Pφ

Like the vast majority of all UTIs, hospital-acquired infections are ascending infections due to pathogens that colonize the periurethral area and distal urethral meatus, and then gain entry to the urinary tract via the ascending route. Instrumentation of the urinary tract facilitates ascending infection. Infection may be confined to the bladder (cystitis) or ascend to involve the kidney (pyelonephritis).

MB

Like all UTIs, the most common cause of health care–associated UTI is Escherichia coli. Depending on the length of hospitalization and prior antibiotic exposure, other pathogens that should be considered include other Enterobacteriaceae (Klebsiella, Enterobacter) and nosocomial gram-negative organisms such as Serratia, Providencia, Citrobacter, and Pseudomonas. Enterococcus species, including vancomycin-resistant enterococci (VRE), may also cause UTI in the hospital.

TP

In noncatheterized patients the clinical presentation will be the same as that for community-acquired UTI; suprapubic tenderness, fever, leukocytosis, and/or other signs of systemic toxicity may be the only clinical findings in patients who have indwelling urinary catheters.

Dx

The diagnosis of UTI should begin with a urinalysis (preferably with microscopic examination) to detect the presence of pyuria, followed by urine culture to confirm the microbiologic diagnosis. Patients with hospital-acquired UTI are at increased risk of antibiotic-resistant pathogens, so a urine culture with susceptibility testing should always be obtained, even if the urinalysis findings are strongly suggestive of UTI. As discussed above, the differentiation of asymptomatic bacteriuria and symptomatic UTI can be challenging, especially in patients with indwelling urinary catheters. Fever, leukocytosis, and other signs of systemic toxicity are suggestive of pyelonephritis rather than simple cystitis, and blood cultures should always be obtained to exclude concomitant bacteremia. Whether cystitis or pyelonephritis, hospital-acquired UTIs are always considered complicated infections.

Pφ

Both peripheral and central venous catheters are associated with catheter-related bloodstream infection. Infection can originate from organisms that colonize the skin at the catheter insertion site or from organisms that may colonize the catheter hub and or lumen at the junction of the catheter and the infusion tubing. Contamination of the infusate is a rare cause of catheter-related BSI but should be suspected in settings where multiple infections due to a single organism occur during a short time period. Catheters in the femoral vein are associated with the highest risk of infection, followed by those in the internal jugular vein, with subclavian vein catheters having the lowest risk of infection.

MB

Coagulase-negative staphylococci are the most common cause of catheter-related BSI, followed by Staphylococcus aureus. Enterococci and Candida species are increasing in incidence as a cause of catheter-related BSI; gram-negative organisms may also cause catheter-related BSI, particularly those associated with femoral vein CVCs.

TP

Fever may be the only symptom of catheter-related BSI, and the IV catheter should most certainly be considered as a likely source of infection in a patient for whom no other source of fever is readily apparent by history and physical examination. Local signs of phlebitis, inflammation, or tenderness at the catheter insertion site are extremely helpful in implicating the IV catheter as the source of infection; however, the IV catheter may still be the source of fever even if these local signs are absent.

Dx

Clinicians caring for patients with new fever and an IV catheter should always obtain blood cultures as part of the evaluation for a potential source of fever. It is necessary always to obtain two sets of blood cultures (from two separate venipuncture sites), especially since coagulase-negative staphylococci are the most common cause of catheter-related BSI and are the most common contaminant in blood cultures. For patients with a CVC, one set of cultures should be obtained from the catheter and one from a peripheral venipuncture. CVCs that are removed because of the possibility of infection should have qualitative culture of the catheter tip; the presence of >15 colony-forming units (utilizing the roll-plate technique) in the presence of a blood culture positive for the same organisms is strong evidence that the catheter was the source of the bacteremia, provided that no other source of infection is apparent on clinical examination.

Pφ

Like community-acquired pneumonias, the majority of HAPs are due to microaspiration of organisms that colonize the upper airways. In patients who are intubated (ventilator-associated pneumonia [VAP]), upper airway secretions may pool around the cuff of the endotracheal tube and are then aspirated during manipulation of the tube for suctioning or during positioning of the patient. HAP may also occur when the lungs are seeded hematogenously by BSI that originates from another site.

MB

Pathogens that commonly cause community-acquired pneumonia may occur in patients with early-onset (within the first 4 days of hospitalization) HAP. Aerobic gram-negative bacilli (including Pseudomonas aeruginosa) and S. aureus must be considered possible pathogens in those patients with onset of infection after 4 days of hospitalization as well as those with risk factors for drug-resistant pathogens. These risk factors include the following: previous antimicrobial therapy, a known high frequency of resistant pathogens in the unit on which the patient is hospitalized, and immunosuppressive therapy or disease.

TP

Fever, cough with sputum production, and worsening dyspnea are typical presenting features in patients with HAP. The clinical presentation may be more subtle in patients who are severely ill or debilitated, and in those with VAP. Focal findings on auscultation of the chest are helpful if present, but the absence of these findings is insufficient to exclude the possibility of pneumonia in patients with fever and respiratory symptoms.

Dx

The diagnosis of HAP should always be confirmed by a chest radiograph that shows a new or worsening infiltrate. Radiographic interpretation may be challenging in patients with preexisting radiographic abnormalities such as pulmonary edema. Efforts should be made to obtain a sputum sample for Gram stain and culture before the institution of empirical antibiotic therapy; a sputum specimen should always be obtained via endotracheal suction from patients who are intubated, as a negative sputum Gram stain in a patient with no recent change in antibiotic therapy virtually excludes the diagnosis of VAP. Blood cultures should also be obtained in all patients in an attempt to confirm a microbial etiology of the infection, although blood cultures are positive in a minority of patients with HAP.

Pφ

C. difficile is found among the normal colonic flora in <5% of healthy individuals in the community, but >20% of individuals who are hospitalized may become colonized with this organism. When the normal colonic flora are disrupted by the use of antimicrobial therapy, toxogenic strains of C. difficile may multiply and produce two exotoxins, toxin A and toxin B. These toxins are highly cytotoxic via the disruption of the cytoskeleton of colonic mucosal cells, leading to mucosal injury and inflammation.

MB

C. difficile is an anaerobic gram-positive bacillus. The organism forms spores that are resistant to antimicrobial therapy and frequently contaminate environmental surfaces, where they may serve as a source of nosocomial transmission. A new strain of C. difficile (the B1/Nap1 strain) has recently been recognized and appears to be responsible for epidemics of severe disease reported both in the United States and in other areas of the world.

TP

The most common clinical presentation of CDI is diarrhea that is typically large in volume and watery without associated blood or mucus. A small proportion of patients (≤5%) may actually present with constipation, rather than diarrhea. Patients may have associated abdominal cramping and lower abdominal pain. The spectrum of illness can range from mild diarrhea that spontaneously resolves with cessation of the antimicrobial therapy to severe disease accompanied by toxic megacolon and septic shock, often necessitating total colectomy. Leukemoid reactions, acute renal failure, severe hypoalbuminemia, and need for ICU admission are characteristic of the new epidemic strain.

Dx

The diagnosis of CDI must be considered in patients with diarrhea that occurs in association with antibiotic therapy, either current or recent (within the preceding 3 months). CDI has also been reported in association with certain antineoplastic agents. Virtually any antibiotic may predispose patients to CDI, and disease has been described after even a single dose of antibiotics given for perioperative prophylaxis. The diagnosis is confirmed by demonstration of the cytotoxin, rather than by culture, since patients may be colonized with the pathogen without disease. Traditional tissue culture–based cytotoxin assays are expensive and require special technical expertise; therefore, enzyme immunoassay techniques are most commonly used to demonstrate toxin A and/or B and confirm the diagnosis. Available assays are only about 75% sensitive, and a repeat assay may have to be performed in patients for whom there is a high index of clinical suspicion for CDI. Newer assays (glutamate dehydrogenase and polymerase chain reaction) appear to be more sensitive. The diagnosis may also be made by endoscopy that reveals pseudomembranes, characteristic raised yellowish lesions with skip areas of normal colonic mucosa.