Surveillance for Asymptomatic and Hospital-Acquired Urinary Tract Infection

Chapter 193

Surveillance for Asymptomatic and Hospital-Acquired Urinary Tract Infection

Generally a patient develops a urinary tract infection (UTI) when microbial colonization leads to adherence, multiplication, and persistent invasion of the urinary tract. However, in some patients bacteria exist within the urinary tract without causing disease or clinical signs, and these patients are said to have bacterial colonization or bacteriuria. Long-term asymptomatic bacteriuria has been documented in human patients; it may result when organisms lack the virulence traits necessary to adhere and cause disease, and these organisms may protect the urinary tract by competing with pathogenic bacterial strains. Although specific diagnostic and therapeutic guidelines have been developed for asymptomatic bacteriuria in human beings, the role and significance of asymptomatic or subclinical bacteriuria is much less clear in veterinary medicine, and evidence-based guidelines are not yet available.


Host factors and bacterial factors both affect whether a microbial organism can persist and cause infection within the urinary tract. Numerous local and systemic components of the host immune system protect against infection, and alterations in these immune defenses can predispose to the development of UTI. Local immunity involves normal micturition (complete and regular voiding), physiologic and anatomic features (peristalsis, length of the urethra, ureterovesical valves), mucosal defense barriers (glycosaminoglycans, mucosal exfoliation, competition from normal distal flora), and antimicrobial properties of urine (urea, organic acids, Tamm-Horsfall proteins, hyperosmolality, and extreme pH), whereas systemic immunity can be humoral or cell mediated.

The majority of UTIs are caused by bacteria that ascend the urogenital tract, and bacteria may possess virulence traits that increase their ability to overcome local defenses and ascend, adhere, and cause disease. These virulence factors can include adhesins (fimbriae, pili), toxins (cytotoxic necrotizing factor, hemolysin), methods of avoiding the host immune system (capsular antigen), and ways to utilize host nutrients (aerobactin). In addition to bacteria, Candida can cause ascending UTI, especially in immunosuppressed patients. Hematogenous spread of bacterial and fungal organisms to the urinary tract occurs less frequently.

Risk Factors

Various studies have evaluated the risk and prevalence of UTI in veterinary patients with specific comorbidities or concurrent therapies. Although most authors consider a finding of more than 1000 colony-forming units (CFU)/ml in a quantitative culture of urine (collected by cystocentesis) to be significant, authors use a variety of definitions of UTI; specific definitions used in each study described here have been included when relevant.

Exogenous and Endogenous Steroids

It has long been believed that glucocorticoid therapy, by suppressing local and systemic immunity, may predispose to UTI. Two studies found positive urine culture results in 39% of dogs (Ihrke et al, 1985) and 18% of dogs (Torres et al, 2005) with chronic skin disorders that received long-term low-dose corticosteroids, compared with no positive urine culture results in dogs with chronic skin disorders that did not receive steroids. In these studies, no dogs had clinical signs of UTI. The type of steroid administered, frequency of administration, duration, and dosage of corticosteroid were not correlated with culture results. Dogs receiving short-term steroid therapy also may be affected because dogs administered dexamethasone in the 48 hours before hospital admission for surgical fixation of intervertebral disk disease were 11.4 times more likely to have a positive urine culture result (>5 CFU/ml) than dogs undergoing such surgery that had not received dexamethasone (Levine et al, 2008). For patients with intervertebral disk disease, this increased risk may be due to the immunosuppressive properties of dexamethasone in combination with altered neurologic function (inability to void completely). Of dogs with naturally occurring hyperadrenocorticism, 46% were found to have a UTI (>1000 CFU/ml), but clinical signs of UTI were rare (Forrester et al, 1999). UTI in these dogs may be caused by systemic immunosuppression, dilute urine causing local alterations in immunity, or concurrent disease. The antiinflammatory properties of glucocorticoids also may influence the development of clinical signs related to UTI and the presence of pyuria on urine sediment examination.

Diabetes Mellitus

Veterinary patients with diabetes mellitus have been considered at increased risk for UTI because of factors such as immunosuppression, inappropriate urine concentration, and glucosuria. In human patients, diabetic individuals with asymptomatic bacteriuria do not have an increased risk of developing symptomatic UTI or other diabetic complications requiring hospitalization; no similar data are available for companion animals. In canine studies, UTI (>1000 CFU/ml) was present in 24% to 37% of dogs with diabetes mellitus, but few patients had clinical signs specific for UTI (Forrester et al, 1999; McGuire et al, 2002). Cats with diabetes mellitus also may be at increased risk of subclinical UTI, with 12% to 13% of diabetic cats found to have bacterial growth in their urine; clinical signs were present in 14% to 44% of those with bacterial growth (Bailiff et al, 2006; Mayer-Roenne et al, 2007). Emphysematous cystitis, most often caused by gas production associated with Escherichia coli invasion of the urinary bladder wall, is a complication of UTI specifically recognized in diabetic veterinary patients as well.

Miscellaneous Systemic Conditions

Numerous other systemic illnesses may predispose dogs and cats to clinical or subclinical UTI. In one study, 12% of hyperthyroid cats had positive urine culture results, but no cats had clinical signs of a UTI (Mayer-Roenne et al, 2007). In dogs with parvoviral enteritis, 23% developed subclinical UTI (>1000 CFU/ml), suspected to be caused by fecal contamination of the urogenital tract combined with neutropenia (Koutinas et al, 1998). It is also commonly believed that veterinary patients receiving chemotherapy or nonsteroidal immunosuppressive therapy (e.g., cyclosporine) are at increased risk of UTI due to immunosuppression. Finally, morbidly obese dogs (>45% body fat) have been documented to have 7.5 times greater risk of asymptomatic UTI than dogs with less than 45% body fat (Lusby et al, 2011).

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Surveillance for Asymptomatic and Hospital-Acquired Urinary Tract Infection
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