Infection caused by Pseudomonas aeruginosa (P. aeruginosa) is common, with the burden of infection in hospitalized patients. The National Nosocomial Infections Surveillance (NNIS) System reports P. aeruginosa to be the second most common organism isolated in nosocomial pneumonia (17% of cases), the third most common organism isolated in both urinary tract infection (UTI) and surgical site infection (11% of cases), and the fifth most common organism isolated from all sites of nosocomial infection (9% of cases) (179). P. aeruginosa is an opportunistic pathogen which rarely causes disease in healthy persons. This organism is commonly considered in the differential diagnosis of a number of gram-negative infections. It is associated with nosocomial infections, often severe and life-threatening, especially in immunocompromised hosts. Chronic infection leads to progressive lung disease in cystic fibrosis, frequently complicated by antimicrobial resistance. If present in large enough numbers of inocula, or there is trauma with a break in epithelium, P. aeruginosa can cause infection in a healthy host. While animal models suggest that both humoral and cell-mediated immunity are involved in host defense against P. aeruginosa, the most important host defense is the neutrophil.
P. aeruginosa is an aerobic gram-negative bacterium and P. aeruginosa is typified by motile, non-spore forming rods that are oxidase positive and lactose nonfermenters. P. aeruginosa is a member of the genus Pseudomonas, colloquially called the pseudomonads. The water-soluble pigments, pyocyanin and pyoverdin, give P. aeruginosa its distinctive blue-green color on solid media. P. aeruginosa produces indophenol oxidase, an enzyme that renders them positive in the “oxidase” test, which distinguishes them from other gram-negative bacteria. The presence of polar flagella and pili gives P. aeruginosa motility.
Like many environmental bacteria, P. aeruginosa live in slime-enclosed biofilms which allow for survival and replication within human tissues and medical devices. Associated with the production of a biofilm protects P. aeruginosa from host-produced antibodies and phagocytes contributing to antibiotic resistance of this organism.
The P. aeruginosa organism thrives in moist environments such as soil and water. It can be found in large numbers on fresh fruits and vegetables. Human colonization begins within the gastrointestinal tract, with subsequent spread to moist cutaneous sites such as the perineum and axilla. It forms smooth fluorescent green colonies at 42oC, with a characteristic sweet (grape-like) odor, making it easy to recognize on solid media in the laboratory.
As a group, pseudomonads have minimal nutritional requirements. Many are capable of using a wide variety of environmental sources for nutrition; P. aeruginosa often only needs acetate and ammonia as the source of carbon and nitrogen, respectively. In additionP. aeruginosa can grow anaerobically, and does not carry out fermentation, rather obtaining energy from the oxidation of sugars. The flexible nutritional requirement permits its growth in marginal environments. They are difficult organisms to eradicate from areas that become contaminated, such as operating rooms, hospital rooms, clinics, and medical equipment (59).
P. aeruginosa, first isolated in 1882 by Gessard from green pus. The ubiquitous life-style of P. aeruginosa allows this bacterium to contribute to frequent infections in humans. It is a highly adaptable bacterium, with soil being the primary habitat; howeverP. aeruginosa also survives in aquatic environments. Its nutritional diversity allows for P. aeruginosa to survive toxic waste degradation.
P. aeruginosa is an important plant pathogen, affecting lettuce, tomatoes, and tobacco plants. It can be found in fresh water environments (streams, lakes, and rivers), as well as sinks, showers, respiratory equipment, even contaminating distilled water (68). Human beings can ingest the P. aeruginosa from such sources; however it does not adhere well to normal intact epithelium. Therefore it may be found as part of normal intestinal flora, and with a healthy immune system, P. aeruginosa does not cause infection (59).
The temperature in hot tubs favors Pseudomonas reproduction, with a hot tub containing up to 100 million organisms per milliliter. P. aeruginosa is adaptable; it finds the hospital and intensive care unit environments accommodating, with reservoirs of P. aeruginosa developing in the water in respiratory equipment. Due to its intrinsic and acquired resistance to many common antimicrobial agents, P. aeruginosa can be cultured from hand creams, hand-washing sinks, and certain cleaning solutions. Respiratory therapy equipment and dialysis tubing, both of which require a wet, body-temperature environment, are particularly susceptible to contamination by P. aeruginosa. Multi-use vials of respiratory medications have been implicated in spread of P. aeruginosa due to contamination with the organism. Artificial fingernails or extenders are not recommended for use by healthcare workers due to the frequent finding of P. aeruginosa colonization of the fingernails. Pseudomonads can even survive in some antiseptic solutions used to disinfect endoscopes and surgical instruments (35, 59, 68, 123, 228).
In a recent analysis of 24,179 adults with nosocomial bloodstream infections in the United States from 1995 to 2002, P. aeruginosa accounted for 4% of cases, and was the third leading cause of gram-negative infection (230). In children in the pediatric intensive care (PICU), the incidence of nosocomial infection was 1.5 per 100 patient-days. Patients with cardiac surgery had the highest nosocomial infection rate, 2.3 per 100 patient-days. Bacteremia (51.7%), respiratory infection (19.0%) and urinary tract infection (17.2%) were the most frequent nosocomial infections observed, and these were associated with use of invasive devices. Coagulase-negative staphylococci (39%) and P. aeruginosa (24%) were the most common organisms isolated (232).
P. aeruginosa is involved in a variety of human infections ranging from neonatal sepsis, to burn sepsis, and acute and chronic lung infections. This organism is a common opportunistic pathogen, leading to infections in patients with defects in host defenses, such as chronic neutropenias and defects of neurtrophil function, hematologic cancers, human immunodeficiency (HIV)/ acquired immunodeficiency syndrome (AIDS), and diabetes mellitus. In addition chronic pulmonary disease is common in patients with cystic fibrosis.
The role of P. aeruginosa in febrile, neutropenic patients is a very real threat. Despite a diminished role of P. aeruginosa as a cause of sepsis since the 1980’s, P. aeruginosa may account for one-third to one-half of gram-negative bacteremia in these patients. The decrease in infections due to P. aeruginosa may be attributed to the change in clinical practice over the past twenty five years, with aggressive early use of anti-Pseudomonal antimicrobials in the febrile neutropenic patient. However when P. aeruginosa infection occurs, mortality is as high as 50-70%.
Neutropenia remains an important predisposing factor to serious P. aeruginosa infections. Patients with human immunodeficiency virus infection or solid-organ transplant recipients receiving myelosuppressive therapies such as ganciclovir should be carefully monitored for decreases in neutrophil count. Patients who become neutropenic should receive granulocyte colony stimulating factors to enhance neutrophil counts. In general, immunosuppressed patients who develop signs or symptoms of serious gram-negative infections should receive high doses of anti-Pseudomonal antibiotics.
P. aeruginosa has been increasingly recognized as nosocomial and community-acquired infections among both adults and pediatric patients with HIV/AIDS (73, 147, 200, 213), with low CD4 lymphocyte counts (3, 220). In a study of 4825 patients with HIV, P. aeruginosa infections were diagnosed in 1.5% (72) patients. Respiratory infection accounted for 47% (34/72), with an overall incidence was 0.07%. Risk factors for a higher rate of P. aeruginosa infection include prior hospitalization and receipt of both dapsone and trimethoprim/sulfamethoxazole (TMP/SMX). Azithromycin use decreased the risk of infection by nearly 70%.
The cystic fibrosis (CF) patient is not immunocompromised in the typical sense; the genetic defect is on chromosome 7, leading to the abnormal production of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein, consequently with malfunction of the chloride channel on the cell surface. Chronic airway infection is the most important cause of morbidity and mortality in cystic fibrosis, and P. aeruginosa is the most significant pathogen in cystic fibrosis (28, 50). This organism infects approximately 60 percent of cystic fibrosis patients overall, with an 80% prevalence in the group of patients 18 years of age and older (51). It is believed in cystic fibrosis patients that the organism is acquired from environmental sources, however cystic fibrosis-patient-to- cystic fibrosis-patient spread of P. aeruginosa has occurred.
Both the presence of P. aeruginosa and its phenotype (e.g., developing a mucoid biofilm due to production of alginate as well as high-level resistance to multiple antibiotics) have been shown to correlate with severity of patient illness (55). This mucoid property predicts chronic infection that cannot be cleared. CF patients with P. aeruginosa have a decreased life expectancy of 30 years, compared with 40 years in non-colonized patients. They also experience a more rapid decline in pulmonary function and more frequent hospitalizations (72). On the other hand, anti-Pseudomonal therapy that decreases sputum colonization is associated with improved pulmonary function and improvement in clinical scores (174) [See chapter on Cystic Fibrosis & P. aeruginosa.] P. aeruginosa in the paranasal sinuses in cystic fibrosis patients frequently leads to acute and chronic infections, commonly complicated by nasal polyps. P. aeruginosa is otherwise an extremely rare finding in the sinuses in the non-cystic fibrosis population.
Contaminated Medical Devices/Equipment
Clusters of P. aeruginosa bacteremia/ sepsis following procedures such as endoscopic retrograde cholangiopancreatography (ERCP), endoscopy, ophthtalmic devices, and transrectal ultrasound (TRUS) have been related to inadequate cleaning or disinfection of reusable medical devices. One cluster of postoperative P. aeruginosa ocular infections occurred when an internal tubing system of automated cataract surgical equipment became contaminated (35, 49, 122).
Neonatal Intensive Care Unit
Sepsis is a frequent infection in premature infants. P. aeruginosa is isolated in approximately 1% of culture-proven causes of early onset sepsis (infection occurring <7 days of life) in very low birth weight preterm infants; mortality from infections with P. aeruginosa is 37% (205). In late-onset sepsis (occurring after 7 days of age) in very low birth weight infants, P. aeruginosa accounts for 2.7% of all infections, with mortality as high as 74.4% (204). Infection by P. aeruginosa in all premature infants was associated with 52.3% mortality, significantly higher than the 13.7% to 23.8% fatality from other gram-negative bacilli (87).
Infections in humans due to P. aeruginosa can be divided into opportunistic infections and those infections occurring in a healthy host. P. aeruginosa infections occur when the immune system is breached, either locally or systemically. Human hands infrequently are colonized with P. aeruginosa; however hospitalization increases the likelihood of finding the bacteria on intact skin. Therefore skin colonization can lead to bacteremia from catheter-related infection, or gastrointestinal colonization can lead to aspiration and pneumonia. Splashing of water from a contaminated sink, or droplets suctioned from a colonized endotrachial tube, can easily facilitate spread of P. aeruginosa. In the normal host, P. aeruginosa, in the proper setting can cause locally invasive disease. Large inocula of the bacteria can overwhelm normal defenses and lead to infection.
Urinary Tract Infections
P. aeruginosa, a common cause of nosocomial urinary tract infections (UTI’s), represents 7% of nosocomially-acquired UTIs in North America and Europe These infections are associated with an indwelling catheter, instrumentation of the urinary system, chronic prostatitis, nephrolithiasis, as well as prior antibiotic therapy. Community-acquired UTI’s are rarely caused by P. aeruginosa (97). In those persons with a neurogenic bladder, or in children with frequent infection from vesicoureteral reflux (VUR), P. aeruginosa UTI infection may occur. P. aeruginosa should be suspected in break-through infections in the urinary tract, especially in a host recently and/ or currently receiving antimicrobial agents, due to its nature to be resistant to many common antibiotics. In the elderly, urosepsis from P. aeruginosa may also follow acquisition of a simple UTI. Treatment regimens depend upon the presence of structural abnormalities or indwelling catheter(s), evidence of systemic sepsis, as well as the site of involvement, and prior antibiotic use. Eradication of the organism remains challenging and requires elimination of the predisposing factors in addition to antibiotic therapy.
Community-Acquired Pneumonia (CAP)
Infection due to P. aeruginosa is generally a rare cause of CAP (100), mainly occurs in HIV-infected patients, solid organ or bone marrow transplant recipients, or patients with neutropenia. However in a recent series of community-acquired bacterial pneumonia in adults, P. aeruginosa caused nearly 7% of the lower respiratory track infections. Nearly all of these patients had a preexisting risk factor for P. aeruginosa infection (9). Sicker adult patients have a high prevalence of severe CAP caused P. aeruginosa as well as Legionella pneumophilia (175).
Ventilator-Associated Pneumonia (VAP)
P. aeruginosa ranks as the leading cause of ventilator-associated intensive care unit (ICU)-acquired pneumonia, accounting for nearly 21% of cases (179). Spread/aspiration of bacteria to the lower respiratory track leads to a ventilator-associated pneumonia (VAP) by P. aeruginosa (161, 162, 221). Infection is common in those who have chronic disease, require respiratory/ventilatory assistance, have cystic fibrosis, or are immunocompromised, such as with cancer and neutropenia and/or hypogammaglobulinemia, (9, 12, 57).
Occasionally, P. aeruginosa, is accompanied by bloodstream infection, septic shock, and acute respiratory distress syndrome (ARDS) as a complication. The dramatic onset of septic shock, followed by death within hours that occurs in some immunocompromised patients with P. aeruginosa bacteremia, is a memorable experience for any observer. However, apart from the appearance of ecthyma gangrenosum, P. aeruginosa bacteremia is usually indistinguishable clinically from other forms of gram-negative bacteremia.
Near universal colonization with P. aeruginosa occurs in adults intubated > 5 days; colonization of tracheotomy sites in adults and children too is common. Risk factors for adults developing VAP include: antibiotic exposure, use of H2-receptor blockers, advanced age, reintubation, and transport from the ICU while intubated. In children in the pediatric intensive care unit three independent risk factors for pediatric VAP include: immunodeficiency, immunosuppression, and neuromuscular blockade (232). In patients with tracheostomy receiving short-term mechanical ventilation, P. aeruginosa can become a common pathogen (177).
Infective endocarditis (IE) due to P. aeruginosa is uncommon, occurring primarily in patients with injection drug use (IDU), with regional epidemics in midwestern U. S. cities (110, 111). Clusters of cases of IE occur particularly in abusers of pentazocine and tripelennamine, likely due to mixing of drugs with contaminated water. IE in patients with IDU frequently have no preceeding valvular or heart disease. The specific heart valve involved is important with respect to clinical manifestations, therapy, and prognoses (88). Infection of the tricuspid valve may have a more subacute presentation, likely due to lower bacterial densities from lower oxygen tension on the right side of the heart. Infection of the mitral valve may present more acutely, with more severe systemic sepsis-like manifestations. In addition, valvular dysfunction may lead to congestive heart failure, and may dictate need for surgical intervention.
Other factors predisposing to Pseudomonas endocarditis include the presence of a prosthetic valve or other intravascular foreign body, underlying malignancy, chemotherapy, and prolonged neutropenia. Increasing reports of Pseudomonas endocarditis following prolonged hospitalization associated with prosthetic endovascular devices (i.e. pacemakers) have been noted (8, 89, 130,180).
Central nervous system (CNS) infection due to P. aeruginosa meningitis is extremely rare, unless there has been penetrating trauma to the head, placement of a CNS shunt (such as a ventriculoperitoneal (VP) shunt), or postneurosurgical procedures (36, 144, 145). Often meningitis or ventriculitis associated with CNS shunts is caused by a mixed bacterial infection, including multiple aerobic gram-negative bacteria, including P. aeruginosa. Gram-negative bacterial infection must be considered, especially when erosion or perforation of the bowel has occurred from a VP shunt catheter, leading to an ascending CNS infection.
In a case series of gram-negative bacterial meningitis, 21% (14 cases) were due to P. aeruginosa. Eight of these 14 cases were postneurosurgical and the overall mortality of Pseudomonas meningitis was 35.7% (144). Mortality is highest if infection results from bacteremia in an immunosuppressed host, underlying infective endocarditis, or malignant otitis externa. Cure is more likely if the meningitis results from neurosurgical procedures involving hardware, such as VP shunts, drains, or reservoirs. An additional group of patients at risk for meningitis secondary to P. aeruginosa bacteremia is those receiving hemodialysis (38).
P. aeruginosa is frequently a cause of infection associated with contaminated contact lens solutions. In addition, eye trauma and recent ophthalmic surgery, as well as contact lens use, are risk factors for sight-threatening infections from P. aeruginosa, leading to corneal ulcerations, keratitis, and endophthalmitis. In addition, cases of orbital cellulitis and endophthalmitis due to P. aeruginosa have resulted as a complication of sepsis in neonates, patients with hematologic malignancy, and HIV/AIDS (23, 148, 173, 228).
There are three major ear infections caused by P. aeruginosa.
Perichondritis of the Ear
With the recent fashion of ear piercing, perichondritis of the auricle due to P. aeruginosa infections has become more common. The pinna may be markedly swollen, red and tender, with infection progressing to necrosis of the cartilage. It is felt that the decreased oxygen tension in the auricle may be more conducive to infection by P. aeruginosa.
Often known as swimmers’ ear, otitis media externa from P. aeruginosa causes a local infection of the external ear canal. Simple otitis media external is associated with warm, humid atmospheric conditions, aural water exposure, and ear canal trauma which may occur with frequent swimming, or when maceration or trauma occurs to the ear canal epithelium. Pain is found in 97.2% (13). Inflammation can be secondary to dermatitis only or it can be caused by active bacteria. Acute otitis externa can occur acutely and become painful. Wax in the ear can swell and block the canal and dampen hearing to varying degrees, creating a temporary conductive hearing loss. In more severe or untreated cases, the infection can rarely spread to the adjacent soft tissues, such as parotid gland and the jaw joint, making chewing painful.
Malignant External Otitis
Malignant (necrotizing) otitis media external is a subset of osteomyelitis caused by P. aeruginosa in which the temporal bone and skull base is involved (92). Patients with diabetes mellitus and advanced age (above 60 years) are at risk for necrotizing otitis externa, perhaps due to a higher pH in diabetic cerumen, and microangiopathy in the ear canal. Otitis externa may also complicate myringotomy tube placement, leading to a chronic otorrhea and subsequent removal of the ear tubes (183). Malignant otitis media external has also been reported in patients with HIV/AIDS.
In malignant external otitis, classic signs of infection including fever, leukocytosis, and systemic toxicity are notably absent, thus making diagnosis difficult. Otalgia followed by severe and often excruciating headache is the most common presenting symptom. Cranial nerve dysfunction, especially facial nerve palsy, is a late complication. Diagnosis rests on the findings of bony erosion and soft tissue abnormalities of the temporal bone and infratemporal fossa on computed tomographic (CT) scan or magnetic resonance imaging (MRI), elevated erythrocyte sedimentation rate (ESR), and isolation of P. aeruginosa from the external auditory canal or mastoid in a patient with a recalcitrant headache (91). In a 1-year prospective comparison, MRI was found to be slightly better than CT at distinguishing medial skull base disease, by delineating changes in the fat content of the marrow (91, 108).
Skin and Soft Tissue Infections
There are seven major skin and soft tissue infections caused by P. aeruginosa.
Hot Tub Folliculitis
Hot tub follculitis is an infection involving the hair follicles can occur as a result of bathing in a contaminated tub. If there inadequate chlorination, P. aeruginosa thrives at the higher temperature environment of hot tubs. Normal hosts with intact skin are affected predominantly in body sites covered by bathing suits, although areas of skin that have abrasion or have recently been shaved, may be at increased risk of infection (34). With a high enough inoculum of P. aeruginosa in the water, normal host defenses are overwhelmed, resulting in infection in immunocompetent hosts (47). Exposure of the head and external auditory canal may result in facial folliculitis or otitis media externa.
Puncture wounds, especially a nail or sharp object through a tennis shoe/sneaker into the plantar aspect of the foot, and lacerations and trauma occurring in fresh water streams and lakes, may lead to infection caused by P. aeruginosa. Soft-tissue infection, as well as osteocondritis, septic arthritis, and/or osteomyelitis of the traumatized bone or joint may occur.Hematogenous osteomyelitis/septic arthritis due to P. aeruginosa in children is extremely rare. More frequently osteomyelitis is found in intravenous drug users with P. aeruginosa bacteremia. Osteomyelitis does occur frequently as a polymicrobial infection in diabetics with foot ulcers, from local trauma and direct inoculation of the organisms(s).
The moist interdigital areas of the feet are ideal sites for colonization with P. aeruginosa. When these areas become infected with dermatophytes, or suffer other trauma to the dermal barrier, secondary bacterial invasion can readily occur.
Green Nail Syndrome
Patients with chronic onycholytic nails who have prolonged immersion exposure to fresh water may develop the green nail syndrome. This characteristic green discoloration is almost always a complication of onycholysis or a chronic paronychia and is usually restricted to one or two nails. Fungi and P. aeruginosa are frequently isolated from the nail. The green color is due to the pigment pyocyanin adhering to the undersurface of the nail plate with accumulated debris below the nail (93).
Ecthyma gangrenosum is a cutaneous manifestation of serious infection due to P. aeruginosa usually associated with bacteremia and sepsis. The lesions of ecthyma gangrenosum involve skin or mucous membranes, resulting from perivascular bacterial invasion of the adventicia of arteries and veins, leading to secondary ischemic necrosis. The painless skin lesions of ecthyma ganrenosum may be multiple, with rapid evolution through stages of macules, nodules, vesicles, and ulcerative eschars; the erythematous nodular lesion evolves into a hemorrhagic, ulcerative and necrotic area. Although not pathognomonic for P. aeruginosainfection, the finding of ecthyma raises the probability of P. aeruginosa systemic infection. Occasionally other skin lesions may occur with dissemination of systemic P. aeruginosa infection. These include macular papular lesions, clusters of pustules, cellulitis that mimics erysipelas, and soft-tissue abscesses. Many lesions become necrotic over time. The lesions contain little, if any, pus. In children the lesions may be more likely to be present on the perineum and buttocks.
Necrotizing fasciitis has been well-described in neutropenic and diabetic hosts (129). Cellulitis due to P. aeruginosa occurs at sites of damage to the dermal barrier, such as puncture sites or surgical wounds. Pyoderma occurs when a preexisting lesion of the skin becomes colonized and subsequently invaded by P. aeruginosa. In patients with facial cellulitis, the mucous membrane of the mouth is often the initial site of infection with subsequent spread to subcutaneous tissue and blood. Rapid progression to gangrene mandates vigorous surgery including extensive debridement and resection (129, 223). Exfoliative skin diseases, venous stasis ulcers, and eczema may predispose to infection. Rare skin disorders such as epidermolysis bullosa may be susceptible to chronic skin infection from P. aeruginosa. Severity of infection may range from a simple localized, nonnecrotic cellulitis to a necrotizing, gangrenous process with associated bacteremia in an immunocompromised host. P. aeruginosa can be cultured from the purulent discharge, but clinical manifestations of erythema, tenderness or warmth should differentiate infection from colonization. Infection may be acute and invasive, or may follow a chronic indolen
Norvasc (Amlodipine Besylate Side Effects, Interactions) Best medicine for travelers diarrhea cipro Cipro (Ciprofloxacin Side Effects, Interactions, Warning)
Arrivi Mikonos Aeroporto Arrivi Voli Mikonos (JMK)
Afrodite - Wikipedia
Mycoplasma Information Package - Rense
Guardia di Finanza - Wikipedia
Gadolinium Side Effects - Gadolinium Toxicity and Reactions