Nosocomial infection

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Chapter 62 Nosocomial infection

Neil Soni

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).

Table 62.1 Principles of diagnosis of nosocomial infections

• Diagnosis of infection usually requires the combination of both clinical findings and the results of diagnostic tests
• Clinical diagnosis of infection from direct observation at surgery, endoscopy or other diagnostic procedure is an acceptable criterion for an infection
• It must be hospital-acquired. There must be no evidence that the infection was present or incubating at the time of hospital admission. Infection acquired in hospital, but only evident after hospital discharge, also fulfils the criteria
• Usually no specific time during or after hospitalisation is given to determine whether an infection is nosocomial or community-acquired. Each infection is examined for evidence that links it to hospitalisation (this is a matter of controversy)

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 site of infection varies with location so that, whereas the urinary tract and the chest are common throughout the hospital, within the ICU surgical wound infection, pneumonia and blood stream infection are far more common (8–12%).

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).

Table 62.2 Risk factors for nosocomial infection

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:

• the acute illness or problem that required ICU admission
• the chronic health status and underlying disease. Conditions such as diabetes predispose to infective problems
• the status of their immunocompetence, which may involve medications, such as steroids
• the integrity of natural defences, such as the skin and mucous membranes. This may be disrupted by burns, surgery or by breakdown of tissues such as pressure areas. The presence of invasive devices (e.g. endotracheal tube, intravenous devices) provides a conduit past the natural defences
• antibiotics given to the patient which may encourage emergence of particular strains or resistant organisms
• blood transfusion has been suggested as a risk factor7

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.

Table 62.3 Common commensals that may cause infection in a vulnerable host

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

Extrinsic organisms may be introduced from the environment, from other patients, from staff or from surfaces. These may be organisms which are thriving in that environment because of local pressures (e.g. antibiotics), or from poor hygiene. Examples include Acinetobacter and, of course, meticillin-resistant Staphylococcus aureus (MRSA). On admission, patients will be carrying a range of organisms that have the potential to cause problems, but during their stay they are likely to acquire a new ecology from their surroundings. In a hospital that ecology may be quite hostile, with multiresistance being common.

The individual characteristics of the organism are important. These include their resilience in the local environment, the ease of transmission and the individual pathogenicity. This clearly interacts with the vulnerability of the host, as some usually innocuous organisms, such as Candida or Serratia marcescens, will only cause problems in vulnerable hosts whereas others, such as some strains of Staphylococcus aureus, Acinetobacter or Clostridium difficile, may be intrinsically more virulent.

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.

Table 62.4 Organisms responsible for the majority of nosocomial infections

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)

Nosocomial infection is dynamic in that it is influenced by many environmental factors, the type of patient, type of surgery or illness, the antibiotic usage profile and many other variables. This dynamism is illustrated by the Gram-positive infections of the 1950s and 1960s, giving way to the Gram-negative infections of the 1970s and, while the multiresistant Gram-positive organisms are a major anxiety currently, they are already being superseded by superresistant organisms, such as Stenotrophomonas and Acinetobacter. The ease of transmission or development of resistance is a key factor in the current explosion in multiresistance.

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.

The organisms causing nosocomial infection may be endogenous or exogenous. Illness and antibiotics may both encourage the emergence and overgrowth of endogenous organisms that were normally suppressed and hence ecological change takes place in the skin, nasopharynx and gut. Alternatively the same factors influence colonisation with exogenous organisms from the environment. Cross-infection plays a significant role, as does the size of the local reservoir of exogenous organisms. The colonising organisms are well placed to invade or be introduced by invasive procedures, by devices or simply through areas of injury. Infection follows.

MULTIRESISTANT ORGANISMS

Many of the organisms that cause nosocomial infection are characterised by multiresistance. There are several mechanisms involved in resistance and in its spread. Enzymes, such as the β-lactamases, render a large array of antibiotics useless. Class 1 β-lactamase is effective against some β-lactam-containing antibiotics but extended-spectrum β-lactamases (ESBL), which incorporate enzymes, such as TEM-24, will produce cross-resistance to multiple classes of antibiotics, including fluoroquinolones and aminoglycosides. Resistance may be produced by a combination of mechanisms, such as in Pseudomonas aeruginosa, where the resistance is due to a combination of derepression of protein efflux systems, cephalosporinases and derepression of AmpC enzyme.

Resistance is acquired in a variety of ways. Mutation of any gene occurs at a rate of one cell in 107 and, if this cell is then presented with antibiotics that it can survive, it will become a dominant cell, reproducing at a rate of 109 overnight. An example of this might be the development of AmpC β-lactamase in Enterobacter, when patients are treated with third-generation cephalosporins. A similar example is the loss of porin OprD in P. aeruginosa in the presence of imipenem.

The big problem, particularly with ESBL, is that they can spread by plasmid transmission which is very rapid. The enzyme production is encoded chromosomally within an organism, and can then be transferred between bacteria by plasmids. Transposons transfer genes between plasmids. Examples of this include:

1 SHV-1 plasmid β-lactamase from Klebsiella
2 plasmid AmpC β-lactamases from Citrobacter
3 aminoglycoside-modifying enzymes from aminoglycoside-producing streptomycetes

The phenomenon of induction is also seen. This is the process whereby the presence of an antibiotic appears to ‘induce’ or speed up the production of the relevant enzyme so that the organism rapidly becomes resistant.

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).

Table 62.5 The influence of extended-spectrum β-lactamases (ESBL) on resistance in Klebsiella

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

Klebsiella

Klebsiella has become increasingly resistant with the acquisition of ESBL, and can be multiresistant. The incidence is incredibly variable between countries.

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

Stenotrophomonas Maltophilia

This is an increasingly common and troublesome environmental organism. It is often resistant to β-lactam antibiotics, quinolones and to aminoglycosides. It also produces a carbapenamase, which makes it resistant to carbapenems.

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

Coagulase-Negative Staphylococci (CNS)

CNS are low-virulence organisms, but are increasingly causing nosocomial infection. Their resilience may be in part due to the production of biofilm. Frequently meticillin-resistant, they are also resistant to multiple classes of antibiotics, but are usually sensitive to glycopeptides. As glycopeptide resistance patterns alter, newer agents, such as quinupristin, dalfopristin and linezolid, will have a role.

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

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