The genus Pseudomonas spp. are Gram negative, non-spore forming bacilli, the majority of which are aerobic (Kayser, Bienz, Eckert, & Zingernagel, 2001). These bacteria are motile due to their polar flagella allowing movement through body fluids – a substantial virulence factor. This genus is known for its rapid growth, biofilm formation and antibiotic resistance, thus making it difficult to eradicate from contaminated areas (Schaechter, Engleberg, DiRita & Dermody, 2013). Of particular note is P. aeruginosa – the most medically important species since it causes the vast majority of pseudomonal infections (Liu & Mercer, 1963). This is an opportunistic pathogen, with some strains being resistant to first- and second generation cephalosporins and penicillins, vancomycin, chloramphenicol, and tetracyclines (Banerjee & Stableforth, 2000). Common reservoirs are water and soil, but it can also be found in normal intestinal and skin microbiota (Schaechter et al., 2013).
Mechanism of Virulence
P. aeruginosa has many mechanisms of virulence, including its secretion of a number of toxins, one of which is the extracellular protease elastase. It can degrade elastin in host cells, as well as acting as a zinc metalloprotease that degrades a myriad of other proteins as well (Stover, Drake, & Montie, 1983).
Clinical Outcome and Disease Progression
Pseudomonas aeruginosa causes infection in immunocompromised patients – usually those with HIV/AIDS, cystic fibrosis, bronchiectasis, diabetes mellitus or burns victims (Aloush, Navon-Venezia, Seigman-Igra, Cabili, & Carmeli, 2005). The lower respiratory tract is the most common site of infection, with severity ranging from colonisation without immunological response to severe necrotising bronchopneumonia. Severe infections in cystic fibrosis patients are almost irremovable and can be fatal (Lister, Wolter & Hanson, 2009). It is accompanied by fever, chills, coughing, and dyspnea (Banerjee & Stableforth, 2000). Other infections that may occur are osteomyelitis, UTIs, gastrointestinal infections, and septicaemia. The incidence of these various infections depends on the portal of entry of the pathogen. For example, osteomyelitis may be caused by a contaminated osseointegrated metal rod, a fomite, that makes contact with the bone.
Mode of Transmission and Impact within Healthcare/Healthcare Systems
Pseudomonas aeruginosa can survive within droplet nuclei and aerosols for long periods of time, thus airborne transmission is a possibility (Bauer, Ofner, Just, Just & Daschner, 1990). Water- and food-borne transmission are also major routes, but the oral infectious dose is very high. However, the routes that pose the greatest health risk are contact transmission and lung exposure. Infected respiratory tracts and contaminated mechanical respiratory ventilators are two common sources of contaminated aerosols (Prasad et al., 2009). Healthy individuals are very rarely affected by P. aeruginosa exposure, however immunosuppression is a large risk factor for infection. There is a considerable impact on the patient’s health, depending on the severity of infection, as well as a notable economic impact. Patients that contract a P. aeruginosa infection undergo longer hospital stays than those without this nosocomial infection. The median difference is 38 days (Bou et al., 2009), varying with the degree of severity of the infection, which is significant and places greater strain on the hospital not only due to the lowered availability of hospital beds for new admissions but also due to the increased cost of the patient’s stay, including fees for diagnostic procedures and pharmaceutical drugs. If there is a P. aeruginosa outbreak in a hospital, healthcare workers must aim to determine the cause of the outbreak and prevent further cases from developing. For example, if the pathogen is spreading via nurse’s hands, then they must use gloves when with a patient and change gloves when they encounter a new patient (Stevens, 2008).
Precautions and Strategies to Control Spread of Infection
The most effective method for controlling the spread of P. aeruginosa infection is transmission based precautions. A-high-incidence-of P. aeruginosa infections-in-hospitals-can-be-attributed-to transmission-between patients via-the-hands-of-medical-staff (Prasad et al., 2009). This-can-be-minimised-by-using proper-hand-washing-technique-before-and-after-handling-a-patient, -as-well-as-when-entering-or-leaving-a-clinical-area, in addition to the use of gloves (Stevens, 2008). Also,-standard-procedures-including-cleaning-and-sterilising medical-equipment-must-be-followed-to-lower-chances-of-infection. P. aeruginosa-is-generally eliminated after sterilisation by steam under pressure at 121oC for 15 minutes. Other primary hazards-that-allow P. aeruginosa to-enter-the-body-and-induce-infection-include parenteral inoculation, ingestion, and inhalation of infectious aerosols (Mena & Gerba, 2009). The latter two transmission mechanisms can be prevented by targeting areas where P. aeruginosa persist and multiply, including moist environments and equipment such as humidifiers in hospital wards, sinks, bathrooms and kitchens. These areas must be regularly disinfected.
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P. aeruginosa develops antibacterial resistance very rapidly (Schaechter et al., 2013), so healthcare workers must employ stringent antimicrobial stewardship practices in order to effectively combat an infection with the bacterium and prevent emergence of drug-resistant strains. The reason for P. aeruginosa’s ability to develop resistance rapidly is due to chromosomally encoded AmpC cephalosporinase, low membrane permeability, and the multidrug efflux pumps (Lister et al., 2009). The empirical therapy for bacteraemia is an aminoglycoside with a beta-lactam penicillin (Banerjee & Stableforth, 2000), causing a synergistic effect. Since patients are usually immunocompromised, these drugs are selected for their bactericidal effects. If the strain of P. aeruginosa is or becomes resistant to these drugs, several other more potent drugs available as a last resort: piperacillin, tazobactam and meropenem, all of which have equivalent antibacterial activity against P. aeruginosa (Bassetti, Vena, Croxatto, Righi & Guery, 2018).
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