscle) damage cell membranes including RBCs produce GAS in tissue HEMOLYSIS: anemia
C. perfringens
ANAEROBIC GPR
gas gangrene: MYONECROSIS, NECROTIZING FASCIITIS
Sx: pain, edema, cellulitis, CREPITUS, HEMOLYSIS
SPORE: contaminated wound
ALPHA TOXIN
high mortality: shock
Dx: smear of tissue and exudate (GPR), cultures anaerobically: SUGAR FERMENTATION and ACID production, DOUBLE ZONE HEMOLYSIS
Tx: penicillin G
Lyme disease
TICK BITE
NORTHERN states, NE (not here in south)
early stage I: ERYTHEMA MIGRANS
early stage II: smaller skin lesions, malaria rash, conjunctivitis, heart and nervous system (palsies and meningitis, AV block)
late: intermittent arthritis (resolves in years without Tx, can use antibiotic to treat but may be refractory to it)
Dx: Lyme Western blot
MTB osteomyelitis
hematogenous spread from lungs PPD, back pain with Hx of TB (treated or not) neg. culture GRANULOMA and CASEATION Pott's: VERTEBRAE Sx: abcesses Tx: RIPE
Osteomyelitis in IVDU
S. aureus (MRSA) and Pseudomonas
also: Candida
unusual sites of infection are common: sternoclavicular, sternochondral joint, pubic symphysis
Iatrogenic effect: osteomyelitis
STAPH doctor did it ALWAYS ask if had recent steroid injection in back potential source of infection Dx: blood culture Tx: broad spectrum antibiotics
staphylococci
G+ cocci in grapelike clusters
catalase
catalase
STAPH
degrade H202: limits neutrophil ability to kill
staphylococcus aureus diseases
normal flora
toxins, pyogenic inflammation
abscesses, septic arthritis, osteomyelitis, endocarditis, food poisoning, scalded skin syndrome, TSS
hospital-acquried PNA leading to empyema/abscess, septicemia, mastitis, surgical wound infections
folliculitis, impetigo, bacterial conjunctivitis
staphylococcus epidermidis
SKIN, MUCOUS MEMBRANES
catalase, NO coagulase, non hemolytic, UREASE, does not ferment mannitol, NOVOBIOCIN sensitive
endocarditis, prosthetic join/hardware infections, IV catheters
BIOFILM
staphylococcus saprophyticus
catalase, coag neg., non-hemolytic, UREASE, does not ferment mannitol, novobiocin resistant
UTI (sex within last 24 hours)
Tx: bactrim or ciprofloxacin
staphylococcus aureus
NOSE, SKIN, some vaginas toxins and pyogenic inflammation catalase, coagulase, staphloxanthin, hemolysin, protein A, teichoic acid, polysaccharide capsule, peptidoglycan, alpha toxin beta hemolysis, ferments mannitol produce beta lactamase CHILDCARE center, IVDU, PRISON, SPORTS can produce biofilm
coagulase
staph aureus
activates prothrombin to thrombin causing activation of fibrinogen to fibrin to form clots
walls off infected site and delays NEUTROPHIL migration to site
test done with RABBIT plasma
beta hemolysis
complete lysis of RBC on blood agar
staph aureus
GAS, GBS, GCS/GGS
mannitol fermentation
staph aureus
beta lactamase
degrades penicillin
staph aureus
mecA gene
staph aureus: MRSA
encodes altered penicillin binding proteins in beta-lactamase-resistant penicillins (methicillin)
staphyloxanthin
staph aureus
carotenoid: causes golden color to colonies
inactivates microbicidal effect of SUPEROXIDES and other ROS in neutrophils
hemolysins
staph aureus
hemolyze RBC to use iron for growth
peptidoglycan
staph aureus
stimulates macrophages to produce cytokines, activates complement/coagulation cascades
SEPTIC SHOCK without endotoxin
protein A
staph aureus
cell wall protein
binds Fc (complement binding site) of IgG and prevents complement activation
NO C3b produced: reduced phagocytosis
teichoic acid
staph aureus
mediate adherence of staph to mucosal cells
lipoteichoic acid induces IL-1 and TNF from macrophages
polysaccharide capsule
staph aureus
11 serotypes: 5 and 8 most commonly cause infection
allows bacteria to attach to artificial materials and resist host cell phagocytosis
also: GAS, GBS
alpha toxin/hemolysin
staph aureus
membrane-damaging hemolytic toxin
forms holes in host cells
causes necrosis of skin and hemolysis
panton valentine (P-V) leukocidin
staph aureus: necrotizing PNA, skin/soft tissue infection, COMMUNITY ACQUIRED MRSA
membrane-damaging hemolytic toxin
pore forming cytotoxin that causes leukocyte destruction by damaging cell membranes and causes tissue necrosis
cell contents leak out of pore
gamma-toxin/leukotoxin
staph aureus
membrane-damaging hemolytic toxin
lyses phagocytes and RBC
scalded skin syndrome
staph aureus EXFOLIATIVE TOXIN A and B NEWBORNS Sx: fever, irritable, diffuse blanching erythema with blisters/bullae a couple days later on flexural areas, butt, hands and feet, serous fluid exudates, dehydration, electrolyte imbalance, FLAKY DESQUAMATION as lesions heal NO SCARRING, recover in 10 days
exfoliatin/exfoliative toxins A and B
staph aureus: scalded skin syndrome, bullous impetigo
protease that cleaves desmoglein in desmosomes leading to separation of epidermis at the granular cell layer
enterotoxin A
staph aureus: food poisoning
vomiting (caused by cytokines that stimulate enteric nervous system to activate vomit center in brain), watery diarrhea
acts as SUPERANTIGEN in GI tract
stimulates IL-1, IL-2 from macrophages and helper T cells
heat resistant: not inactivated by brief cooking, resistant to stomach acid/enzymes
incubate 1-8 hours
bullous impetigo
staph aureus EXFOLIATIVE TOXIN: localized vesicles flaccid bull with clear yellow fluid, later darker and more turbid ruptured bull leave thin brown crust TRUNK
staph toxic shock syndrome
staph aureus
SUPERANTIGEN: TSST
tampons, nasal packing, post op infection, other infections
local infection spreads to blood stream
IL-1, IL-2, TNF
blood cultures NEGATIVE
Sx: fever, hypotension, dizzy, diffuse macular erythroderma that desquamates 1-2 weeks after onset, vomit/diarrhea, severe myalgia, CPK elevates, renal failure, transaminitis, hyperbilirubinemia, thrombocytopenia, AMS
Tx of MSSA
nafcillin/oxacillin, cephalosporins (cefazolin, ceftriaxone, cefepime, ceftaroline)
vancomycin
augmentin (mild infections)
resistant to PCN (produce beta lactamase)
Tx of MRSA
vancomycin, daptomycin
linezolid
ceftaroline
mild: bactrim, clindamycin, doxycycline
Tx VISA/VRSA
daptomycin
linezolid
ceftaroline
MRSA/ MRSE
methicillin resistant staph aureus/epidermidis
MecA gene: change in PBP in cell membrane of bacteria
VRSA
vancomycin resistant staph aureus
genes encode enzymes that substitute D-lactate for D-alanine in peptidoglycan
VISA
vancomycin intermediate staph aureus
synthesis of unusually thick cell wall
D-test
evaluates inducible clindamycin resistance
plate with erythromycin and clindamycin antibiotic disks 2 cm apart
postive for inducible resistance: D shape
negative: circular and clindamycin can be used
Tx of TSS
supportive: extensive fluids, vassopressors (dopamine, NE)
surgical: remove tampon, explore and debride surgical wounds
antibiotics: vancomycin AND clindamycin (suppresses protein synthesis and therefore toxin synthesis: Linezolid also does this)
S. aureus prevention
peri-operative cefazolin +/- vancomycin if MRSA is prevalent in area
intranasal mupirocin to reduce colonization
Hibiclens (chlorexidine gluconate) for bathing +/- antibiotcs (doxy, bactrim)
usually 1 week