Microorganisms that Cause HCAI

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Chapter: Pharmaceutical Microbiology : Public Health Microbiology: Infection Prevention And Control

Although some infectious agents causing HCAI are also involved in community acquired infectious diseases (norovirus, Salmonella spp., Staph. aureus), many HCAIs are caused by organisms particularly associated with healthcare.



Although some infectious agents causing HCAI are also involved in community acquired infectious diseases (norovirus, Salmonella spp., Staph. aureus), many HCAIs are caused by organisms particularly associated with healthcare. These bacteria are generally characterized by two properties: they tend to be resistant to many antibiotcics and have been selected by pressure of antibiotic usage in healthcare, and they are also generally opportunist pathogens with less capacity to produce illness in otherwise fit and healthy people but able to cause severe and life-threatening infection in those who are vulnerable and most susceptible because of their underlying diseases and/or their treatment. Some, in particular, can be associated with artificial implants and prostheses.


Staphylococcus aureus, Including MRSA


Staph. aureus is inextricably linked with human health and disease. Its natural habitat is the human skin particularly the anterior nares and the warm, moist skin folds of the perineum (and groin) and axilla and at any one time about one third of people are colonized with Staph. aureus, alternatively known as ‘carriers’. The nose is the principle carriage site in most (probably all but not always detectable) carriers with the skin sites also colonized in a smaller number. Staph. aureus has always been the most common cause of wound infections (accidental and surgical) and a leading cause of HCAIs. When penicillin was first used clinically in the early 1940s, almost all Staph. aureus strains were susceptible to it and it was widely used. By the late 1950s, 95% were resistant to penicillin due to natural selection of penicillinase (β-lactamase) producing strains. Meticillin (formerly known as methicillin), and the later oxacillin, cloxacillin and flucloxacillin, was developed to resist breakdown by β-lactamase and restore treatment options. Within a year of introduction, the first meticillin-resistant Staph. aureus (MRSA) strain was described. MRSA were interesting rarities in the 1960s and through the 1970s. In the 1980s, some MRSA strains (now called epidemic strains; EMRSA with sequential numbers) caused isolated and restricted outbreaks of HCAI which were mostly contained by a ‘search and destroy’ approach (i.e. isolate and treat the patient; screen all contacts among patients and staff for carriage; give decolonization treatment to any found to be positive). However, in the early 1990s in the UK, two EMRSA strains, 15 and 16, emerged with greater capacity to spread in healthcare settings and to cause a higher proportion of severe disease. Their spread through the healthcare system was not controlled and these strains became a major HCAI problem and the subject of media publicity, pressure group campaigns, and political concern in the early years of the 21st century. These strains were difficult to treat and caused significant morbidity and mortality. However, it must be remembered that MRSA is not a disease; it is a group of Staph. aureus strains that cause a wide range of HCAIs—wound and soft tissue infections, VAP, catheter-associated UTI, as well as the bacteraemias that have been a major focus for surveillance and preventive measures as being the most severe end of the spectrum of MRSA disease


Staphylococcus epidermidis (Coagulase-Negative Staphylococci)


Everyone carries Staph. epidermidis, and sometimes other coagulase-negative staphylococci (CNS), on their skin as part of the normal flora. These CNS are often antibiotic resistant (including being meticillin resistant) but have much less pathogenic potential than Staph. aureus for healthy people. However, they are one of the most common causes of HCAI associated with indwelling artificial devices and prosthesis. Despite the emphasis on MRSA bacteraemia, S.epidermidis is the most common cause of intravenous line-associated bacteraemia, but with more low-grade or ‘grumbling ’ clinical presentations and fewer severe and fatal infections than MRSA. It is also the commonest cause of late onset deep infections of implanted prostheses such as hip and knee joints and heart valves. In this respect they cause significant morbidity and treatment often requires removal and replacement of the original implant.


Gram-Negative Bacteria


Several distinct groups of Gram-negative bacilli have the capacity to cause opportunist infections in vulnerable patients, particularly those with various forms of immuno-suppression. All share a general characteristic of being able to survive in moist environmental conditions and being resistant to a range of antibiotics so that their survival and spread is selected by the widespread use of antibiotics in hospitals and other healthcare settings. This group of opportunist pathogens has long included organisms such as Pseudomonas aeruginosa (or other Pseudomonas species), Acinetobacter spp. and the resistant enterobacterial relatives of Escherichia coli EnterobacterSerratia and Klebsiella spp. All have caused serious infections in immuno-compromised patients, e.g. patients undergoing chemotherapy for a malignant disease in whom Gram-negative bacteraemias have a high incidence, often leading to clinical sepsis and death. Ps. Aeruginosa causes similar infections but also has a long association with pulmonary infection in cystic fibrosis patients.


Two further challenges from Gram-negative bacteria are causing concern with the emergence of new antibiotic resistance markers. The ß-lactaen antibiotics (penicillions and cephalosporins) have been mainstays of treatment of E. coli and related Gram-negative bacteria for many years. Strains of E. coli have now emerged that have acquired genes for the production of extended spectrum β-lactamases that break down all β-lactam agents. These ESBL-producing E. coli have become widely established in patients in hospitals and in other health and social care settings. Gut colonization is linked to urinary tract infection, especially when the patients are catheterized, and this can then result in bacteraemias that are very difficult to treat. Carbapenen antibiotics (e.g. imipenem) are important for treatment of these resistant Gram-negative HCAIs, so it is of special concern that some carbapenemase-producing Klebsiella spp. and other Gram-negative species are now being found in some UK and other European hospitals.


Glycopeptide-Resistant Enterococci


Enterococci (Enterococcus faecalis and Ent. faecium) have been recognized causes of HCAI in immunocompromised patients, e.g. post-transplant (including bonemarrow recipients) and cancer chemotherapy. These organisms are intrinsically resistant to many antibiotics and the mainstays of treatment where the glycopeptides vancomycin and teicoplanin. There was particular concern in the early 2000s when glycopeptide-resistant strains of Ent. faecium caused small but severe outbreaks in transplant and chemotherapy units. A suggested link to glycopeptide use in agriculture has not been proven, and although such strains still cause some serious infections, they have not become a widespread problem in other patient groups.


Clostridium difficile


Cl. difficile was discovered to be the major cause of antibiotic-associated diarrhoea and colitis simultaneously by groups in the UK and the USA in 1978. Although the subject of much interest and research amongst anaerobe microbiologists and a few infectious diseases physicians, it did not reach popular notoriety until the middle of the first decade of the 21st century. Cl. difficile is an anaerobic spore-forming organism found in the gut of many species of animal, including humans. With conventional bacteriological methods, about 3% of healthy people are found to carry Cl. difficile in their faeces. However, the figure is much greater in hospitalized patients and in residential nursing and care home residents. Patients with Cl. difficile diarrhoea excrete large numbers of spores into their surrounding environment where they can survive for weeks, months and even years. People with a normal, healthy gut flora can swallow Cl. difficilespores without ill effect, but in patients whose normal intestinal flora is disturbed, especially and most commonly by use of broad-spectrum antibiotics, the normal inhibition of Cl. difficile germination and growth is removed and Cl. difficile grows rapidly. The vegetative Cl. difficile cells attach to the gut mucosa and produce two toxins (A and B) that cause the disease. Toxin A is specifically called an enterotoxin whereas toxin B is a cytotoxin, but they show considerable structural and functional overlap and toxin B in particular can produce severe disease on its own when a strain that is A-negative/B-positive is the cause of the infection. The toxins cause diarrhoea, ranging from mild to profuse and debilitating, and colonic ulceration (which appears as erupting volcanoes on microscopy and biopsy specimens) that can develop into pseudo-membranous colitis with, at worst, toxic megacolon and colonic perforation.


The directly attributable mortality in several well-documented outbreaks has been around 10% during the initial stages of infection, but in the cohorts of elderly patients who have had CDI, the overall mortality over a period of 2–3 months can be as high as 40%.


The precipitating factor of antibiotic use and the range of severity of CDI have been recognized since the late 1970s and the infection was well documented in the 1980s in surgical patients from over-use of clindamycin and the cephalosporin antibiotics for surgical prophylaxis (and in immunocompromised groups), but it was not regarded as a priority. In an outbreak amongst elderly patients in hospital in the winter of 1991 in Manchester, there were more than 170 cases with 17 deaths. The patients were on open ‘Nightingale’ wards and most had received antibiotics for chest infections. For the first time, strain typing (by pyrolysis mass spectrometry at that stage) proved that the outbreak was caused by a single strain spread by cross-infection in the hospital setting. A subsequent Department of Health and Public Health Laboratory Service review and report provided guidance and recommendations that remained relevant a decade later but were not generally applied and acted upon with the rigour that was needed. The number of cases reported rose steadily during the 1990s and reached epidemic proportions by the early 2000s when the general increase was compounded by the emergence (in North America, the UK and Europe) of a new strain designated ribotype 027 with increased virulence and specific resistance to fluoroquinolone antibiotics which were being used increasingly in community and hospital practice. The serious impact of this disease meant that health services in the UK and elsewhere had to take specific and vigorous actions to bring down the unacceptably high incidence of CDI which was compromising the delivery of healthcare. Not only were patients suffering from a serious infection that compromised their underlying medical problems, but the management of these patients placed great pressure on hospital services overall and were a serious drain on health service resources.




Norovirus infections cause very significant disruption to hospital and social care services. This virus infection causes an explosive vomiting and diarrhoea with rapid onset and little preliminary warning that the patient is about to be ill. The vomitus and diarrhoea are heavily laden with the virus and the aerosols created by both are key to its rapid spread among contacts. The virus can spread directly by aerosol to the mucous membranes (mouth, nose, pharynx) of people in the same area. It will also contaminate items throughout the environment that can then themselves be a source of infection when those items of furniture, fittings, equipment, etc. are handled. The infection has a very high attack rate among those exposed and the post-infection immunity is generally very short-lived, so previous infection provides little protection. Both patients or residents and staff are usually affected in these outbreaks. Control of norovirus infection requires prompt and vigorous infection control precautions.


Fortunately, although unpleasant and debilitating when it occurs, norovirus infection is usually short-lived and recovery is quick in most patients. The acute vomiting and diarrhoea symptoms usually last for only 36–48 hours and most people then have only a few days of convalescence before feeling well again. Staff are usually able to resume work about 72 hours after the vomiting and diarrhoea has ceased, by which time they are no longer infectious. However, in health and social care settings where patients and residents are elderly and often frail, with severe underlying conditions, norovirus can be a more severe disease with significant associated morbidity and some mortality.


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