Pseudomonas, Burkholderia, and Stenotrophomonas

Keywords

• bacteremia

• biofilm

• burn wound sepsis

• conjunctivitis

• cystic fibrosis

• ecthyma gangrenosum

• immunosuppressed

• neutropenia

• urinary tract infection

• ventilator-associated pneumonia

Etiology

Pseudomonas aeruginosa is a gram-negative rod and is a strict aerobe. It can multiply in a great variety of environments that contain minimal amounts of organic compounds. Strains from clinical specimens do not ferment lactose, are oxidase positive, and may produce β-hemolysis on blood agar. Many strains produce pigments, including pyocyanin, pyoverdine, and pyorubrin, that diffuse into and color the surrounding medium. Strains of P. aeruginosa are differentiated for epidemiologic purposes by a variety of genotyping methods, including restriction fragment length polymorphisms using pulsed-field gel electrophoresis, multilocus sequence typing, and more recently, whole genome sequencing.

Epidemiology

P. aeruginosa is a classic “opportunist.” It rarely causes disease in people who do not have a predisposing risk factor. Compromised host defense mechanisms resulting from trauma, neutropenia, mucositis, immunosuppression, or impaired mucociliary transport explain the predominant role of this organism in producing opportunistic infections. In pediatric settings, it is most frequently seen in the respiratory secretions of children with cystic fibrosis (CF). P. aeruginosa was found in 1% of neonates with fever and bacteremia in a review of 6 U.S. centers. One series of neonatal intensive care unit (NICU) infections reported that 3.8%episodes of neonatal bacteremia from 1989–2003 were caused by P. aeruginosa . Another children's hospital reported 232 episodes of P. aeruginosa bacteremia over a 10 yr period, with half the infected children diagnosed with an underlying malignancy.

P. aeruginosa and other pseudomonads frequently enter the hospital environment on the clothes, skin, or shoes of patients or hospital personnel, with plants or vegetables brought into the hospital, and in the gastrointestinal (GI) tract of patients. Colonization of any moist or liquid substance may ensue; the organisms may be found growing in any water reservoir, including distilled water, and in hospital kitchen sinks and laundries, some antiseptic solutions, and equipment used for respiratory therapy and urinary procedures. Colonization of skin, throat, stool, and nasal mucosa of patients is low at admission to the hospital but increases to as high as 50–70% with prolonged hospitalization and with the use of broad-spectrum antibiotics, chemotherapy, mechanical ventilation, and urinary catheters. Patients’ intestinal microbial flora may be altered by the broad-spectrum antibiotics, reducing resistance to colonization and permitting P. aeruginosa in the environment to populate the GI tract. Intestinal mucosal breakdown associated with medications, especially cytotoxic agents, and nosocomial enteritis may provide a pathway by which P. aeruginosa spreads to the lymphatics or bloodstream.

Pathology

The pathologic manifestations of P. aeruginosa infections depend on the site and type of infection. Because of its elaboration of toxins and invasive factors, the organism can often be seen invading blood vessels and causing vascular necrosis. In some infections there is spread through tissues with necrosis and microabscess formation. In patients with CF, focal and diffuse bronchitis/bronchiolitis leading to bronchiolitis obliterans has been reported.

Clinical Manifestations

Most clinical patterns are related to opportunistic infections in immunocompromised hosts (see Chapter 205 ) or are associated with shunts and indwelling catheters ( Chapter 206 ). P. aeruginosa may be introduced into a minor wound of a healthy person as a secondary invader, and cellulitis and a localized abscess that exudes green or blue pus may follow. The characteristic skin lesions of P. aeruginosa, ecthyma gangrenosum , whether caused by direct inoculation or a metastatic focus secondary to septicemia, begin as pink macules and progress to hemorrhagic nodules and eventually to ulcers with ecchymotic and gangrenous centers with eschar formation, surrounded by an intense red areola ( Table 232.1 and Fig. 232.1 ).

Outbreaks of dermatitis and urinary tract infections (UTIs) caused by P. aeruginosa have been reported in healthy persons after use of pools or hot tubs. Skin lesions of folliculitis develop several hours to 2 days after contact with these water sources. Skin lesions may be erythematous, macular, papular, or pustular. Illness may vary from a few scattered lesions to extensive truncal involvement. In some children, malaise, fever, vomiting, sore throat, conjunctivitis, rhinitis, and swollen breasts may be associated with dermal lesions. UTIs caused by P. aeruginosa are most often nosocomial and are often associated with the presence of an indwelling urinary catheter, urinary tract malformations, and previous antibiotic use. UTIs may be minimized or prevented by prompt removal of the catheter and by early identification and corrective surgery of obstructive lesions when present.