Medscape is available in 5 Language Editions – Choose your Edition here.


Pseudomonas Infection

  • Author: Selina SP Chen, MD, MPH; Chief Editor: Russell W Steele, MD  more...
Updated: Mar 09, 2016


In 1882, Gessard first discovered Pseudomonas, a strictly aerobic, gram-negative bacterium of relatively low virulence. The organism is ubiquitous, with a predilection to moist environments, primarily as waterborne and soilborne organisms. Pseudomonal species have been found in soil, water, plants, and animals; Pseudomonas aeruginosa colonization reportedly occurs in more than 50% of humans, and P aeruginosa is the most common pseudomonal species.

Pseudomonas is a clinically significant and opportunistic pathogen, often causing nosocomial infections. In addition to causing serious and often life-threatening diseases, these organisms exhibit innate resistance to many antibiotics and can develop new resistance after exposure to antimicrobial agents. Some pseudomonal species that previously were considered the causative agents of old diseases now are being reexamined for their potential use as biological warfare agents.

The current classification of the genus Pseudomonas is divided into 5 groups based on ribosomal RNA (rRNA)/DNA homology. Of the more than 20 pseudomonal species that have been found from human clinical specimens, the following 4 representative organisms are discussed in this article:

  • P aeruginosa (homology group I)
  • Burkholderia (Pseudomonas) cepacia (group II)
  • Burkholderia (Pseudomonas) pseudomallei (group II)
  • Burkholderia (Pseudomonas) mallei (group II)


Pseudomonas aeruginosa

Although P aeruginosa is a common human saprophyte, it rarely causes disease in healthy persons. Most infections with this organism occur in compromised hosts. Examples of compromising conditions include disrupted physical barriers to bacterial invasion (eg, burn injuries, intravenous [IV] lines, urinary catheters, dialysis catheters, endotracheal tubes) and dysfunctional immune mechanisms, such as those that occur in neonates and in individuals with cystic fibrosis (CF),[1] acquired immunodeficiency syndrome (AIDS), neutropenia, complement deficiency, hypogammaglobulinemia, and iatrogenic immunosuppression.

The complete sequence of the genome of P aeruginosa strain, PAO1, is noted for its large size and diverse metabolic capacity. The pathogenesis of this organism is multifactorial and involves various toxins and proteases (eg, exotoxin A, lecithinase) and the glycocalyx "slime." P aeruginosa is both invasive and toxigenic. The 3 stages of Pseudomonas infections are (1) bacterial attachment and colonization, (2) local infection, and (3) bloodstream dissemination and systemic disease.

Efflux systems are thought to contribute to antimicrobial resistance in P aeruginosa; thus, efflux pump inhibitors are thought to be useful in reducing the invasiveness and antimicrobial resistance of P aeruginosa and may be promising as new anti-infectious agents. The genome annotation is continually updated, and the database functionality is being expanded to facilitate accelerated discovery of P aeruginosa drug targets and vaccine candidates.

Pseudomonal infection, as described by Pollack, occurs in 3 stages: (1) bacterial attachment and colonization, followed by (2) local invasion and (3) dissemination and systemic disease.[2]

In healthy children, disease is primarily limited to the first 2 stages (as in diseases such as otitis externa, urinary tract infections (UTIs), dermatitis, cellulitis, and osteomyelitis), although recent case reports describe bacteremia, sepsis, and GI infections in previously healthy children.

In immunocompromised hosts, including neonates, infection can progress rapidly through the 3 stages and cause pneumonia, endocarditis, peritonitis, meningitis, ecthyma gangrenosum (EG), bacteremia, and overwhelming septicemia.

Pseudomonas cepacia

In 1949, Walter Burkholder of Cornell University first described P cepacia (now known as Burkholderia cepacia) as the phytopathogen responsible for the bacterial rot of onions.[3] In the 1950s, B cepacia was first reported as a human pathogen that causes endocarditis. Subsequently, the organism has been found in numerous catheter-associated UTIs, wound infections, and IV catheter–associated bacteremias.

In 1971, this species was reported as the causative organism of foot rot in US troops on swamp training exercises in northern Florida; it also was isolated from troops serving in Vietnam's Mekong Delta. In 1972, B cepacia was discovered as an opportunistic human pathogen in a patient with CF. Since then, B cepacia has emerged with increasing frequency as the cause of pneumonia and septicemia in children with CF.

Pseudomonas mallei

P mallei (now known as Burkholderia mallei) causes glanders, a serious infectious disease of animals (primarily horses, although it has also been isolated in donkeys, mules, goats, dogs, and cats). Transmission is believed to occur through direct contact. Glanders transmission to humans is rare and presumably occurs through inoculation of broken skin or the nasal mucosa with contaminated discharges. Manifestation of the disease in humans varies, ranging from an acute localized suppurative infection, acute pulmonary infection, or acute septicemic infection to chronic suppurative infection. Fulminant disease with multiple organ system involvement occurs with septicemic infection.

Pseudomonas pseudomallei

P pseudomallei (now known as Burkholderia pseudomallei) causes melioidosis (from the Greek, "resemblance to distemper of asses"). Melioidosis, also called Whitmore disease, clinically and pathologically resembles glanders but has an entirely different epidemiologic profile from B mallei. It occurs in many animals (eg, sheep, goats, horses, swine, cattle, dogs, cats). Transmission is believed to occur through direct contact, although inhalation reportedly is a possible route of acquisition. Since the first description of the disease from North Queensland, Australia, in 1962, melioidosis has spread to Southeast Asia.

B pseudomallei is found in contaminated water and soil. The pathogen spreads to humans and animals through direct contact with a contaminated source. In otherwise healthy hosts, disease manifestations range from acute to chronic local suppurative infections to septicemia with multiple abscesses in all organs of the body.




United States

According to data from the Centers for Disease Control and Prevention (CDC) National Nosocomial Infections Surveillance System, P aeruginosa can be rated as follows:

  • Number 1 cause of intensive care unit (ICU)–related pneumonia
  • Number 1 cause of osteochondritis
  • Number 2-ranked gram-negative organism, responsible for 9% of all nosocomial bacterial and fungal isolates
  • Number 2 cause of nosocomial pneumonia
  • Number 3-ranked isolate in hospital-acquired UTIs
  • Number 4 cause of surgical site infections and of hospital-acquired gram-negative rod bacteremia
  • Number 5 hospital pathogen
  • Number 8-ranked bloodstream isolate
  • Causes 10% of nosocomial infections
  • Most common bacteria isolated from mild-to-severe form of external otitis and chronic suppurative otitis media
  • Most common gram-negative organism isolated from corneal ulcers and endocarditis
  • Frequent cause of contact lens–associated keratitis
  • Second most frequent cause of brain abscess and meningitis in patients with cancer
  • Third most common cause of recurrent UTIs complicated by obstruction, catheters, or stones
  • Fifth most common cause of recurrent UTIs in schoolchildren

B cepacia is associated with increased illness and death in patients with CF. In several small focal hospital outbreaks that involved patients who did not have CF, the typical cause was a contaminated common source (eg, IV solutions, disinfectant preparations). In the early 1980s, the organism emerged as a major threat, causing superinfection in as many as 40% of patients in some CF centers. Approximately 35% of patients infected with B cepacia develop accelerated pulmonary deterioration or fulminant necrotizing pneumonia with rapidly fatal bacteremia, a condition also referred to as cepacia syndrome.

A retrospective analysis of the U.S. National Hospital Discharge Surveys from 1996-2010 found that Pseudomonas aeruginosa septicemia incidence declined from 6.5 per 10,000 in 1996 to 3.1 per 10,000 in 2001 and then increased to 6.5 per 10,000 in 2010.[4]


Numerous B cepacia epidemics associated with CF have been reported. A particular highly transmissible strain, which spread epidemically within and between CF centers in Western Europe and the United States, carries the cblA gene. This cblA strain has spread across Canada and now has been isolated in 50% of CF centers in the United Kingdom. Another strain of B cepacia has been found in CF centers in 4 regions of France. The propensity for transmission evidently varies among strains; most strains are not involved in epidemics but appear to be acquired independently without evidence of epidemic transmission.

A study reviewed German NICU surveillance data on more than 44,000 infants below 1500 g birth weight with the aim to quantify the pathogen-specific risk of a blood stream infection in preterm infants after an index case of the same pathogen in the NICU department. The relative risk was markedly elevated for Serratia and Pseudomonas aeruginosa.  With only 38 cases of Pseudomonas aeruginosa out of the 2004 culture-positive infections, the relative risk was still high at 64.5.[5]

Glanders caused by B mallei has not occurred in the United States since the 1940s, although it remains common in domestic animals in Africa, Asia, the Middle East, Central America, and South America.

Melioidosis caused by B pseudomallei is endemic in Southeast Asia. The highest concentrations of cases occur in Vietnam, Cambodia, Laos, Thailand, Malaysia, Myanmar (formerly Burma), and northern Australia. Melioidosis also occurs in the South Pacific, Africa, India, and the Middle East. The B pseudomallei organism is so prevalent that it is often found as a contaminant.


Pseudomonal infections (eg, bacteremic pneumonia, sepsis, burn wound infections, meningitis) are associated with an extremely high mortality rate.

Monocular blindness is primarily due to bacterial keratitis, the causes of which include pseudomonal infection. Colonization with B cepacia has been associated with increased morbidity and mortality in patients who are immunocompromised, especially those with CF.

Untreated glanders and melioidosis bloodstream infections are usually fatal within 7-10 days. P aeruginosa bacteremia has an estimated mortality rate exceeding 50% and is associated with fatality rates higher than those associated with other gram-negative bacteremic infections. Pseudomonal pneumonia, especially the bacteremic type, is associated with mortality that typically occurs 3-4 days after the first signs or symptoms of pulmonary or extrapulmonary infection. Ventilator-associated pneumonia (VAP) caused by P aeruginosa is associated with higher mortality rates (estimated to be as high as 68%) than VAPs caused by other infectious organisms. The mortality rate is high for the septicemic form of EG and is approximately 15% for the nonsepticemic form of the disease.


Black men reportedly have an increased incidence of pseudomonal endocarditis.


Sternoarticular pyarthrosis caused by pseudomonal infections occurs in young men, particularly those who engage in IV drug abuse. Some studies cite a 5.4:1 male-to-female ratio of P aeruginosa endocarditis.


Infants younger than 1 year have direct vascular communication with the epiphysis across the growth plate, allowing direct spread of pseudomonal osteomyelitis from the metaphysis to the epiphysis and, eventually, the joint. In older children, the growth plate provides a barrier; thus, the epiphysis and the joints seldom are involved.

Children have a higher predilection than adults to pseudomonal osteochondritis infections following puncture wounds of the foot. Older patients are more susceptible to pseudomonal bone and joint infections. Children have a higher likelihood of developing pseudomonal folliculitis than adults. Endocarditis occurs most often in young (mean age 29 y) black men.

In patients with CF, prevalence of pseudomonal pneumonia ranges from 21% in those younger than 1 year to more than 80% in those older than 19 years. The increasing longevity of patients with CF has created a significant shift in the proportion of adult patients with CF; their proportion has increased 4-fold, from 8% in 1969 to 33% in 1990.

Contributor Information and Disclosures

Selina SP Chen, MD, MPH Assistant Professor of Pediatrics, Department of Internal Medicine, John A Burns School of Medicine, University of Hawaii; Internal Medicine and Pediatric Hospitalist, Kapiolani Medical Center for Women and Children; Internal Medicine Hospitalist, Straub Clinic and Hospital; Electronic Medical Record Physician Liaison and Trainer

Selina SP Chen, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians-American Society of Internal Medicine, Society of Hospital Medicine

Disclosure: Nothing to disclose.


Ralph Rudoy, MD 

Ralph Rudoy, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Leonard R Krilov, MD Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics, Winthrop University Hospital; Professor of Pediatrics, Stony Brook University School of Medicine

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

  1. Bendiak GN, Ratjen F. The approach to Pseudomonas aeruginosa in cystic fibrosis. Semin Respir Crit Care Med. 2009 Oct. 30(5):587-95. [Medline].

  2. Pollack M. The Virulence of Pseudomonas aeruginosa. Rev Infect Dis. 1984. 6:S617-26.

  3. Burkholder W. Sour skin, a bacterial rot of onion bulbs. Phytopathology. 1950. 40:115-8.

  4. Werth BJ, Carreno JJ, Reveles KR. Shifting trends in the incidence of Pseudomonas aeruginosa septicemia in hospitalized adults in the United States from 1996-2010. Am J Infect Control. 2015 May 1. 43 (5):465-8. [Medline].

  5. Reichert F, Piening B, Geffers C, Gastmeier P, Bührer C, Schwab F. Pathogen-Specific Clustering of Nosocomial Blood Stream Infections in Very Preterm Infants. Pediatrics. 2016 Mar 8. [Medline].

  6. Rosenfeld M, Emerson J, McNamara S, et al. Risk factors for age at initial Pseudomonas acquisition in the cystic fibrosis epic observational cohort. J Cyst Fibros. 2012 May 1. [Medline].

  7. Morgan DJ, Rogawski E, Thom KA, et al. Transfer of multidrug-resistant bacteria to healthcare workers' gloves and gowns after patient contact increases with environmental contamination. Crit Care Med. 2012 Apr. 40(4):1045-51. [Medline].

  8. Kielhofner M, Atmar RL, Hamill RJ, Musher DM. Life-threatening Pseudomonas aeruginosa infections in patients with human immunodeficiency virus infection. Clin Infect Dis. 1992 Feb. 14(2):403-11. [Medline].

  9. Giamarellou H, Antoniadou A. Antipseudomonal antibiotics. Med Clin North Am. 2001 Jan. 85(1):19-42, v. [Medline].

  10. [Guideline] Committee on Infectious Diseases. The use of systemic fluoroquinolones. Pediatrics. 2006 Sep. 118(3):1287-92. [Medline].

  11. Douidar SM, Snodgrass WR. Potential role of fluoroquinolones in pediatric infections. Rev Infect Dis. 1989 Nov-Dec. 11(6):878-89. [Medline].

  12. Carmeli Y, Troillet N, Eliopoulos GM, Samore MH. Emergence of antibiotic-resistant Pseudomonas aeruginosa: comparison of risks associated with different antipseudomonal agents. Antimicrob Agents Chemother. 1999 Jun. 43(6):1379-82. [Medline].

  13. Altemeier WA, Tonelli MR, Aitken ML. Pseudomonal pericarditis complicating cystic fibrosis. Pediatr Pulmonol. 1999 Jan. 27(1):62-4. [Medline].

  14. Arbulu A, Holmes RJ, Asfaw I. Tricuspid valvulectomy without replacement. Twenty years' experience. J Thorac Cardiovasc Surg. 1991 Dec. 102(6):917-22. [Medline].

  15. Ashdown LR, Guard RW. The prevalence of human melioidosis in Northern Queensland. Am J Trop Med Hyg. 1984 May. 33(3):474-8. [Medline].

  16. Baltch AL, Griffin PE. Pseudomonas aeruginosa bacteremia: a clinical study of 75 patients. Am J Med Sci. 1977 Sep-Oct. 274(2):119-29. [Medline].

  17. Baum J, Barza M. Topical vs subconjunctival treatment of bacterial corneal ulcers. Ophthalmology. 1983 Feb. 90(2):162-8. [Medline].

  18. Brewer SC. Clinical Investigations in Critical Care: Ventilator-Associated Pneumonia due to Pseudomonas aeruginosa. Chest. 1996. 109:4:1020-30.

  19. Byrne S, Maddison J, Connor P, et al. Clinical evaluation of meropenem versus ceftazidime for the treatment of Pseudomonas spp. infections in cystic fibrosis patients. J Antimicrob Chemother. 1995 Jul. 36 Suppl A:135-43. [Medline].

  20. Cleveland RP, Hazlett LD, Leon MA, Berk RS. Role of complement in murine corneal infection caused by Pseudomonas aeruginosa. Invest Ophthalmol Vis Sci. 1983 Feb. 24(2):237-42. [Medline].

  21. Cunha BA. Antibiotic resistance. Med Clin North Am. 2000 Nov. 84(6):1407-29. [Medline].

  22. Davis SD, Sarff LD, Hyndiuk RA. Comparison of therapeutic routes in experimental Pseudomonas keratitis. Am J Ophthalmol. 1979 May. 87(5):710-6. [Medline].

  23. Edgeworth JD, Treacher DF, Eykyn SJ. A 25-year study of nosocomial bacteremia in an adult intensive care unit. Crit Care Med. 1999 Aug. 27(8):1421-8. [Medline].

  24. EORTC International Antimicrobial Therapy Cooperative Group. Ceftazidime combined with a short or long course of amikacin for empirical therapy of gram-negative bacteremia in cancer patients with granulocytopenia. N Engl J Med. 1987 Dec 31. 317(27):1692-8. [Medline].

  25. Fagon JY, Chastre J, Domart Y, et al. Nosocomial pneumonia in patients receiving continuous mechanical ventilation. Prospective analysis of 52 episodes with use of a protected specimen brush and quantitative culture techniques. Am Rev Respir Dis. 1989 Apr. 139(4):877-84. [Medline].

  26. Germiller JA, El-Kashlan HK, Shah UK. Chronic Pseudomonas infections of cochlear implants. Otol Neurotol. 2005 Mar. 26(2):196-201. [Medline].

  27. Giamarellou H. Empiric therapy for infections in the febrile, neutropenic, compromised host. Med Clin North Am. 1995 May. 79(3):559-80. [Medline].

  28. Giamarellou H. Malignant otitis externa: the therapeutic evolution of a lethal infection. J Antimicrob Chemother. 1992 Dec. 30(6):745-51. [Medline].

  29. Gitterman B. In Brief: Aminoglycosides. Pediatrics in Review. 1998 Aug. 19(8):285.

  30. Griffiths AL, Jamsen K, Carlin JB, et al. Effects of segregation on an epidemic Pseudomonas aeruginosa strain in a cystic fibrosis clinic. Am J Respir Crit Care Med. 2005 May 1. 171(9):1020-5. [Medline].

  31. Harris A, Torres-Viera C, Venkataraman L, et al. Epidemiology and clinical outcomes of patients with multiresistant Pseudomonas aeruginosa. Clin Infect Dis. 1999 May. 28(5):1128-33. [Medline].

  32. Highsmith AK, Le PN, Khabbaz RF, Munn VP. Characteristics of Pseudomonas aeruginosa isolated from whirlpools and bathers. Infect Control. 1985 Oct. 6(10):407-12. [Medline].

  33. Ho PL, Chan KN, Ip MS, et al. The effect of Pseudomonas aeruginosa infection on clinical parameters in steady-state bronchiectasis. Chest. 1998 Dec. 114(6):1594-8. [Medline].

  34. Husson MO, Richet H, Aubert A, et al. In vitro comparative activity of meropenem with 15 other antimicrobial agents against 1798 Pseudomonas aeruginosa isolates in a French multicenter study. Clin Microbiol Infect. 1999 Aug. 5(8):499-503. [Medline].

  35. Isles A, Maclusky I, Corey M, et al. Pseudomonas cepacia infection in cystic fibrosis: an emerging problem. J Pediatr. 1984 Feb. 104(2):206-10. [Medline].

  36. Kang CI, Kim SH, Park WB, et al. Clinical features and outcome of patients with community-acquired Pseudomonas aeruginosa bacteraemia. Clin Microbiol Infect. 2005 May. 11(5):415-8. [Medline].

  37. Karlowicz MG, Buescher ES, Surka AE. Fulminant late-onset sepsis in a neonatal intensive care unit, 1988- 1997, and the impact of avoiding empiric vancomycin therapy. Pediatrics. 2000 Dec. 106(6):1387-90. [Medline].

  38. Kerem E. The Role of Pseudomonas aeruginosa in the Pathogenesis of Lung Disease in Cystic Fibrosis: More Questions than Answers. Pediatric Pulmonology- Supplement. 1997. 14:403-11.

  39. Komshian SV, Tablan OC, Palutke W, Reyes MP. Characteristics of left-sided endocarditis due to Pseudomonas aeruginosa in the Detroit Medical Center. Rev Infect Dis. 1990 Jul-Aug. 12(4):693-702. [Medline].

  40. Koprnova J, Beno P, Korcova J, et al. Bacteremia due to Pseudomonas aeruginosa: results from a 3-year national study in the Slovak Republic. J Chemother. 2005 Oct. 17(5):470-6. [Medline].

  41. Lahiri T. Approaches to the treatment of initial Pseudomonas aeruginosa infection in children who have cystic fibrosis. Clin Chest Med. 2007 Jun. 28(2):307-18. [Medline].

  42. Malaty J, Lee JC, Zhang M, et al. Click here to read Hearing loss and extent of labyrinthine injury in Pseudomonas otitis media. Malaty J, Lee JC, Zhang M, Stevens G, Antonelli PJ. Department of Otolaryngology, University of Florida, Gainesville 32610-0264, USA. Otolaryngol Head Neck Surg. 2005 Jan. 132(1):25-9. [Medline].

  43. Malaty J, Lee JC, Zhang M, et al. Hearing loss and extent of labyrinthine injury in Pseudomonas otitis media. Otolaryngol Head Neck Surg. 2005 Jan. 132(1):25-9. [Medline].

  44. Marchetti F, Bua J. More evidence is needed in the antibiotic treatment of Pseudomonas aeruginosa colonisation. Arch Dis Child. 2005 Nov. 90(11):1204. [Medline].

  45. Masekela R, Green RJ. The role of macrolides in childhood non-cystic fibrosis-related bronchiectasis. Mediators Inflamm. 2012. 2012:134605. [Medline]. [Full Text].

  46. Medical Letter. Drugs for sexually transmitted infections. Med Lett Drugs Ther. 1999 Sep 24. 41(1062):85-90. [Medline].

  47. Medical Letter. The choice of antibacterial drugs. Med Lett Drugs Ther. 1999 Oct 22. 41(1064):95-104. [Medline].

  48. Milner SM. Acetic acid to treat Pseudomonas aeruginosa in superficial wounds and burns. Lancet. 1992 Jul 4. 340(8810):61. [Medline].

  49. Morrison AJ Jr, Wenzel RP. Epidemiology of infections due to Pseudomonas aeruginosa. Rev Infect Dis. 1984 Sep-Oct. 6 Suppl 3:S627-42. [Medline].

  50. Mukhopedhyay S, Singh M, Cater JI. Nebulized antipseudomonal antibiotic therapy in cystic fibrosis: A meta-analysis of benefits and risks. Thorax. 1996. 51:364.

  51. Mull, CC. Case Report: Ecthyma gangrenosum as a Manifestation of Pseudomonas Sepsis in a Previously Healthy Child. Annals Emerg Med. 2000 Oct. 36:4.

  52. Nagaki M, Shimura S, Tanno Y, et al. Role of chronic Pseudomonas aeruginosa infection in the development of bronchiectasis. Chest. 1992 Nov. 102(5):1464-9. [Medline].

  53. Neo EN, Haritharan T, Thambidorai CR, Suresh V. Pseudomonas necrotizing fasciitis in an immunocompetent infant. Pediatr Infect Dis J. 2005 Oct. 24 (10):942-3. [Medline].

  54. Obritsch MD, Fish DN, MacLaren R, Jung R. Nosocomial infections due to multidrug-resistant Pseudomonas aeruginosa: epidemiology and treatment options. Pharmacotherapy. 2005 Oct. 25(10):1353-64. [Medline].

  55. Pandey A, Malenie R, Asthana AK. Beta-lactamase producing Pseudomonas aeruginosa in hospitalised patients. Indian J Pathol Microbiol. 2005 Oct. 48(4):530-3. [Medline].

  56. Paul M, Leibovici L. Combination antibiotic therapy for Pseudomonas aeruginosa bacteraemia. Lancet Infect Dis. 2004 Aug. 4(8):519-27. [Medline].

  57. Radford R, Brahma A, Armstrong M, Tullo AB. Severe sclerokeratitis due to Pseudomonas aeruginosa in noncontact-lens wearers. Eye. 2000 Feb. 14 (Pt 1):3-7. [Medline].

  58. Rajashekaraiah KR, Rice TW, Kallick CA. Recovery of Pseudomonas aeruginosa from syringes of drug addicts with endocarditis. J Infect Dis. 1981 Nov. 144(5):482. [Medline].

  59. Roilides E, Butler KM, et al. Pseudomonas Infections in Children with Human Immunodeficiency Virus Infection. Pediatric Infect Dis J. 1992. 11:547-53.

  60. Saiman L. The use of macrolide antibiotics in patients with cystic fibrosis. Curr Opin Pulm Med. 2004 Nov. 10(6):515-23. [Medline].

  61. Schimpff SC, Moody M, Young VM. Relationship of colonization with Pseudomonas aeruginosa to development of Pseudomonas bacteremia in cancer patients. Antimicrobial Agents Chemother. 1970. 10:240-4. [Medline].

  62. Tabbara KF, El-Sheikh HF, Aabed B. Extended wear contact lens related bacterial keratitis. Br J Ophthalmol. 2000 Mar. 84(3):327-8. [Medline].

  63. Tablan OC, Chorba TL, Schidlow DV, et al. Pseudomonas cepacia colonization in patients with cystic fibrosis: risk factors and clinical outcome. J Pediatr. 1985 Sep. 107(3):382-7. [Medline].

  64. Taneja N, Meharwal SK, Sharma SK, Sharma M. Significance and characterisation of pseudomonads from urinary tract specimens. J Commun Dis. 2004 Mar. 36(1):27-34. [Medline].

  65. Tsekouras AA, Johnson A, Miller G, Orton HI. Pseudomonas aeruginosa necrotizing fasciitis: a case report. J Infect. 1998 Sep. 37(2):188-90. [Medline].

  66. Tumaliuan JA, Stambouly JJ, Schiff RJ, et al. Pseudomonas pericarditis and tamponade in an infant with human immunodeficency virus infection. Arch Pediatr Adolesc Med. 1997 Feb. 151(2):207-8. [Medline].

  67. Whitehead B, Helms P, Goodwin M, et al. Heart-lung transplantation for cystic fibrosis. 2: Outcome. Arch Dis Child. 1991 Sep. 66(9):1022-6; discussion 1016-7. [Medline].

  68. Wu BY, Peng CT, Tsai CH, Chiu HH. Community-acquired Pseudomonas aeruginosa bacteremia and sepsis in previously healthy infants. Acta Paediatr Taiwan. 1999 Jul-Aug. 40(4):233-6. [Medline].

  69. Yeung CK, Lee KH. Community acquired fulminant Pseudomonas infection of the gastrointestinal tract in previously healthy infants. J Paediatr Child Health. 1998 Dec. 34(6):584-7. [Medline].

  70. Over-the-Counter Topical Antiseptic Products: Drug Safety Communication - FDA Requests Label Changes and Single-Use Packaging to Decrease Risk of Infection. FDA. 11/13/2013. Available at

  71. Zegans ME, DiGiandomenico A, Ray K, Naimie A, Keller AE, Stover CK, et al. Association of Biofilm Formation, Psl Exopolysaccharide Expression, and Clinical Outcomes in Pseudomonas aeruginosa Keratitis: Analysis of Isolates in the Steroids for Corneal Ulcers Trial. JAMA Ophthalmol. 2016 Feb 4. [Medline].

Erythematous papulopustules of pseudomonas folliculitis. Courtesy of Mark Welch, MD.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.