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.
MICROORGANISMS THAT CAUSE HCAI
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.
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
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.
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 Enterobacter, Serratia 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.
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.
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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