Pseudomonas, Stenotrophomonas and  Burkholderia

Pseudomonads are Gram-negative, aerobic, rod-shaped bacteria with widespread occurrence in nature, especially in damp biotopes. The most important species from a medical point of view is Pseudomonas aeruginosa. Free O₂ is required as a terminal electron acceptor to grow the organism in cultures. The pathogenesis of Pseudomonas infections is complex. The organism can use its attachment pili to adhere to host cells. The relevant virulence factors are: exotoxin A, exoenzyme S, cytotoxin, various metal proteases, and two types of phospholipase C. Of course, the lipopolysaccharide of the outer membrane also plays an important role in the pathogenesis. Pseudomonas infections occur only in patients with weakened immune defense systems, notably pneumonias in cystic fibrosis, colonization of burn wounds, endocarditis in drug addicts, postoperative wound infection, urinary tract infection, sepsis. P. aeruginosa frequently contributes to nosocomial infections. Diagnosis requires identification of the pathogen in cultures. Multiple resistance to anti-infective agents presents a therapeutic problem.

Numerous other Pseudomonas species and the species of the genera Burk-holderia and Stenotrophomonas are occasionally found in pathogenic roles in immunosuppressed patients. B. mallei causes malleus (glanders) and B. pseu-domallei causes melioidosisl.

Pseudomonas aeruginosa

Occurrence, significance. All pseudomonads are widespread in nature. They are regularly found in soils, surface water, including the ocean, on plants and, in small numbers, in human and animal intestines. They can proliferate in a moist milieu containing only traces of nutrient substances. The most important species in this group from a medical point of view is P. aeruginosa, which causes infections in person with immune defects.

Morphology and culture. P. aeruginosa are plump, 2-4 µm long rods with one to several polar flagella. Some strains can produce a viscous extracellular slime layer. These mucoid strains are frequently isolated in material from cystic fibrosis patients. P. aeruginosa possesses an outer membrane as part of its cell wall. The architecture of this membrane is responsible for the natural resistance of this bacterium to many antibiotics.

P. aeruginosa can only be grown in culture mediums containing free O2 as a terminal electron acceptor. In nutrient broth, the organism therefore grows at the surface to form a so-called pellicle. Colonies on nutrient agar often have a metallic sheen (P. aeruginosa; Latin: aes = metal ore). Given suitable conditions, P aeruginosa can produce two pigments, i.e., both yellow-green fluorescein and blue-green pyocyanin.

Pathogenesis and clinical pictures. The pathomechanisms involved are highly complex. P. aeruginosa usually enters body tissues through injuries. It attaches to tissue cells using specific attachment fimbriae. The most important virulence factor is exotoxin A (ADP ribosyl transferase), which blocks translation in protein synthesis by inactivating the elongation factor eEF2. The exoenzyme S (also an ADP ribosyl transferase) inactivates cytoskeletal proteins and GTP-binding proteins in eukaryotic cells. The so-called cytotoxin damages cells by creating transmembrane pores. Various different metallo-proteases hydrolyze elastin, collagen, or laminin. Two type C phospholipases show membrane activity. Despite these pathogenic determinants, infections are rare in immunocompetent individuals. Defective nonspecific and specific immune defenses are preconditions for clinically manifest infections. Patients suffering from a neutropenia are at high risk. The main infections are pneumonias in cystic fibrosis or in patients on respiratory equipment, infections of burn wounds, postoperative wound infections, chronic pyelonephritis, endocarditis in drug addicts, sepsis, and malignant otitis externa. P. aeruginosa frequently causes nosocomial infections (see p. 343).

Diagnosis. Laboratory diagnosis includes isolation of the pathogen from relevant materials and its identification based on a specific pattern of metabolic properties.

Therapy. The antibiotics that can be used to treat P. aeruginosa infections are aminoglycosides, acylureidopenicillins, carboxylpenicillins, group 3b cepha-losporins (see p. 190), and carbapenems. Combination of an aminoglycoside with a betalactam is indicated in severe infections. Susceptibility tests are necessary due to frequent resistance.

Epidemiology and prevention. Except in cystic fibrosis, P. aeruginosa is mainly a hospital problem. Since this ubiquitous organism can proliferate under the sparest of conditions in a moist milieu, a number of sources of infection are possible: sinks, toilets, cosmetics, vaporizers, inhalers, respirators, anesthesiology equipment, dialysis equipment, etc. Infected patients and staff carrying the organism are also potential primary sources of infection. Neutropenic patients are particularly susceptible. Preventive measures i.e., above all disinfection and clinical hygiene, concentrate on avoiding exposure.

Other Pseudomonas species, Stenotrophomonas and Burkholderia

Opportunistic pseudomonads. Other Pseudomonas species besides P. aeruginosa are capable of causing infections in immunosuppressed patients. These nosocomial infections are, however, infrequent. It would therefore not be particularly useful here to list all of the species that occasionally come to the attention of physicians. Classic opportunists also include Stenotrophomonas maltophilia (formerly Xanthomonas maltophilia) and Burkholderia cepacia (formerly Pseudomonas cepacia). These species all occur in hospitals and frequently show resistance to anti-infective agents. Antibiotic therapy must therefore always be based on a resistance test.

Burkholderia mallei. This species is the causative organism in malleus or glanders, a disease of solipeds. The bacteria invade the human organism through microtraumata, e.g., in the skin or mucosa, and form local ulcers. Starting from these primary infection foci they can move to other organs, either lymphogenously or hematogenously, and cause secondary abscesses there. Malleus no longer occurs in Europe.

Burkholderia pseudomallei. This species is the causative organism in me-lioidosis, a disease of animals and humans resembling malleus. The natural reservoirs of B. pseudomallei are soil and surface water. The pathogen invades the body through injuries of the skin or mucosa and causes multiple subcutaneous and subserous abscesses and granulomas. Starting from primary foci, the infection can disseminate and cause abscesses in a number of different organs. This disease is observed mainly in Asia.