CHAPTER 02: INFECTION Flashcards
What are the organisms usually found in human and animal bites?
Usually Staphylococcus aureus
Human Bites → mixed aerobe and anaerobes
o Aerobic
- Staph aureus
- Staph epidermidis
- Strep
o Anaerobic
- Peptostreptococcus - Peptococcus
- Bacteroides
- Eikenella corrodens
Cat and Dog bites → Pasteurella multocida
Leeches – Aeromonas - Ciprofloxacin
What is wound infection?
What does it cause to the healing process?
Wound infection = bacterial count in wound > 105 bacteria per gram of tissue
- Infection impairs wound healing. All phases of the wound healing cascade are affected.
- ↓ tissue pO2
- ↑inflammatory phase
- ↓leukocyte chemotaxis and migration
- ↓ phagocytosis and intracellular killing
- ↓angiogenesis and ↓ epithelialisation
- Bacteria break down collagen so weaken wound strength and contraction
- infection may colonise, spread locally or systemically, depending on virulence of organism and host defences
Necrotising fasciitis definition
Life threatening infection that progresses along fascial planes and subcutaneous tissues
Described by Wilson 1953
Type 1 poly microbial
- most common, bacterial synergism with lytic toxins increasing spread of anaerobes
Type 2 mono microbial
- Group A β-haemolytic streptococcus (pyogenes) infection usually
Type 3 clostridium perfringens, gas gangrene
Necrotising fasciitis classification
Can be described by:
- tissue planes affected (fasciitis, myositis)
- extent of invasion
- anatomical site
- causative pathogens
What is the pathogenesis?
- Production of pyrogenic toxins
- Haemolysins
- Hyaluronidase
- Streptokinase
- NF occurs possibly due to lack of antibodies to M-Proteins, various strep endotoxins
e. g. Group A strep in nose/throat of 15% of population – some just get sore throat, others scarlet fever, and others go on to get necrotising fasciitis
What are the risk factors of necrotising fasciitis?
IDDM Minor trauma Surgery NSAIDs (minor correlation) Varicella zoster virus infection More common in IVDA Malnutrition Obesity Chronic Alcoholism and cirrhosis Peripheral Vascular disease Chronic Lymphoid Leukaemia Steroids Renal failure Immunocompromised Bad prognosis if female, ↑ age, ↑infection, delay ↑Creatinine, ↑Lactate, ↓organ function at diagnosis
What are the clinical features?
- No obvious entry portal
- Local swelling, redness and intense pain
- Very rapid spread sc & superficial fascia
- Systemic toxicity – apathy, confusion, septic shock, elderly may not have pyrexia
- Dusky hue, areas of purple necrosis
- ↑ WBC (15+) ↓ Na (<135mmmol)
Cellulitis → rapid spread in subcutaneous tissues and superficial fascia → Liquefactive necrosis → vascular thrombosis and myonecrosis → cutaneous blood vessels last to be affected (pt may initially present septic with innocuously-appearing cellulitis but violent infection beneath)
Prognosis: 53% with treatment, 100% without
What are the 6 variables in the laboratory risk indicator for necrotizing fasciitis (LRINEC) score to help discriminate between necrotizing and nonnecrotizing soft-tissue infections?
Wong et al 2004 C-reactive protein, mg/L <150 0 >150 4 WBC count, cells/mm3 <15 0 15–25 1 >25 2 Hemoglobin level, g/dL >13.5 0 11–13.5 1 <11 2 Sodium level, mmol/L >135 0 <135 2 Creatinine level, mg/dL <1.6 0 >1.6 2 Glucose level, mg/dL <180 0 >180 1
LRINEC score, Probability of Risk (category points), NSTI (%)
Low <|= 5 <50%
Intermediate 6–7 50–75%
High >|= 8 >75%
Diagnosis of nec fasc
Treatment of nec fasc
Dx
- Clinical
- Finger test - loosened tissue planes, cloudy exudate, lack of bleeding
- Tissue biopsy
- Radiology
- X-ray
- CT
- MRI
- Doppler USS
Treatment
- Resus, aggressive fluid resus
- IV antibiotics - clindamycin (stops endotoxins and M protein prod), gentamicin, imipenem (chase micro)
- Radical surgical debridement, relook
- ITU: ventilation/oxygenation, inotropes and dialysis
- HBO
What is Fournier's gangrene Meleney gangrene Gas gangrene NOMA
Fournier’s - abrupt, rapidly progressive, gangrenous infection of the external genitalia, perineum or abdominal
Meleney - Lethal and rapidly progressive soft tissue infection, due to microaerophilic strep. Synergistic gangrene: symbiosis of anaerobic streps and staphs.
Gas gangrene: Clostridium perfringens (Gram +ve, spore-forming anaerobic bacillus in GI tract, soil), can also be Bacteroides, anaerobic strep, coliforms Surgical emphysema (crepitus) due to hydrogen production
NOMA - Necrotising Ulcerating Stomatitis, Stomatitis Gangrenosa, Cancrum Oris
140,000 cases per year worldwide – mainly children
Gingival infection - Fusobacterium necrophorum, Prevotella spp, Strep spp, Actinomyces, Pseudomonas
Tell me about penicillin
- Beta-lactam ring fused to a thiazolidine ring.
- Change to phenoxymethyl side branch to make it acid resistant = oral preparation
- Add amino group to phenyl radical → Gram -ve & +ve cover.
- modify → protection from penicillinase (beta-lactamase, staphs)
Mechanism - block cross-linking of bacterial cell wall mucopeptide formation
Resistance - Beta-Lactamase producers
Interactions - Penicillins inactivate aminoglycosides when mixed in the same solution.
Toxicity - Hypersensitivity, encephalopathy, tubulo-interstitial nephritis.
- Ampicillin if given to infectious mononucleosis 90% get rash.
What are the indications for penicillin?
Indications
- Benzyl Pen – IV/IM, esp. for endocarditis
- Pneumococcus, Meningococcus, Streptococcus, Gonococcus, Clostridia, Actinomycosis, Anthrax and Spirochetes (Syphilis) - Pen V (phenoxymethyl) - oral, rheu fever
- Flucloxacillin – for penicillinase producers
- Methicillin – IV for penicillinase producers
- Ampicillin – also Gram -ves e.g. Salmonella, Shigella, E.Coli, H.Inf, Proteus (good for UTI and URTI)
- Amoxicillin – same as Amp, better absorbed
- Clavulanic Acid – inhibits beta-lactamase
- Carbenicillin and Ticarcillin also cover Pseudomonas
- Acylureidopenicillin derivatives (Azlocillin, Mezlocillin and Piperacillin) better at gram negs and Pseudomonas but are susceptible to beta-lactamases so no good for staphs.
Tell me about Cephalosporins
- Innately resistant to staph penicillinases.
- Activity against gram neg and gram pos
- Beta lactam ring assoc with dihydrothiazine ring.
1st generation = Cephazolin, Cephalexin - only +ve cocci.
2nd generation = Cefuroxime, Cefaclor (oral) Cephradine (oral), better against E coli, Klebsiella, Pr. mirabilis. Use for resistant H.Inf, mixed aerobic-anaerobic infections (combined with aminoglycoside)
3rd generation = Cefotaxime (penetrates CSF), Ceftazidime. Broad spectrum, better against aerobic gram negs, Esp. good for Enterobacter, Pseudomonas, Bacillus and Nisseria.
Cephalosporins - mechanism, indications, resistance, interactions and toxicity
Mechanism
Inhibit bacterial cell wall synthesis.
Indications
Serious systemic infections. Post op infection, immunocompromise, leukaemics etc
Resistance
Usually OK for beta-lactamases so no real problems
Interactions
Increased nephrotoxicity if used with other nephrotoxic drugs such as aminoglycosides and diuretics,
Toxicity
Allergy. 1st generations caused proximal tubule damage, later ones better.
Tell me about Carbapenems
Carbapenems
- Imipenem
- Highly resistant to beta lactamase
Mechanism
- Inhibits cell wall synthesis
- administered with cilastatin
Indications
- Very broad spectrum active against +ve cocci, (similar to penicillin) –ve organisms and anaerobes (similar to metronidazole and clindamycin).
- nosocomial infections, multiple resistant gram –ve bacilli, mixed aerobe, anaerobic infections suspected
Toxicity
- Similar to penicillins. Nausea vomiting and diarrhoea. No evidence of renal toxicity or coagulation problems.
