The pathogenesis of catheter-associated urinary
tract infection
JMT Barford*, ARM Coates
Medical Microbiology, Centre for Infection, Division of Cellular and Molecular Medicine, St George's, University of London,
Email: jbarford@sgul.ac.uk
*Corresponding author
Accepted: 4 September 2008
Key words: Urinary catheterisation, urinary tract infection, bacteriuria, aetiology
Abstract
C atheter-associated urinary tract infection (CAUTI)
remains one of the most common types of hospital-
acquired infections. Further progress in the pre-
vention of CAUTI requires a better understanding of its
pathogenesis. Bacteria may enter the bladder through
contamination of the tip during insertion with the ora of
the distal urethra or from bacteria ascending the outside
or the inside of the catheter. Residual urine in the bladder
of catheterised patients increases the risk of bacteriuria.
During the process of infection, bacteria need rst to
adhere to the epithelial cells of the urinary tract and/or
the surface of the catheter. They will then develop into
biolms on the catheter surface and are resistant to the
immune system and antibiotics. Catheters by themselves
may cause immediate physical damage to the bladder
epithelium; they may be toxic and also cause inamma-
tion. Bacteria can also damage the epithelium and cause
inammation and the combination of both may be syner-
gistic in producing symptoms in the patient. Most epi-
sodes of catheter-associated bacteriuria are asymptomatic
but it is not known why some patients are symptomatic
and others are not. Further research into the pathogene-
sis of CAUTI needs to be carried out. A suggestion for the
prevention of CAUTI is the use of catheters with an addi-
tional eye-hole beneath the balloon to prevent residual
urine in the bladder or to remove the tip and balloon alto-
gether, with the additional benet of having no tip to cause
Peer reviewed paper
damage or inammation to the bladder epithelium.
Introduction
Catheter-associated urinary tract infection (CAUTI) is one of the most
common types of hospital acquired infection (Gravel et al, 2007; Lee
et al, 2007) and contributes to excess morbidity, mortality, hospital
stay and costs (Saint, 2000; Tambyah et al, 2002). However, there is
confusion about its clinical relevance and this is due, in part, to the
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lack of a clear denition of CAUTI. In this review, the term CAUTI will
be used to describe a symptomatic urinary tract infection (UTI) asso-
ciated with a urinary catheter. This is distinct from catheter-associated
bacteriuria (CAB), which refers to the presence of bacteria in the urine
without symptoms.
Although infection rates are reduced if catheter use is minimised
(Cornia et al, 2003; Reilly et al, 2006; Topal et al, 2005) and closed
drainage systems are used (Allepuz-Palau et al, 2004; Thornton and
Andriole, 1970), other preventive measures, such as antiseptic or
antibiotic-coated catheters, remain controversial (Jahn et al, 2007;
Schumm and Lam, 2008). For example, most clinical trials involving
silver alloy-coated catheters have found a reduction in rates of CAB
and CAUTI (Ahearn et al, 2000; Gentry and Cope, 2005; Karchmer
et al, 2000; Liedberg and Lundeberg, 1990; Liedberg et al, 1990;
Newton et al, 2002; Rupp et al, 2004; Seymour, 2006; Verleyen et al,
1999), but some found no signicant difference compared with con-
trol catheters (Bologna et al, 1999; Lai and Fontecchio, 2002;
Srinivasan et al, 2006). Also, silver oxide-coated catheters have not
been found to be effective (Brosnahan et al, 2004; Saint et al, 1998).
Further progress in the prevention and treatment of CAUTI requires
a better understanding of its development, which is also termed
pathogenesis. This review will cover what is known about the differ-
ent aspects of the pathogenesis of CAUTIs, focusing on indwelling
catheters rather than intermittent or suprapubic catheters. This is
because more is known about indwelling catheters and because they
cause the highest rates of infection (Horgan et al, 1992; Igawa et al,
2008; Saint et al, 2006). The review will not include discussion of
uncomplicated UTIs, which is a much broader topic and has been
covered elsewhere (Finer and Landau, 2004; Moore et al, 2002;
Schaeffer et al, 2001).
Pathogenesis of CAUTI
Inoculation/route of infection
How do micro-organisms get into the urinary tract? There are consid-
ered to be three main routes (Figure 1). Firstly, when the catheter is
Infection Prevention Society 2009
SAGE Publications
10.1177/1757177408098265
 C were not always responsible for the bacteriura, indicating that perhaps
Bladder
A susceptible to both urethral colonisation and bacteriuria. These nd-
B 2004), which also found an association between positive meatal cul-
Bacteria Catheter
Catheter
Bacteria
Figure 1. The potential routes for infection of the catheterised bladder (A) The catheter
pushes bacteria colonising the distal urethra into the bladder while being inserted.
(B) Bacteria colonising the distal urethra climb up the outside of the catheter after
it has been inserted. (C) Bacteria contaminating the drainage bag or catheter/bag
junction climb up the inside of the catheter
inserted, bacteria which colonise the distal urethra may be picked
up on the tip and pushed into the bladder. Secondly, after catheter
insertion, bacteria, again from the colonised distal urethra, may climb
up the outside of the catheter within the urethra through growth or
motility. The third possibility is that bacteria may contaminate
the lumen of the catheter, due to colonisation of the catheter bag or
contamination of the junction between the catheter and the catheter
bag, for example, if it is accidentally disconnected, and these bacteria
may then move up the inside of the catheter into the bladder. There
are no studies providing convincing evidence of which of these routes
is the most common or important or under which circumstances they
occur. However, there have been a number of studies which provide
indirect evidence.
Support for the contamination on insertion route of infection is
provided by a study (Barford et al, 2008a), which investigated the
colonisation of whole catheters removed from patients and compared
them with catheters removed from an in vitro ow model in which
bacteria were inoculated in the distal urethra prior to catheter inser-
tion. It was found that the patterns of colonisation on the patient
catheters were consistent with those found on catheters from the
model, suggesting that tip contamination on insertion might be a
possible route of infection. The possibility of bacteria moving up the
outside of the catheter has been conrmed (Kass and Schneiderman,
1957) by inoculating the periurethral area of three patients with
Serratia marcesans, subsequently recovered from the urine.
Making assumptions about the origin of bacteriuria based on the
detection of bacteria in the urine and catheter bag at different times
has been used in one study (Tambyah et al, 1999) to determine the
route of infection in patients. The probable route was determined in
69% of CAB cases, of which 18% were judged to be from catheter
insertion, 48% from the extraluminal route and 34% from the intralu-
minal route. A catheterised animal model (Nickel et al, 1985) showed
that contamination within the closed system and intraluminal ascend-
ing colonisation led to rapid infection of the bladder but that if the
Peer reviewed paper
sterile closed system was maintained, the extraluminal route was
more important, although the development of infection took longer.
Several studies have compared the micro-organisms found in the
urine with those colonising the urethral meatus, periurethral area or
rectum. In patients with spinal cord injury (Schaeffer and Chmiel,
1983), the source of 35% of bacteriuria episodes was the urethra and
the density of bacteria on the urethral meatus was greater in patients
who were bacteriuric. However, the strains that colonised the urethra
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host susceptibility is also important and some patients may be more
ings are supported by other studies (Garibaldi et al, 1980; Waites et al,
tures and bacteriuria, and a further study (Silva et al, 2007) found that
patients with Candida vaginal colonisation were more likely to
develop candiduria. The routes of infection may vary with gender
because urethral colonisation with the same organism preceded CAB
in 67% of women but only 29% of men and rectal colonisation pre-
ceded CAB in 78% of women but again only 29% of men (Daifuku
and Stamm, 1984). This suggests that colonisation of the periurethral
area may be an important risk factor for the development of CAB in
women but perhaps not so important in men.
Migration of bacteria along catheter surfaces has also been demon-
strated in vitro, including intraluminally against the ow of urine
(Johnson et al, 1997; Jones et al, 2004; Kumon et al, 2001; Nickel
et al, 1992; Rogers et al, 1996; Sabbuba et al, 2002).
Disruption of normal defences
The normal working of the urinary tract is altered by the presence of a
catheter. This makes it easier for bacteria to become established in the
bladder and cause infection. In indwelling catheters, the eye-hole
through which urine drains is above the balloon. This means that
urine can ll the bladder until it reaches this point before it drains
away and a residual pool of urine is probably constantly in the
bladder. This provides a reservoir in which bacteria can grow. The
normal ushing out of urine is also absent, which makes it easier for
bacteria to remain within the bladder. There is some disagreement in
the literature over whether residual urine is a risk factor for UTIs or
bacteriuria. Studies of patients undergoing assessment of bladder
emptying (Hampson et al, 1992) and patients in nursing homes
(Omli et al, 2008) found no additional risk of bacteriuria and symp-
tomatic UTI, respectively, with residual urine of greater than 100 ml.
However, elderly women with a large post-void residual volume had a
greater risk of recurrent UTI (Stern et al, 2004) and men undergoing
prostate evaluation were also at higher risk of developing bacteriuria if
the residual volume was greater than 180 ml (Truzzi et al, 2008). The
different conclusions from different studies could be due to the differ-
ent patient groups that were studied. However, the two studies that
found no increased risk used a cut-off of 100 ml to dene increased
residual urine but Truzzi et al (2008) found that 180 ml actually pro-
vided the best sensitivity and specicity for predicting positive urine
culture. The only evidence found in the literature to conrm that a
residual pool of urine in the bladder of catheterised patients actually
increases the risk of bacteriuria is a study (Rubino and Scialabba,
1983) showing that an additional eye-hole in the catheter below the
balloon, through which urine can drain, prevented the pool of residual
urine and also decreased the numbers of patients with bacteriuria.
Adhesion of bacteria
In order for bacteria to establish infection, they rst have to adhere to
the urinary tract and/or the catheter. When bacteria adhere to uroepi-
thelial cells, they use specic adhesins, often on projections from the
bacterial cell surface called pili or mbriae. This may help in initiating
or sustaining infection in the urinary tract (Daifuku and Stamm, 1986;
Mobley et al, 1987) and is partly dependent on the susceptibility of
the patient's epithelial cells (Schaeffer et al, 2001).
However, different mechanisms may be involved in adherence to
catheter materials. Bacteria may adhere directly to catheters: Proteus
mirabilis uses mannose-resistant (MR/P) mbriae (Rocha et al, 2007),
Providencia stuartii uses mannose-resistant Klebsiella-like (MR/K)
haemagglutinin (Mobley et al, 1988), Staphylococcus epidermidis uses
capsular polysaccharide adhesion (Muller et al, 1993) and Escherichia
Journal of Infection Prevention 51
 coli uses non-specic adhesion involving the capsular polysaccharide
colanic acid, electrostatic and van der Waals forces (Razatos et al,
1998; Reid et al, 1996), although the role of colanic acid is not certain
(Hanna et al, 2003). In vivo, the catheters may be coated with host-
derived proteins and other molecules to which bacteria can then attach,
for example, E. coli will adhere to surfaces coated in monomannose by
the specic type 1 mbrial adhesin FimH (Thomas et al, 2004).
Biolms
Once bacteria have attached to surfaces such as catheters, they form
biolms, which are communities of bacteria and secreted extracellular
polysaccharide attached to a surface (Donlan and Costerton, 2002).
These biolms can also be responsible for, and form part of, encrusta-
tions, consisting of calcium and magnesium phosphates. These miner-
als are precipitated from the urine as a result of an increase in pH
caused by the enzyme urease, which breaks down urea into ammonia
and is produced by certain bacteria such as P. mirabilis (Stickler et al,
2003). Bacteria which live as part of biolms can be very different
physically and behaviourally to bacteria growing in a liquid (Choong
and Whiteld, 2000). Some of the bacteria are very slow-growing or
dormant and resistant to antibiotics and the immune system (Anderl
et al, 2003). Some characteristics of bacteria are associated with or aid
biolm formation, for example, toxin, toxin and bronectin-binding
protein A in methicillin-resistant Staphylococcus aureus (MRSA)
(Ando et al, 2004) and the enzymes involved in the synthesis of inter-
cellular polysaccharide adhesin (ica genes) in S. epidermidis (Cho
et al, 2002). In E. coli, the rcsC sensor kinase helps to regulate the
production and secretion of colanic acid (Ferrieres and Clarke, 2003).
Type 3 mbriae (Burmolle et al, 2008; Ong et al, 2008), the outer
membrane protein OmpA (Orme et al, 2006) and the extracellular
structures called curli (Ryu et al, 2004) are also all involved in biolm
formation by E. coli. Quorum sensing molecules cause changes in a
biolm once a threshold of numbers is reached and is a type of com-
munication between bacteria (Stickler et al, 1998).
Bacteria combined with implants or foreign bodies on which they
can form biolms cause much more persistent infections than free
bacteria and are difcult to eradicate because of their innate resistance
to the immune system and antibiotics (Kadurugamuwa et al, 2005;
Ward et al, 1992; Zimmerli et al, 1982).
Effects of catheters and bacteria on the lower urinary tract
epithelial cell lining
Catheters and bacteria may have separate or combined effects on the
epithelium of the urinary tract, which may predispose to CAUTI.
Catheters may cause physical damage to, and exfoliation of, cells of
the bladder epithelium (Barford et al, 2008b). This increases the per-
meability of the uroepithelium because the impermeable supercial
umbrella cells are removed and may allow urea and other toxic com-
ponents of the urine into the tissue, causing irritation and inamma-
tion (Lavelle et al, 2002; Rajasekaran et al, 2006). Physical irritation of
the urethra may also cause nerve-mediated vascular permeability
(Abelli et al, 1991). Irrigation of the bladder may actually increase
damage to a vulnerable, already inamed bladder epithelium (Elliott
et al, 1989; Rao and Elliott, 1988) and negative pressure in the catheter
can suck the bladder mucosa into the eye-holes of the catheter causing
haemorrhagic pseudopolyps (Lowthian, 1991; Milles, 1965). Catheters
Peer reviewed paper
made out of different materials differ in the roughness of their surfaces
and the friction that they cause (Khoury et al, 1991; Lawrence and Turner,
2006), but it is not known how this may affect the damage that they
can cause to the urinary tract. Physical damage to the uroepithelium
may make it easier for bacteria to adhere and cause infection.
Catheter materials, especially latex, may be toxic to cells of the urinary
tract. Again, this may make it easier for bacteria to cause infection
but may also contribute to symptoms experienced by the patient.
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Latex catheters reduce viability, metabolic activity and cell proliferation/
DNA synthesis in animal and human cell lines and human urothelial
cells (Liedberg et al, 1990; Nacey et al, 1986; Pariente et al, 1998a,
1998b, 2000; Ruutu et al, 1985), but silicone catheters are non-toxic.
Catheters may cause inammation in the lower urinary tract, which
may contribute to the pathogenesis of CAUTIs. Increased numbers of
leucocytes were found in the urine (Anderson, 1979) and from ure-
thral swabs (Vaidyanathan et al, 1994) after catheterisation. As with
toxicity, latex catheters appear to stimulate more inammation than
silicone ones in patients (Bruce et al, 1976; Edwards et al, 1983;
Nacey et al, 1985; Talja et al, 1990), animals (Liedberg, 1989) and in
vitro (Barford et al, 2008b). Patients may also develop polypoid cysti-
tis, an inammatory reaction in the bladder, often due to catheters
(Anderstrom et al, 1984; Ekelund and Johansson, 1979), and the
grade of catheter reaction in the bladder correlates with the duration
of catheterisation (Goble et al, 1989).
It is known that bacteria stimulate the synthesis of cytokines such as
interleukin-6 (IL-6) and IL-8 by uroepithelial cells (Agace et al, 1993;
Funfstuck et al, 2001; Hedges et al, 1992, 1994) in vitro and these
cytokines are also found in urine from patients with UTI (Kassir et al,
2001; Olszyna et al, 2001; Otto et al, 1999, 2005; Rao et al, 2001),
although they are not specic to these infections. The secretion of
IL-8 has also been shown to recruit neutrophils to the site of infection,
which travel between the epithelial cells into the lumen of the bladder
(Agace et al, 1995; Cramer et al, 1980). This provides an explanation
for the correlation of bacteria and white blood cells in the urine of
infected patients (Stamm, 1983), which is less strong in catheterised
patients (Tambyah and Maki, 2000b).
There is little information in the literature about the effect of bacteria
and catheters combined on inammation. One study (Barford et al,
2008b) found that IL-6 and IL-8 were secreted from bladder epithelial
cells in culture after stimulation by E. coli, whereas silicone catheter
sections did not cause cytokine secretion. When both catheter sections
and E. coli were present there were higher levels of the cytokines than
either alone, but this was not statistically signicantly different. In
contrast, physical damage to the cell membranes of the epithelial cells
as measured by lactate dehydrogenase release was immediate due to
the catheter sections but delayed when caused by the bacteria. These
data suggest that whilst silicone catheters may damage the lining of
the urinary tract, bacteria cause inammation.
CAUTI and symptoms in patients
In catheterised patients, the presence of bacteriuria is not associated
with symptoms and most are asymptomatic (Steward et al, 1985;
Tambyah and Maki, 2000a). This may be partly because bacteria in
the urine and inside the catheter have no contact with the urethra,
which would normally be inamed and produce symptoms in uncom-
plicated UTIs. Another possible explanation could be that, as the
presence of the catheter makes it easier for bacteria to colonise the
urinary tract, there is less of a need for specic virulence factors to be
present to cause infection and so bacteria responsible for CAUTI are
less virulent than those responsible for uncomplicated UTIs (Venier
et al, 2007). This means that they may be less able to invade the
uroepithelium and cause serious damage to give the patient symp-
toms. It is easier for the bacteria to colonise the urinary tract but once
there cannot do much damage. Why some people with catheters and
bacteriuria develop symptoms and others do not is not known. Inam-
mation of the bladder may reduce the threshold for mechanical stimu-
lation to cause pain (McMahon et al, 1995).
Encrusted catheters may cause symptoms if they become blocked
and urine is retained within the bladder, causing distension. Infected
urine may be forced up the ureters if this condition is not treated, lead-
ing to pyelonephritis, kidney damage and/or septicaemia (Johnson
et al, 1993; Morris et al, 1999; Wilson, 2008).
 Prevention and control
Many different methods have been tried to prevent catheter-related
infection but few have been effective. The only really effective strategy
was the introduction of closed drainage to prevent intraluminal
ascending infection (Allepuz-Palau et al, 2004; Thornton and Andriole,
1970). Minimising catheter use also reduces the number of patients
that develop CAUTI (Cornia et al, 2003; Reilly et al, 2006; Topal et al,
2005). It is suggested that the best way to discover a means of pre-
venting these infections is to look at the pathogenesis of infection and
determine what makes catheterised patients more susceptible to colo-
nisation and infection than uncatheterised patients. One strategy to
be considered is minimising the effect a catheter has on the urinary
tract to reduce the disruption of normal functioning, which keeps the
urinary tract sterile. For example, catheters can be tted with taps or
valves (Addison, 1999; German et al, 1997) instead of bags so that
urine can be ushed out periodically instead of being continuously
drained in small amounts. Although they have not been demonstrated
to reduce infection rates in vivo, catheter valves are generally preferred
by patients (German et al, 1997; Wilson et al, 1997). Another possi-
bility is to have a catheter without the tip or balloon ending instead at
the internal urethral sphincter so that there is no pool of urine in the
bladder in which bacteria can multiply. A ow model (Barford et al,
2008a) has been used to test this theory and it was found that growth
of bacteria was delayed in the bladder compared with a control
catheter (unpublished data). The additional advantage of this model
is that there is no foreign body in the bladder and, therefore, no
damage or inammation of the bladder epithelium caused by the tip.
However, the method of securing the catheter in place remains to be
designed. A compromise might be to modify existing catheters by
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