Bacteremia Exam Notes PDF

BACTEREMIA Determining the primary (original) source of this infection is critical ○ May be the cause or consequence of another infection Epidemiology & Common Etiologies Hospital-acquired: respiratory tract, indwelling catheters Community acquire...

BACTEREMIA Determining the primary (original) source of this infection is critical ○ May be the cause or consequence of another infection Epidemiology & Common Etiologies Hospital-acquired: respiratory tract, indwelling catheters Community acquired: UTIs Post-operative: soft tissue, intra abdominal infections Gram-positive ○ Increased over past decades (aging population, device-related procedures) ○ Staph aureus = most common Gram-negative ○ Most common associated with CAB ○ E coli= most common Pathophysiology- reproducing bacteria lead to septicemia due to immune system failure Cellular innate and adaptive immune responses responsible for initial microbe clearance Liver and spleen filtration of active bacteria in circulating blood Complications May cause endocarditis, osteomyelitis, meningitis, and other complicating infections, as well as progression to sepsis and multiorgan dysfunction that can be fatal Clinical presentation FEVER Chills and/or rigors; do not need to be present When it leads to sepsis and septic shock ○ Hypotension, altered mental status decreased urine output due to hypovolemia from leaky capillaries Diagnosis Identifying or presuming the source dictates the diagnostic workup (ex UTI- urine) When suspected labs include blood cultures: ○ 2 sets (1 from each arm) assessing for aerobic and anaerobic organisms 2 bottles from 1 arm 2 bottles from other arm ○ WBC- often elevated (non-specific) Approach to Treatment Urgent and appropriate antibiotics required ○ Broad-spectrum, bactericidal, high dose Antibiotic selection based on: ○ Community vs hospital-acquired ○ Recent healthcare exposure, surgery? ○ Local antibiotic resistance patterns (antibiogram) ○ Rapid diagnostic tools when available Other Considerations Route ○ IV preferred initially ○ Oral: afebrile > 48 hours, clinically improved & stable unless complicated by other infection, high bioavailability drug Duration ○ Based on source and its control ○ Gram positive- 14 days, complicated may be 4-6 weeks Evaluation of Therapeutic Outcomes Clinical ○ Resolved signs and symptoms ○ Source identified and eradicated ○ Drug specific toxicity ○ No complicating infections Microbiological ○ Susceptibility data ○ Sterilization of blood cultures · Infective Endocarditis o Pathogenesis sequence – slide 12 o Know the following 3 specific listed risk factors for endocarditis: § Previous endocarditis, prosthetic heart valve, injection drug use – slides 10-11 § Treatment approach – Slide 20 INFECTIVE ENDOCARDITIS = endovascular infection Inflammation of lining membrane of heart (endocardium) Epidemiology Classifications ○ Acute or subacute ○ Native valve or prosthetic valve ○ Community acquired or health-care associated ○ By microbiological etiology Impact ○ High mortality (20-30%) ○ Fatal without antimicrobial therapy ○ Rising incidence Acute bacterial Health-care associated Staph aureus assoc with both Risk factors ○ Predisposing heart conditions Valve replacement therapy- treatment will differ  ○ PWID Direct inoculation Clinical manifestations differ ⅔ have no underlying heart disease Predilection for tricuspid valve- local damage to endocardium Only 35% with heart murmurs on admit Risk factors (AHA predisposing heart conditions) High risk Moderate risk Low or no-risk Pathogenesis 1. Pathogen accesses bloodstream ○ Dental, IV catheter, PWID 2. Adheres to valve surface ○ Abnormal blood flow predisposes (at risk) 3. Pathogen persists and proliferates ○ Vegetation forms Bacterial haven 4. Pathogen disseminates ○ Metastatic infections Approach to Treatment Directed therapy ○ Pathogen is known when IE is determined ○ Approach based on most likely pathogen, “culture negative” IE approach Bactericidal drugs High dose Parenteral (IV) Long duration (6-8 weeks or more) ○ May require outpatient parenteral antimicrobial therapy ○ Rationale for long treatment course: Organisms produce biofilm on valve structure; difficult to penetrate vegetation Non-reproductive bacterial growth phase High risk of recurrence MENINGITIS =Inflammation of meninges Likely common pathogens based on gram stain results Streptococcus pneumoniae (58-72%) ○ Gram-positive cocci in pairs ○ Ceftriaxone + vancomycin (for resistance risk)  Strept agalactiae ○ Gram-positive cocci ○ Ampicillin + gentamicin Listeria monocytogenes ○ Gram positive rods ○ Ampicillin or PCN +/- gentamicin Neisseria meningitidis ○ Gram-negative diplococci ○ Ceftriaxone Haemophilus influenzae ○ Gram-negative rod ○ ceftriaxone Approach to treatment Pathophysiology- treatment ○ 1. Bacteria multiply in CSF ○ 2. CSF typically blacks antibodies and complement ○ 3. Thus, antibacterials that inhibit bacterial growth are not enough! ○ 4. Bactericidal drugs required to sterile the CSF ○ 5. Antibacterials must cross BBB ○ Tissue damage is due to inflammation from bacteria in CSF; enhanced with bacterial lysis from bactericidal drugs- anti-inflammatory corticosteroids to mitigate Approach ○ 1. Start antibiotics EMPIRICALLY, then based on patient specific CSF culture data Obtaining CSF fluid may be delayed for patient safety (ex on warfarin) Antibacterial and antiviral (acyclovir) often both initiated ○ 2. Empiric antibacterial backbone 3rd gen IV cephalosporin + IV vancomycin Risk for nosocomial GNR- ceftazidime or cefepime ○ 3. Add IV ampicillin for listeria monocytogenes risk ○ 4. High doses to penetrate BBB to access CSF OSTEOMYELITIS AND SEPTIC JOINT General classifications Infective arthritis ○ Inflammatory reaction within JOINT SPACE associated with purulent effusion ○ Most common in young children, elderly Osteomyelitis ○ Inflammation of BONE, especially the marrow  Infective arthritis Osteomyelitis Duration Acute: < 7 days Acute: recent onset, > 7 days chronic or symptoms for 1 week irreversible damage Chronic: longer than 1-4 weeks, initial infection relapse Etiology Gonococcal, Presence or absence of nongonococcal peripheral vascular disease and vascular insufficiency What’s affected Number of joints Portion of bone (knee=most common affected, patient’s site), monoarticular vs physiologic status, local polyarticular environment Etiology Infective arthritis Osteomyelitis Cause? Bacteria, viruses, fungi, bacteria parasites Most common Adults: Hematogenous (spread pathogens Staph aureus through bloodstream) (48%) S. aureus Strept species H. influenzae Less often (common in gram-negative children prior to vaccines) Salmonella species Children: Direct Inoculation & 4: S. aureus outside of body) S. aureus Polymicrobial ○ E coli ○ Pseudomo nas aeruginos  a ○ Strept species ○ Staph epidermidi s Characteristics of synovial fluid for infectious arthritis diagnosis IA OM ESR, CRP increased increased Serum WBC Increased with left shift Acute: increased WBC differential with left shift Chronic: may be normal Blood culture Positive 50%; 20% Positive in 50% gonococcal hematogenous Other tests Needle aspiration of X-ray: bone changes joint (synovial fluid): 10-14 days after onset Arthrocentesis 50% of bone matrix Purulent fluid must be decalcified to Positive gram detect stain & culture WBC 50-200 x MRI- most sensitive, 10^3/mm^3 common WBC differential with > 90% Bone aspiration/biopsy polymorphonucle ar leukocytes Culture of abscess Low glucose High lactic acid (non-gonococcal) Approach to treatment Empiric therapy initiated before pathogen is identified ○ IA: based on gram stain of synovial fluid ○ Prosthetic joint infection- combination therapy often includes rifampin Antibiotics must penetrate readily into bone/joint space ○ Start with IV in high doses  IA OM Source control Joint drainage Surgical debridement of bone may be needed Long duration 3-4 weeks in adults, 10 4-6 weeks in adults (8 days in children w/ weeks for MRSA); acute normalized CRP hematogenous in children 3 weeks minimum Inpatient to outpatient IV initiated in hospital “” with placement of long-term I access- to OPAT Necrotizing soft tissue infections- focus on necrotizing fasciitis Types, most common risk factor = diabetes Complications: TSS, compartment syndrome, septic shock SLIDE 66 Type 1 Most common (80%) Anaerobes and facultative bacteria act synergistically to cause destruction of fat and fascia Type 2 More common in younger patients, MRSA increasingly common Streptococcal gangrene = flesh eating bacteria Rapidly extending necrosis of SC tissues; early onset shock/organ failure Type 3 Involves skeletal muscle Prominent gas production, muscle necrosis Type 4 Rare; fungal etiology, traumatic wounds, burns Clinical presentation and approach to treatment Location: typically abdomen, perineum, lower extremities In contrast to cellulitis ○ Severe pain, disproportional to clinical findings ○ Fails to respond to initial antibiotic therapy (if IV or PO) Determined from appearance during surgery ○ Swollen, dull-gray fascia Treatment ○ Requires surgical management immediate/aggressive surgical debridement of all necrotic tissues ○ Antibiotics Broad empiric coverage, IV route ○ IV fluid replacement Maintain hydration ○ IVIG - may benefit strep infections ○ Hyperbaric oxygen