Chapter 62 Nosocomial infection
Nosocomial or hospital-acquired infections are a major problem in hospitals, affecting up to 9% of inpatients at any one time. Intensive care units (ICUs) represent 2–10% of hospital beds, but are responsible for 25% of all nosocomial blood stream and pulmonary infections. In the European Prevalence of Infection in Intensive Care (EPIC) snapshot of prevalence the infection rate in ICU was 20.62%.1 Nosocomial infection is, at least in theory, a preventable cause of morbidity and mortality (Table 62.1).
EPIDEMIOLOGY
The prevalence of nosocomial infection is reported as being between 3 and 12% in most institutions but varies considerably between different sites within each institution.2 The vulnerability of the patient population, the nature of interventions and cross-infection are but three of many factors. This is seen clearly if one compares the range between ophthalmology and critical care – 0–23%.3
The impact of nosocomial infection is impressive. Ventilator-associated pneumonia (VAP) is common, has significant morbidity with increased length of stay, associated costs and a twofold increase in mortality.4 It has been suggested that blood stream infections, surgical wound infections and nosocomial pneumonia result in 14, 12 and 13 attributable extra hospital days respectively.5 Catheter-related blood stream infection (CR-BSI) was also associated with major morbidity although, curiously, not necessarily mortality.6 The mortality rates directly due to these infections are hard to separate from the mortality attributed to the presenting severity of illness, which in its own right may have predisposed to infection. What is clear is that nosocomial infection is associated with increased mortality, and huge financial and resource costs.2
THE MECHANISMS INVOLVED IN NOSOCOMIAL INFECTION
A range of factors come together to enable nosocomial infection to occur. Some may be risk factors in their own right whereas other may simply represent an identifier of a sicker and therefore more vulnerable population (Table 62.2).
Patient |
Severity of illness |
Underlying diseases |
Nutritional state |
Immunosuppression |
Open wounds |
Invasive devices |
Multiple procedures |
Prolonged stay |
Ventilation |
Multiple or prolonged antibiotics |
Blood transfusion |
Environment |
Changes in procedures or protocols |
Multiple changes in staff; new staff |
Poor aseptic practice – poor hand-washing |
Patient-to-patient: busy, crowded unit, staff shortages |
The organism |
Resistance |
Resilience in terms of survival |
Formation of slime or ability to adhere |
Pathogenicity |
Prevalence |
HOST
The vulnerability of a potential host will be determined by several factors:
ENVIRONMENT
Local environmental pressures play their part. The combination of antibiotics, in particular multiple antibiotics, and cross-infection predisposes a vulnerable population to pseudomembranous colitis from Clostridium difficile toxin.8 Epidemiological patterns, such as the prevalence of Enterococcus faecalis as a common pathogen in the surgical population, may be linked to widespread cephalosporin usage. Much of the multiresistance problem probably originates from antibiotic pressures.9 Cross-infection is the biggest single problem in intensive care and transmission is by various means, but still the most common is by hands.10
ORGANISM
The host usually lives in synergistic or symbiotic tranquillity with a huge range of organisms (Table 62.3). Antibiotics suppress many normal organisms and allow the emergence and overgrowth of a usually insignificant organism or resistant organism of the same type. For example, an intrinsic organism such as Candida will flourish in the presence of broad-spectrum antibiotics and this overgrowth may result in symptomatic or even invasive candidiasis. Cephalosporin use may encourage the intrinsically resistant but quiescent enterococci to emerge as a dominant and problematic organism.
Site | Common commensal organisms |
---|---|
Skin | Staphylococcus epidermidis, streptococci, Corynebacterium (diphtheroids), Candida |
Throat | Streptococcus viridans, diphtheroids |
Mouth | Streptococcus viridans, Moraxella catarrhalis, Actinomyces, spirochaetes |
Respiratory tract | Streptococcus viridans, Moraxella, diphtheroids, micrococci |
Vagina | Lactobacilli, diphtheroids, streptococci, yeast |
Intestines | Bacteroides, anaerobic streptococci, Clostridium perfringens, Escherichia coli, Klebsiella, Proteus, enterococci |
THE ORGANISMS
A vast range of organisms can cause nosocomial infection (Table 62.4). It must be emphasised that each hospital and each ICU will have its own local ecology and knowing this ecology is important. Regional, national and international surveys give indications of general trends but this does not supplant local knowledge.
Methicillin-resistant Staphylococcus aureus (MRSA) |
Coagulase-negative Staphylococcus (CNS) |
Enterococcus spp. (E. faecalis, E. faecium) |
Pseudomonas aeruginosa |
Acinetobacter baumanii |
Stenotrophomonas maltophilia |
Enterobacter spp. |
Klebsiella spp. |
Escherichia coli |
Serratia marcescens |
Proteus spp. |
Candida spp. (C. albicans, C. glabrata, C. krusei) |
Other organisms may be a problem in the severely immunocompromised, such as those with acquired immunodeficiency syndrome (AIDS: see Chapter 60)
The combination of sick patients and widespread use of potent antibiotics selects out problematic organisms and, as this epitomises intensive care practice, it is in ICU where multiresistance is common.
MULTIRESISTANT ORGANISMS
Staphylococcal resistance to meticillin occurs due to an altered penicillin-binding protein, which has low affinity for all β-lactam agents. It is linked to a MecA gene. This gene does not develop readily and spread of meticillin resistance is by vector transmission, not de novo production of resistance7 (Table 62.5).
Antibiotics | ESBL-negative (% resistant) | ESBL-positive (% resistant) |
---|---|---|
Gentamicin | 8 | 76 |
Amikacin | 3 | 52 |
Ciprofloxacin | 3 | 31 |
All the above | 0 | 5 |
(Reproduced from Livermore DM, Yuan M. Antibiotic resistance and production of extended-spectrum beta-lactamases amongst Klebsiella spp. from intensive care units in Europe. J Antimicrob Chemother 1996; 38: 409–24.)
SOME COMMON ORGANISMS
See Table 62.4 for organisms responsible for the majority of nosocomial infections.
Escherichia Coli
E. coli was one of the first organisms to become multiresistant. The spread of its resistance is a model of how the problem develops in different environments. Currently in Europe, about 4% of E. coli is resistant to ceftazidime but in Turkey this figure is 26%. The trend towards an increase in resistance seems to correspond with the use of quinolones.11
Enterobacter species, cloacae and Aerogenes
Part of the normal intestinal flora, these species tend to develop ESBL relatively easily, making them multiresistant to a wide range of antibiotics, including ceftazidime. The prevalence of resistance in many western ICUs is running at about 35% and rising. This organism has been implicated in cross-colonisation in ICU and the relevant enzymes, including TEM-24, impart cross-resistance to multiple classes of antibiotics. Prompt recognition and treatment are usually effective.12
Pseudomonas
Pseudomonas are versatile opportunistic pathogens common in the critically ill; they may colonise patients with chronic lung disease. Resistance is able to develop in a range of ways and produces a very broad spectrum of resistance, making it potentially very difficult to treat and resulting in the increased popularity of combination therapy.13 It is associated with adverse outcome in the critically ill.14
Acinetobacter Baumanii
Acinetobacter baumanii is an increasing and major problem. It survives even in dry environments and, despite its name, spreads and cross-infects readily (a cineto: without movement). They are multiresistant and, although they were sensitive to carbapenems, they are increasingly resistant even to these agents, presumably through gene exchange. They become rapidly resistant and the profile of resistance is unpredictable but can be extremely broad, with some organisms recently only sensitive to colistin.15
Staphylococcus Aureus
This is a virulent pathogen causing a wide range of infections. Meticillin resistance started in the early 1960s, and although rates between countries and ICUs vary considerably, there has been an inexorable rise in its prevalence in most countries. It is easily identified. It both colonises and infects, but is relatively easily treated with glycopeptides. More recent reports of occasional glycopeptide-resistant organisms are therefore a major source of concern. It has been a model of the failure of some infection control methods. It is being increasingly assessed in terms of suppressibility with a selective decontamination of the digestive tract (SDD)-style approach to elimination.16
Enterococcus Faecalis and Faecium
These organisms emerged with increased third-generation cephalosporin use. E. faecalis is more commonly isolated and may still be sensitive to ampicillin but more than 30% are resistant to aminoglycosides. This contrasts with E. faecium, which has a resistance rate of 7% to vancomycin (and rising), 53% to ampicillin and 30% to aminoglycosides. Glycopeptide resistance is increasing and vancomycin-resistant enterococcus (VRE), unheard of 10 years ago, is now being regularly identified.17