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
urease
S. epidermidis, saprophyticus
hydrolysis of urea into CO2 and ammonia
novobiocin sensitive
S. epidermidis
resistant: saprophyticus
biofilm
S. epidermidis
once introduced into body, foreign materials become coated with host proteins (fibrinogen, fibronectin, etc.) which serve as receptors for staph surface proteins (ADHESINS)
extracellular polysaccharide matrix or slime is produced that encases bacteria and serves as barrier to antibiotic penetration and may interfere with jost defenses
S. epidermidis TX
MSSE: oxacillin, nafcillin
MRSE: vancomycin
prosthetic valve endocarditis: rifampin or gentamycin
REMOVE device
mannitol fermentation
staph aureus
strep
G+ pairs or chains
catalase neg., type of hemolysis distinguishes
streptococcus pyogenes
Group A strep
skin, oropharynx
pyogenci inflammation, exotoxin, immunologic
M protein, polysaccharide capsule, hyaluronidase, streptokinase, DNase, C5a peptidase, streptococcal chemokine protease, streptolysin O/S, erythrogenic toxin, pyrogenic exotoxin A, extoxin A/B/C
beta hemolytic
bacitracin sensitive
pharyngitis, cellulitis/impetigo/erysipelas, necrotizing fasciitis, TSS, scarlet fever, pueroperal sepsis, endometritis, rheumatic fever, glomerulonephritis
streptococcus agalactiae
Group B strep
vagina (acquired in urtero), colon
beta hemolytic: narrow
lack of hydrolysis of bile esculin
hydrolyzes hippurate
bacitracin resistant
CAMP test
polysacchride capsule
risk factor: premature rupture of membrane (PROM) in colonized women, babies prior to 37 weeks, children whose mothers lack Ab
neonatal sepsis, meningitis, PNA
adults: invasive infections: septic arthritis, cellulitis, osteomyelitis,
association: DIABETES, BREAST CA
Dx: gram stain, culture, rapid DNA test for vaginal/rectal
Tx: penicillin, ampicillin, vancomycin if PCN allergy
prevention: screen women between 35-37 weeks: IV PCN G/ampicillin at delivery
enteroccous faecalis/faecium
Group D strep
colon
gamma hemolytic
can grow in hypertonic saline or in bile
low virulence, capsule, enzymes that injure host
hospital acquired UTIs, blood stream infections, endocarditis, intra-abdominal infections
Tx: combination antibiotics required: PCN/Vanc (depends on susceptibility) and aminoglycoside
if vanc resistant (more likely E. faecium): linezolid or daptomycin
streptococcus bovis (galaliticus)
Group D strep gamma hemolytic ENDOCARDITIS in patients with COLON CA does not grow in hypertonic saline Tx: PCN, ceftriaxone, vacomycin
Viridian group streptococci
alpha hemolytic
mouth, colon
resistant to lysis by bile, optochin resistant
enter blood stream after DENTAL SURGERY in patients with CAVITIES
no enzymes/exotoxins
glycocalyx: attach to heart valve
BRAIN (or liver, abdominal) ABSCESS, ENDOCARDITIS,
includes: sp. anginosus, milleri, intermedius, mutans, sanguis
Tx: depends on susceptibilities, PCN or ceftriaxone
endocarditis Tx with intermediates susceptibility to PCN: add gent
peptostreptococcus
anaerobe
flora: gut, mouth, vagina
found in mixed anaerobic infections/abscesses: BRAIN, ABDOMEN, PELVIC ABSCESS
Tx: penicillin
streptococcus pnuemoniae
alpha hemolytic
optochin resistant
lysed by bile
Group C and G strep
beta hemolysis
streptococcus dysgalactiae subspecies equismilis
flora of URT, asymptomatic colonizer of skin, GI, vagina
emerging cause of human infection: invasive infections, pharyngitis, bacteremia, meningitis, puerperal infections
ACQUIRED VIRULENCE FROM GAS: capsule, superantigen, etc.
rapid tests do not detect GCS/GGS
Group A strep
streptococcus pyogenes
Group B strep
streptococcus agalactiae
Group D strep
enteroccous faecalis/faecium
streptococcus bovis
hydrolyzes esculin in presence of bile
gamma hemolytic
M protein
GAS
anti-phagocytic
protrudes from outer surface of cell and interferes with ingestion by phagocytes
lots of types
polysaccharide capsule
GAS
anti-phagocytic
made of hyaluronic acid
hyaluronidase
GAS
degrades hyaluronic acid
spreading factor in cellulitis and skin infections
streptokinase
GAS
activates plasminogen to plasmin, dissolves fibrin in clots, thrombi and emboli
streptodornase (DNase)
GAS
degrades DNA in exudates/necrotic tisse
protect bacteria from being trapped in neutrophils extracellular traps (NETs)
C5a peptidase
GAS
cleaves C5a: minimizes influx of neutrophils early in infection
streptococcal chemokine protease
GAS
prevention of migration of neutrophils into site of infection by degrading chemokine IL-8 (neutrophil recruiter)
streptolysin O
GAS
cytotoxic, protect from phagocytic killing and enhance bacterial influence
HEMOLYSIN
OXYGEN LABILE: beta hemolysis only when colonies grow under surface of blood agar plate
Ab formed
streptolysin S
GAS more modest effect on virulence HEMOLYSIN OXYGEN STABLE: causes beta hemolysis on surface of the plate no Ab formed
pharyngitis
GAS
Sx: sore throat, inflamed tonsils with pharyngeal exudate, N/V, tender enlarged cervical lymph nodes
ABSENCE of URI Sx
Dx: RAPID STREP antigen TEST (specific, not sensitive), throat culture if neg. rapid test
neg culture: DISCONTINUE antibiotics
rapid strep antigen test
pharyngitis
detects bacterial antigen in throat swab
antigens react with Ab bound to latex particles
positive: agglutination of latex particles
GAS Tx
all 10 days except Z pac oral PCN V: 2-3x/day amoxicillin, cephalexin: 2x/day Pen allergy: azithromycin 2-5 days clarithromycin, clindamycin: 3x/day
complications of untreated GAS pharyngitis
immune mediated: rheumatic fever
local extension: otitis media, sinusitis, mastoiditis, meningitis, peritonsillar/retropharyngeal abscess
erysipelas
GAS
rapidly spreading erythematous cutaneous swelling that may begin in face
sharp well-demarcated, serpiginous border
BUTTERFLY on face
cellulitis
GAS
dermis and subcutaneous fat infection
impetigo
GAS
papules progressing to vesicles then pustules that rapidly break down to form adherent crusts with golden appearance
necrotizing fasciitis
GAS: M protein 1/3, exotoxins A/B/C, trypsinlike protease
infection of deeper tissues, progressive destruction of muscle fascia and overlying subQ fat
infection spreads along muscle fascia due to poor blood supply
Sx: PAIN, erythematous, swollen, warm, shiny, crepitus
acute, rapid progression: skin changes from red-purple to blue-gray
advanced infection: fever, tachycardia, systemic toxicity
associated with: strep TSS
predisposing factors: skin injury, blunt trauma, surgery, IVDU, childbirth
NO NEUTROPHILS
trypsinlike protease
GAS: necrotizing fasciitis
degrades IL-8: no neutrophil recruitment
erythrogenic toxin
GAS: scarlet fever
SUPER ANTIGEN responsible for rash
pyrogenic exotoxin A
GAS: TSS
SUPERANTIGEN
fever inducing
superantigen
causes large release of cytokines
exotoxin B (extracellular cysteine protease)
GAS: necrotizing fasciitis
rapidly destroys tissue
strep TSS
GAS most often
entry: skin, vagina, pharynx
trauma that develops deep infection in 2-3 days: often soft tissue of extremity
Sx: diffuse erythema, fever, chills, myalgia, N/V/D
complications: DIC, AKI, ARDS
Dx: isolate GAS from sterile site
Tx: penicillin plus clindamycin (or linezolid)
scarlet fever
GAS children erythrogenic toxin Tx: sore throat, DIFFUSE ERYTHEMA on head and neck spreads to trunk, SAND PAPER SKIN, rash desquamates, STRAWBERRY TONGUE complication of pharyngitis
post-strep glomerulonephritis
GAS
poor socioeconomic status
Ag-ab complexes on glomerular basement membrane
complication of SKIN INFECTION, pharyngitis
Sx: HTN, facial, LE edema, DARK URINE, subclinical
most patients recover completely
acute rheumatic fever
GAS
Ab against GAS proteins cross-react with host antigens: M protein
Jones Criteria: polyarthritis, carditis, nodules, erythema marginatum, Sydenham chorea
2 weeks after untreated pharyngitis or scarlet fever
Dx: ASO titer: STREPTOLYSIN O
Tx: even though infection was weeks ago, full antibiotics
prevent strep infections with Hx of RF: PCN IM monthly for many years
lack of hydrolysis of bile esculin agar
GBS
does hydrolyze esculin: GDS: black pigment
hydrolyzes hippurate
GBS
bacitracin resistant
GBS
sensitive: GAS
CAMP test
GBS
protein is produced that enhances hemolysis on sheep blood agar when combined with beta-hemolysin of S. aureus
grows in hypertonic saline
enterococcus faecalis/faecium
NOT: streptococcus bovis (galaliticus)
resistant to lysis by bile
viridans group strep
lysed by bile: S. pneumo
optochin resistant
Viridian group strep
sensitive: S. pneumo
glycocalyx
strep viridans
allow organism to attach to heart valve
streptococcus mutans
cause of dental carries
synthesizes polysaccharides in dental plaque
alpha hemolysis
green on blood agar: partial hemolysis
viridans group strep, S. pneumoniae
gamma/non-hemolytic
GDS: S. bovis and enterococcus
native acute infectious arthritis
bacterial infection in joint: suppurative/pyogenic/septic arthritis
Sx: intense pain, LIMITED ROM in 1-2 week period, swelling, red, warmth
mycobacterial and fungal are more chronic and slowly progressive
usually MONOARTICULAR: KNEE, hip, shoulder, wrist, ankle
HIP in children most common
Dx: ARTHROCENTESIS REQUIRED; leukocytosis, elevated ESR and CRP
can get X-ray/CT/MRI: early: normal osseous structures, late: joint space loss, bony erosion
ultrasound to guide needle aspiration
Tx: antibiotics, drain +/- irrigation and debridement
SURGICAL EMERGENCY
pathophysiology of septic arthritis
depends on adherence of organisms to synovial membrane, bacterial proliferation in synovial fluid and host inflammatory response
joint disease/injury: increased exposure of ECM proteins (fibronectin, collagen, elastin, hyaluronic acid) that promote bacterial attachment
mycobacterial arthritis
MTB
chronic granulomatous mono arthritis (usually homogeneous from lung)
knee, hip, ankle
PPD
Dx: synovial biopsy (granulomas), acid fast stain, PCR
Tx: RIPE for 8 weeks, then INH and RIF for 6 months
mycobacterial arthritis risks
- older than 65
- female
- immigrant from high TB region
- low SE status
- incarceration
- alcohol abuse
- immunosuppressed/HIV
- pre-existing joint disease
prosthetic joint infection
highly susceptible to infection
joint inoculation during Sx or early post operation
S. aureus most common (next coag. neg. staph, strep, GNB, enterococci)
lower leukocyte count than native; neg. culture does not rule out Dx
Tx: remove prosthesis, prolonged antibiotics
viral arthritis
Rubella, Parvo B19, HCV, HBV
immune complex
Sx: arthralgia or arthritis
most short duration and resolve spontaneously
small joints of hand most common, can get large joints
osteomyelitis
S. aureus most common (express high affinity adhesins)
infection localized to bone
bone destruction, sequestra (dead bone)
develop from: contagious spread from joint/soft tissue (mono bacterial), hematogenous (polymicrobial), direct inoculation
difficult to treat
Sx: nonspecific pain, draining sinus tract
Dx: MRI/CT (sensitive); X-ray (cheap, not sensitive), elevated ESR and CRP, needle aspiration to identify organism
most common organism for osteomyelitis
What if you stepped on a nail?
STAPH
others: strep, enterococci, gram neg. (Pseudomonas, E. coli, serratia), anaerobes, MTB
Nail: Pseudomonas
rare: dimorphic fungi, Salmonella, other mycobacteria
Tx: Sx (remove hardware, drain, debride), antibiotics
osteomyelitis Tx
4-6 weeks IV
most common: beta-lactams, Vancomycin
linezolid (oral): due to AE: limit to VRE and those intolerant to vanc.
daptomycin: G+
vertebral osteomyelitis and spondylodiskitis
source: skin/ soft tissue infection, GU tract infection, infective endocarditis, IVDU, post-op, hematogenous (most common)
most common: STAPH
endemic regions: MTB, Brucella
Sx: epidural abscess, motor/sensory deficit
Dx: high suspicion in high risk, MRI
Tx: at least 6 weeks antibiotics
osteomyelitis in DM or vascular insufficiency
FOOT
Dx: MRI
Tx: surgery, broad spectrum antibiotics (zosyn, ertapenem, cephalosporins, flagyl, cipro, other quinolones), revascularization in PVD
risk: DM 10+ yrs, poor glucose control, retinal or renal complicaitons, peripheral neuropathy, callus, PVD
acute hematogenous osteomyelitis in children
STAPH, STREP
METAPHYSES of long bone (tibia, femur)
neonatal: septic arthritis of adjacent joint; GBS, E. COLI
Dx: clinical, MRI, blood culture
Tx: antibiotics (switch from IV to oral when afebrile) for 3 weeks
pathogenesis of acute hematogenous osteomyelitis in children
capillary ends of artery make sharp loops under growth plate: slow turbulent blood flow
minor trauma: obstruction of capillaries: avascular necrosis, then seeded from transient bacteremia
capillaries lack phagocytes
osteomyelitis in sickle cell disease
SALMONELLA, Staph
mostly children
capillary occlusion secondary to skirling may devitalize and infarct gut permitting salmonella invasion
reduced liver and spleen function: can’t clear organisms
bone also devitalized
myositis
inflammation of muscles
infection uncommon
bacteria, mycobacteria, fungi, virus, parasites
source: contiguous spread, hematogenous
pyomyositis
acute bacterial infection of skeletal muscle
TROPICS
STAPH AUREUS, then strep
large muscles: lower extremities, turn, shoulder
Sx: fever, localized muscle pain, stiff/swell/tender, pus accumulation
previous bacteremia along with minor muscle injury
Dx: imaging: MRI best
Tx: drain ABSCESS, vancomycin
if not Dx: sepsis, striking erythema, very tender, fluctuance
risk factors for pyomyositis
- HIV
- IVDU
- alcoholic liver disease
- corticosteroids
- hematologic malignancy
rare: post partum, post abortion, post op
