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 im 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 fluo-rescein 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.

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Essentials of Human Physiology

Essentials of Human Physiology

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