Pseudomonas aeruginosa Infections

Pseudomonas aeruginosa is an opportunistic pathogen that is widespread in the environment, a major cause of nosocomial infections, and an occasional cause of community-acquired infections, meaning infections acquired outside hospital or other medical facilities. Community-acquired infections include skin rashes from contaminated swimming pools and hot tubs, serious infections of the foot bones from stepping on nails, serious eye infections from contaminated contact lens solutions, heart valve infections in injected-drug abusers, external ear canal infections in swimmers and others who fail to dry their ears properly, and biofilms in the lungs of individuals with the inherited disease cystic fibrosis. ■ Pseudomonas, p. 281

In hospitals, the bacterium is the leading cause of nosocomial lung infections and a common cause of wound infections, especially of thermal burns. Burns have large exposed areas of dead tissue free of any body defenses and, therefore, are ideal sites for infection by bacteria from the environment or normal flora. Almost any opportunistic pathogen can infect burns, but Pseudomonas aeruginosa is among the most common and hardest to treat.


In burns and other wounds, P. aeruginosa can often color the tissues green from pigments released from the bacteria (figure 27.6a, b). It is especially dreaded because it often invades the bloodstream and causes chills, fever, skin lesions, and shock.

Causative Agent

Pseudomonas aeruginosa is motile by means of a single polar fla-gellum (figure 27.6c). The organisms grow readily and rapidly; some strains can grow in a variety of aqueous solutions, even in distilled water. The bacterium generally utilizes oxygen as the final electron acceptor in the breakdown of nutrients. Under certain circumstances, however, it can also grow anaerobically, as when nitrate is available. Nitrate substitutes for oxygen as a final electron acceptor, an example of anaerobic respiration. Strains of P. aeruginosa often produce one or more water-soluble pigments, which can be red, yellow, blue, or dark brown. Commonly they produce a fluorescent yellowish pigment called pyoverdin, which combines with a blue pigment, pyocyanin, to produce the striking green color characteristically seen in infected wounds and in growth media. ■ anaerobic respiration, pp. 137,149


The overall effect of P. aeruginosa infection of burns and other wounds is to produce tissue damage, prevent healing, and increase the risk of septic shock. Septic shock results from pathogens circulating in the bloodstream, as opposed to toxic shock caused by the circulation of specific exotoxins. Most strains produce an extracellular enzyme called exoenzyme S that in vitro catalyzes the transfer of an ADP-ribose fragment of NAD to G proteins. The signaling mechanism from host cell surface receptors to the appropriate genes is thereby impaired. In other words, exoenzyme S functions in vitro in the same way as the toxins of Vibrio cholerae and Bordetella pertussis. Strains of P. aeruginosa having an experimentally impaired gene for the enzyme show

Pseudomonas Burn Infection

10 mm

Figure 27.6 Pseudomonas aeruginosa (a) Extensive burn infected with P. aeruginosa. Notice the green discoloration. (b) Culture.The green discoloration of the medium results from water-soluble pigments diffusing from the P. aeruginosa colonies. (c) P. aeruginosa has a single polar flagellum.

10 mm

Figure 27.6 Pseudomonas aeruginosa (a) Extensive burn infected with P. aeruginosa. Notice the green discoloration. (b) Culture.The green discoloration of the medium results from water-soluble pigments diffusing from the P. aeruginosa colonies. (c) P. aeruginosa has a single polar flagellum.

marked decrease in virulence. ■ signaling, p. 70 ■ Bordetella pertussis, p. 580 ■ Vibrio cholerae, p. 611

Most strains of P. aeruginosa also produce toxin A, an exoenzyme that has a mode of action identical to that of the toxin of Corynebacterium diphtheriae, a Gram-positive rod. The two toxins, however, are antigenically distinct and target different cells. These toxins halt protein synthesis by the host cell and are enhanced by lowering the concentration of iron. Toxin A deficient mutants of P. aeruginosa show a marked decrease in virulence. Experimentally, most strains of P. aeruginosa produce proteases

Chapter 27 Wound Infections

Table 27.2 Leading Causes of Wound Infections

Causative Organism



Staphylococcus aureus

Gram-positive cocci in clusters, coagulase-positive

Delayed healing; abscess formation; extension into tissues, artificial devices, or bloodstream; occasional strains can cause toxic shock syndrome

Streptococcus pyogenes

Gram-positive cocci in chains; Lancefield group A

Same, except occasional strains can cause "flesh-eating" necrotizing fasciitis

Pseudomonas aeruginosa

Aerobic Gram-negative rod, green pigment

Delayed healing; abscess formation; extension into tissues, artificial devices, or bloodstream; septic shock

that cause localized hemorrhages and tissue necrosis. Also, many strains produce a heat-labile hemolysin, a phospholipase C, identical in mode of action to the principal toxin of the gas gangrene bacillus to be discussed later in this chapter, Clostridium per-fringens. Phospholipase C hydrolyses lecithin, an important lipid component of cell membranes. The pigments released from P. aeruginosa may also contribute to pathogenicity by inhibiting competing bacteria and helping it acquire iron. ■ Corynebacterium diphtheriae, p. 568 ■ elongation factor, p. 178 ■ required elements p. 90


Pseudomonas aeruginosa is widespread in nature, in soil and water, and on plants, including fruits and vegetables. It is introduced into hospitals on shoes, on ornamental plants and flowers, and on produce. It can persist in most places where there is dampness or water, and it can contaminate soaps, ointments, eyedrops, contact lens solutions, cosmetics, disinfectants, many kinds of hospital equipment, swimming pools, hot tubs, the inner soles of shoes, and illegal injectable drugs, all of which have been sources of infections.

Prevention and Treatment

Prevention involves elimination of potential sources of the bacterium and prompt care of wounds. Careful removal of dead tissue from burn wounds, followed by application of an antibacterial cream such as silver sulfadiazine, is often effective in preventing infection with P. aeruginosa. Established infections are notoriously difficult to treat because P. aeruginosa is usually resistant to multiple antibacterial medications. Antibiotic susceptibility tests are done to guide the selection of an effective regimen. Medications must usually be administered intravenously in high doses.

Table 27.2 compares the leading causes of wound infections.

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  • elanor
    What are the causative agent of shock?
    4 years ago
  • bandobras
    What is the cause of pigments in pseudomonas?
    3 years ago
  • Kai Kiiskinen
    What is the causative agents of pseudomonas auginosa?
    2 years ago
  • Ishbel
    What is the causative agent of plseudomonas aeruginosa?
    2 years ago
  • hannah
    What are pheudomonas and their causative?
    2 years ago
  • asphodel
    What is the causative agent for psuedomonas aeruginosa?
    1 year ago

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