Nosocomial infections

Common organisms

• MRSA
• Enterococcus faecium/faecalis
• Coagulase-negative staphylococcus
• Pseudomonas
• Acinetobacter baumanii
• Stenotrophomonas maltophila
• Enterobacter
• Klebsiella
• Serratia marcescens
• Proteus
• Candida (albicans, glabrata, krusei)

Multiresistant organisms

• Class I beta-lactamase
• Extended-spectrum beta-lactamases (ESBL)
  • Enzymes such as TEM-24 produce cross-resistance to multiple classes of antibiotics including fluoroquinolones and aminoglycosides
  • Can spread by plasmid to other species. Transposons transfer genes between plasmids despite being coded in chromosomal genetic material
  • E.g. SHV-1 plasmid beta-lactamase from Klebsiella
  • Plasmid AmpC beta-lactamase from Citrobacter
  • Aminoglycoside-modifying enzymes from streptomyces

Beta-lactamases

• Class A
  • Resistance to monobactams, third-gen cephalosporins
  • Inhibited by clavulanate and tazobactam
  • E.g. Klebsiella pneumoniae carbapenemase
• Class B
  • Resistance to penicillins, cephalosporins and carbapenems
  • NOT inhibited by clavulanate and tazobactam
  • Aka Metallo-beta-lactamases
  • E.g. NDM-1 enzyme

Beta-lactamases

• Class C
  • Resistance to cephalosporins; not usually inhibited by clavulanate or tazobactam
  • ESCAPPM organisms
• Class D
  • Oxacillinases. Resistance to carbapenems is slightly inhibited by clavulanate

Multiresistant organisms

• Pseudomonas
  • Derepression of protein efflux systems, cephalosporinases and derepession of AmpC enzyme
  • Can develop loss of porin OprD in presence of imipenem within days
• Enterobacter
  • AmpC beta-lactamase can develop in the presence of third-generation cephalosporins within days of initiation
• Induction
  • Presence of antibiotic induces resistance
  • Seen with ESBL’s that show susceptibilty in vitro but not in vivo
• Methicillin-resistance in Staph is due to altered PBP with low affinity for all beta-lactams 
  • Linked to MecA gene
  • Spreads by vector transmission NOT de novo production (does not develop readily de novo)

E. coli

• One of the first multiresistant organisms
• Increasing third-generation cephalosporin and quinolone resistance

Enterobacter and Aerogenes

• Part of normal gut flora but develop ESBL easily leading to ceftazidime resistance
• TEM-24 enzyme confers resistance to a wide range of antibiotic classes

Klebsiella

• Increasingly resistant due to acquiring ESBL

Pseudomonas

• May colonise chronic lung disease
• Very broadly resistant

Stenotrophomonas

• Increasingly common environmental organism
• Often resistant to beta-lactams, quinolones and aminoglycosides
• Also produces carbapenemase

Acinetobacter baumanii

• Survives in dry environments and cross-infects readily
• Multiresistant including sometimes to carbapenems
• Become rapidly resistant and may only be sensitive to colistin

Coagulase-negative staph

• Usually methicillin-resistant – hence vancomycin use
• As glycopeptide resistance rises, quinpristin, dalfopristin and linezolid may have a role

Staphylococcus aureus

• Relatively easily treated with glycopeptides if MRSA
• Vancomycin resistance is rising
• VRE/VISA

Enterococcus

• With increasing third-generation cephalosporin use, E. faecalis and E. faecium have risen in incidence
• E. faecalis is more common and may still be sensitive to ampicillin but >30% are resistant to aminoglycosides
• E. faecium has a resistance rate of 7% to vancomycin (VRE), 53% to ampicillin and 30% to aminoglycosides

Colonisation vs. infection

• MRSA colonises readily and causes infection in a significant proportion of cases
• VRE is still relatively uncommon and colonisation rates far exceed infection rates
• Acinetobacter colonises and infects readily, can take days to identify and is difficult to treat

Nosocomial pneumonia

• 15-30% of ventilated patients
• Aspiration from nasopharyn, local spread or haematogenous spread
• 45% of healthy adults aspirate in their sleep
• In the sick patient, the nasopharynx is colonised with Gram-negatives
• Pneumonia will develop in 25% of colonised patients vs. 3% in non-colonised patients
• Colonisation of upper GI tract can lead to colonisation of nasopharynx

Nosocomial pneumonia

• Organisms:
  • Aerobic Gram-negatives predominate: Pseudomonas, Enterobacter, Klebsiella, E. coli, Serratia marcescens and Proteus
  • Staph (MRSA in particular) account for small but significant number
  • Early-onset VAP (48 hours to 5 days) may be due to community organisms such as MSSA, S. pneumoniae and H. influenzae as well as Gram-negative enteric bacilli
  • Late-onset VAP (>5 days) involves more resistant agents such as MRSA, Pseudomonas, Stenotrophomonas and Acinetobacter
• Treatment: 8 day course likely adequate

Wound infections

• Skin commensals are common (Staph, Strep)
• Gram-negatives also implicated

Line sepsis

• CVL: Colonisation rates of 5-40% with 10% of colonised catheters leading to infection
• Colonised catheter: >15 CFU from a proximal or distal catheter segment in absence of accompanying symptoms/signs
• CR-BSI: Isolation of same organism from catheter specimen and peripheral blood culture with signs of infection and absence of other source
  • Defervescence with catheter removal provides indirect confirmation
• 25% incidence of coagulase-negative staph (increasingly pathogenic)
• S. aureus and MRSA also prevalent
• Enterococci increasingly seen and fungi can occur

Line sepsis

• Treatment
  • Remove line
  • 5-7 day course of glycopeptide for Coagulase-negative staph
  • 10-14 day course for S. aureus (unless invasive illness – 6 weeks)
  • 10-14 days for Gram-negatives and fungi
  • Culture lines
  • Try to avoid replacing CVL if possible for a few days if removed

Last Updated on October 2, 2020 by Andrew Crofton