The ‘chain of infection’ is the phrase used to describe the process by which infection can spread from one susceptible individual to another. It has been criticized for being a biomedical model as opposed to a biosocial model, focusing on the microbiological, physical and environmental aspects of the infection process, and excluding the various social and psychological factors that play a role in cross-infection (Elliott, 2009). However, it has its origins in what is known about the nature of microorganisms and how they are transmitted, and the concept of there being a ‘chain’ in the infection process is one which has become firmly established and utilised widely within infection prevention and control. For an infection to occur, all of the links in the chain must be intact and in the correct order. In order to break the chain, it is important that healthcare workers understand how the different components of the chain interact and facilitate the spread of infection. Then, the basic principles of infection prevention and control can be applied to clinical practice to break the chain.
Link 1: causative organism
This can be any organism that demonstrates pathogenicity and/or virulence, which are not necessarily one and the same thing. Pathogenicity is the ability of the organism to cause infection.
Not all organisms are pathogenic, and those that are may cause infections that range from asymptomatic or mild, to severe. Virulence refers to the organism’s ability to cause severe disease, and while all pathogens are able to cause disease, some are more virulent than others. The degree of virulence is dependent on the host’s susceptibility and the virulence factors that the organism possesses (see Chapter 5).
Fact Box 8.6 Virulence
An example of virulence can be demonstrated by looking at Shigella and Salmonella, two medically important bacteria which cause severe diarrhoea. While 10–1000 Salmonella cells are required to cause salmonellosis, only 10 Shigella cells will cause diarrhoea, making Shigella a more virulent organism than Salmonella (Engelkirk and Duben-Engelkirk, 2011).
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Fact Box 8.7 Reservoirs and sources
Patients can become a source of infection if they have infected skin lesions, skin scales, secretions and excretions which can easily be transferred to other people. Organic material such as dirt, blood and body fluids can harbour bacteria and viruses, and any equipment that has been in contact with the patient can serve as both a reservoir and a source of infection.
Bed frames, mattresses and manual handling equipment have all been implicated in the spread of infection (O’Connor, 2002).
Links 3 and 4: portal of exit and portal of entry
There are many different portals of exit, which are the routes by which the organism leaves the reservoir and enters the host. These include the respiratory and gastro-intestinal tracts and the skin and mucosa, with organisms carried in blood and body fluids, in respiratory droplets and on the surface of the skin. In some organisms, the portal of exit can be the same as the portal of entry, such as the respiratory tract in tuberculosis, or it may be different; in Salmonella infections, the route of entry is the mouth as Salmonella has to be ingested, and the exit route is in the faeces.
Link 5: mode of transmission
This refers to the way in which the organism is spread and acquired.
Direct contact with infected body fluids, secretions and lesions can transmit infections such as HIV, the common cold and impetigo. The hands of healthcare workers are the most important source of cross-infection, transferring resident and transient skin flora (see Chapter 14). Fomites are objects which can become contaminated with organisms from patients or staff, and subsequently become a source of cross-infection. They include IV stands, pumps and monitors, bed linen, computer keyboards and telephones. The risk that these pose depends largely on the degree or extent to which the object or piece of equipment is contaminated, the microbial load and the amount of direct contact that it has with the patient. However, even if it does not come into contact with the patient, the hands of any healthcare workers who may have had contact with it could serve as vehicles for cross-infection.
Airborne transmission of particles such as dust, water and respiratory droplets, which can all contain microorganisms, can result in infection if they are inhaled or if they settle on equipment or wounds. Legionella is present in aerosols which can, depending on wind speed, travel up to 500 m and infect large numbers of people. Pathogens may be expelled from the respiratory tract during coughing, sneezing and talking. These droplets partially evaporate to form droplet nuclei, where they remain suspended in the air for long periods of time and can subsequently be inhaled. Other droplets, or large dust particles, may fall rather rapidly and settle on furniture, bedding or equip- ment, and although they are unlikely to become airborne again, they can still cause infection.
Bacteria may be ingested through consuming contaminated food or water (e.g. cholera, Campylobacter and Salmonella). Patients may also acquire some infections as a result of faecal-oral transmission, whereby their hands have become contaminated and they subsequently move their hands to their mouth (e.g. C. difficile). Norovirus can be spread by both the airborne and the faecal-oral routes (Chapter 23).
Transmission of blood-borne viruses such as HIV and hepatitis B and C via inoculation injury, either from a contaminated sharp (see Chapters 14 and 24) or a splash of blood or body fluids into the mucosa, can pose a big risk to healthcare workers.
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As described in this chapter, some infections may also be spread endogenously – they are acquired as the result of the patient’s own body flora being transferred from one body site to another.
Link 5: the susceptible patient
Any patient in a hospital bed is potentially at risk of contracting an infection during their in-patient stay, but there are many factors which significantly increase that risk.
Age: With increasing age, the ability of the immune system to fight infection naturally declines.
This affects the efficiency of both the innate and the acquired responses, particularly decreased antibody and lymphocyte responses, and lowered response to vaccination. This is a natural decline known as immunosenescence (Dieffenbach et al., 2009).
Fact Box 8.8 Immunosenescence
A weakened immune response means that fever, which is a normal clinical response to infection, may be absent or suppressed, and the first indications of an infection may actually be non-specific signs such as lack of appetite, confusion and malaise (Rajagopalan and Yoshikawa, 2001; Destarac and Ely, 2002). Elderly individuals often have a reduced cough reflex and are more vulnerable to serious respiratory tract infections, particularly pneumonia, as up to 40% of lung function decreases by the age of 70 (Knight and Nigam, 2008a). The skin is more easily damaged and prone to tears due to the weakening of the collagen content of the dermis, which means that the skin loses some of its elasticity or ‘bounce-back’ (Bianchi and Cameron, 2008). While gastric acid secretion is part of the immune defence, creating an inhospitable, acidic environment for microorganisms, it can cause gastric ulcers by weakening and damaging the protective stomach lining or mucosa (Knight and Nigam, 2008b). To reduce gastric acid secretion and prevent gastric ulcers, proton pump inhibitors such as Omeprazole are prescribed. However, the downside of this is that they can increase the risk of colonisation or infection with C. difficile (Dial et al., 2004).
Babies in the uterus are sterile up until the membranes rupture, and then they are exposed to the genital and perineal flora of the mother during childbirth, and to the outside world, and they rapidly become colonised (Ryan and Ray, 2010). Premature infants are particularly susceptible to infection, and have no immunological memory together with a reduced ability to develop specific antibodies against the microorganisms that they are exposed to (Petrova and Mehta, 2007). Their protection against infection is mostly dependent upon innate immune defences. However, due to their prematurity, natural barriers such as the skin and mucosa are weakened. They have an immature and undeveloped population of T lymphocytes, and decreased neutrophil efficiency (although the neutrophil count rises abruptly within the first 24 hours after birth and stabilizes within 72 hours, neutrophil production in response to an infection is underwhelming) (Petrova and Mehta, 2007), and they are deficient in some components of the complement cascade (Petrova and Mehta, 2007; Anderson-Berry and Bellig, 2010).
Nutritional status: Poor nutritional intake compromises the immune system and increases the risk of infection (Cowan et al., 2003; Kenkmann et al., 2010). Malnutrition, which affects 40–60%
of older people admitted to hospital (Morse and High, 2004), results in low concentrations of
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serum albumin (hypoalbuminemia), which can be a poor prognostic indicator when treating serious infections, for example severe C. difficile infection (see Chapter 22).
Loss of mobility: This can breach the body’s first line of defence, the skin, leading to skin damage and potential pressure sore formation.
Co-existing illness or disease: The presence of a known or undetected underlying illness increases an individual’s susceptibility to infection. For example, wound infection is a major complication of diabetes as a result of impaired leukocyte function and delayed migration of neutrophils and macrophages to the wound or site of inflammation (Hirsch et al., 2008), and the risk of surgical wound infection is estimated to be 2–5 times greater in diabetics, as compared to non-diabetics (Golden et al., 1999).
Immunocompromised as a result of underlying illness or treatment: In individuals who are immunocompromised as a result of chemotherapy or radiotherapy, damage occurs to the mucosal barriers in the mouth and GI tract, leading to inflammation, ulceration and diarrhoea. Neutrophils can become severely depleted owing to suppression of the bone marrow, giving rise to a potentially life-threatening condition known as neutropenia, which is a neutrophil count of less than 1000/
mm3, with the risk of infection increasing substantially if the count drops below 500 mm3 (see Chapter 9).
Medication: The balance of the resident microbial population of the colon can be adversely affected by the administration of antibiotics. While the colonic micro-flora is generally resistant to colonisation by C. difficile, which is part of the normal bowel flora in 2–5% of the population and readily acquired in the healthcare setting, with carriage rates reported of approximately 15%
(Poutanen and Simor, 2004), C. difficile can grow unchecked, proliferating within and colonising the colon, and giving rise to systemic infection (see Chapter 22).
The presence of invasive indwelling devices: The presence of an invasive indwelling device that breaches the skin (e.g. a peripheral intravenous cannula) or a sterile organ (e.g. a urinary catheter inserted into the bladder) significantly increases the risk of infection as critical lines of defence are breached.
Duration of hospital stay: The duration of hospital stay and bed occupancy hospital rates increase the risk of patients becoming colonised with MRSA (see Chapter 20) or C. difficile. The average bed occupancy rates in 1996–1997 were 80.8%, increasing to 86.5% in 2002–2003; in 2008/09–2009/10, one-quarter of NHS Trusts had bed occupancy rates exceeding 90%. Trusts with greater than 90% occupancy were found to have MRSA rates that were 10 times greater than those with bed occupancy rates of less than 85% (Department of Health, 2007).
Think of a microorganism, or reflect on a colonised or infected patient care in your care, and then work your way through the chain of infection, considering each of the remaining five links in turn and the infection control precautions and preventions that need to be taken in order to interrupt each link.