Pseudomonas aeruginosa infections of the eye, ear, urinary tract, gastrointestinal tract, and central nervous system

INTRODUCTION — Pseudomonas aeruginosa is an important pathogen in the differential diagnosis of several common infections. Consideration of this organism is important because it has the potential to cause severe infections, especially in immunocompromised hosts, and to be multidrug resistant.

The clinical manifestations, diagnosis, and treatment of P. aeruginosa eye, ear, urinary tract, gastrointestinal tract, and central nervous system infections will be reviewed here.

The general principles of antimicrobial treatment of infections caused by P. aeruginosa, including antibiotic options and decisions on combination therapy, are discussed in detail elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections".)

The clinical manifestations and management of other P. aeruginosa infections and the epidemiology and pathogenesis of infection with this organism are also discussed separately.

●(See "Epidemiology, microbiology, and pathogenesis of Pseudomonas aeruginosa infection".)

●(See "Pseudomonas aeruginosa pneumonia".)

●(See "Pseudomonas aeruginosa bacteremia and endocarditis".)

●(See "Pseudomonas aeruginosa skin and soft tissue infections".)

●(See "Cystic fibrosis: Antibiotic therapy for chronic pulmonary infection", section on 'Pseudomonas aeruginosa' and "Cystic fibrosis: Antibiotic therapy for pulmonary exacerbations".)

EYE INFECTIONS — P. aeruginosa is capable of causing both minor and vision-threatening infections of the eye. These infections include dacryocystitis, blepharoconjunctivitis, and orbital cellulitis. P. aeruginosa can also be directly introduced into the cornea, anterior chamber, or vitreous via trauma, surgery, or contaminated optic medications (eg, artificial tears) [1]. P. aeruginosa has been implicated in some cases of ophthalmia neonatorum and scleral abscesses. Hematogenous infection of the vitreous occurs rarely in patients with P. aeruginosa bacteremia. (See "Orbital cellulitis" and "Bacterial endophthalmitis" and "Conjunctivitis", section on 'Bacterial conjunctivitis'.)

In a single-center retrospective study from Japan, 9 of 108 cases of gram-negative bacillary ocular infections were caused by P. aeruginosa; hospitalization and age ≥65 years were associated with drug-resistant P. aeruginosa infection [2].

Corneal and conjunctival infections

Clinical syndromes

Corneal infections — Corneal infections due to P. aeruginosa usually result from minor trauma to the cornea. These infections may manifest as focal or diffuse inflammation of the cornea (keratitis) or as corneal ulcers if inflammation results in tissue loss and corneal erosion.

P. aeruginosa is the most common cause of bacterial keratitis among contact lens wearers. Pseudomonas keratitis has been observed among patients using hydrophilic lenses and extended wear lenses, as the polymer matrix provides a suitable surface for Pseudomonas adherence. Extended lens wearing provides more time for lens surface coatings to accumulate, which promotes further bacterial adherence. Lens wear can then lead to bacterial accumulation on ocular surface by shielding the cornea from the immune components found in tears and from the wiping action of the eyelids. Although poor lens care practices such as use of contaminated solutions or tap water to clean lenses is commonly reported among affected individuals, P. aeruginosa can colonize contact lenses despite proper lens hygiene.

Traumatic epithelial defects also play a very important role in promoting keratitis secondary to contact lenses. Previous experimental models showed that corneal disease develops predominantly in corneas exposed to trauma, which can occur during lens insertion or removal [3]. Other predisposing conditions include use of topical steroids for other ocular diseases, contaminated ocular medications (eg, artificial tears), and prior ocular irradiation [1]. (See "Complications of contact lenses", section on 'Infectious keratitis'.)

P. aeruginosa corneal ulcers usually start with a small lesion that rapidly spreads concentrically, in some cases leading to corneal perforation over a 48-hour period. Corneal ulcers can also be indolent, evolving slowly over days to weeks. Clinical findings include eye redness, decreased visual acuity, pain, eyelid swelling, photophobia, yellow infiltrates, and corneal epithelial defects visualized by fluorescein staining. Fever and other systemic manifestations are generally absent. Typically, there is a necrotic gray ulcer with adherent mucopurulent discharge and surrounding epithelial edema. P. aeruginosa corneal ulcers can result in secondary hypopyons or panophthalmitis.

Blepharoconjunctivitis — Critically ill patients, neonates, or burn patients may develop unilateral or bilateral conjunctivitis due to P. aeruginosa. Conjunctival infection can occur with or without associated infection of the eyelids (blepharitis). Patients on mechanical ventilation are at increased risk for colonization of the eye with this organism, which can subsequently lead to conjunctivitis. Contamination of the conjunctiva with P. aeruginosa can occur during tracheal suctioning, when ventilator intubation tubes are disconnected, allowing eye inoculation from aerosols or direct contact with secretions [4].

Diagnosis — The diagnosis of a corneal ulcer, keratitis, or conjunctivitis due to P. aeruginosa can be easily confirmed by obtaining scrapings from the bed of the ulcer or the conjunctiva for Gram stain and culture.

Treatment — The treatment of corneal and conjunctival infections usually consists of topical and systemic (table 1) antipseudomonal agents. In general, treatment should be based on available susceptibility results and continued until the clinical signs of active infection have resolved. Antibiotic selection for pseudomonal infections is detailed separately. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections".)

In one series, subpalpebral lavage with antibiotics was used with good results [5]. Other adjunctive therapies that have been used in case reports or experimental models include hyperbaric oxygen and topical chlorhexidine [6-8]. (See "Complications of contact lenses", section on 'Infectious keratitis'.)

Endophthalmitis

Predisposing causes — Five mechanisms can lead to P. aeruginosa endophthalmitis:

●Perforating corneal ulcers

●Penetrating ocular injuries

●Postoperative complication of eye surgery

●Hematogenous spread

●Use of contaminated eye medications or solutions (eg, artificial tears) [1]

Unlike most forms of postoperative endophthalmitis, which occur when commensal colonizing ocular flora are inoculated into the eye, postsurgical P. aeruginosa endophthalmitis is more likely to result from exogenous sources, such as contaminated intraoperative air, irrigation fluids, intraocular lens, or even surgical equipment [9,10]. As an example, in an outbreak of post-operative P. aeruginosa endophthalmitis in an Indian hospital, polymerase chain reaction (PCR) analyses demonstrated that the main source of infection was a contaminated air-conditioning system [10]. (See "Bacterial endophthalmitis".)

Clinical features — The course of pseudomonal endophthalmitis is typically fulminant, developing over hours. Patients characteristically have intense ocular pain and decreased visual acuity. Findings of panophthalmitis, including conjunctivitis with chemosis, lid edema, and anterior uveitis, may also be present.

A retrospective review of 28 cases of P. aeruginosa endophthalmitis reported poor visual outcomes despite prompt treatment with intravitreal antibiotics to which the organisms were sensitive [11]. In this case series, 64 percent of affected eyes were either enucleated or eviscerated (ie, contents of the eye were removed, leaving only the sclera and attached ocular muscles).

Diagnosis — Endophthalmitis is diagnosed clinically by the presence of the characteristic symptoms and signs detailed above and the absence of a red reflex. The clinical diagnosis should be confirmed by aspiration of the anterior chamber or vitreous. Subsequent Gram stain and cultures will usually confirm the diagnosis either immediately or within 24 to 36 hours.

Treatment — Therapy includes vitrectomy and intravitreal antibiotics. Treatment of bacterial endophthalmitis is discussed separately. (See "Bacterial endophthalmitis".)

EAR INFECTIONS — P. aeruginosa causes four types of ear infection:

●Simple otitis externa (or "swimmer's ear")

●Malignant external otitis

●Otitis media

●Perichondritis

Otitis externa — P. aeruginosa is the most common cause of acute external otitis, accounting for more than 70 percent of cases in one series [12,13]. Otitis externa due to P. aeruginosa is common in swimmers and in residents of tropical or humid climates. In a prospective study of 99 cases of otitis externa, the peak incidence occurred in summer and early autumn months; exposure to water and previous use of ear drops and cotton-tipped applicators predisposed to infection [14]. In contrast to acute otitis externa, chronic otitis externa is generally caused by allergies or underlying inflammatory dermatologic conditions [13].

Patients with otitis externa typically complain of itching and pain, worsened by traction on the pinna. Characteristically, there is a thick purulent discharge from the ear, and on examination, the external auditory canal is usually tender, edematous, and occluded with debris. The color or odor of the aural discharge is not useful in distinguishing between infection due to P. aeruginosa and otitis externa due to fungi or other organisms [14]. (See "External otitis: Pathogenesis, clinical features, and diagnosis".)

The treatment of external otitis is discussed separately. (See "External otitis: Treatment".)

Skull base osteomyelitis — In some patients, particularly elderly patients with diabetes mellitus, otitis externa may progress to a more severe and even life-threatening illness. Skull base osteomyelitis (also known as malignant external otitis) occurs when P. aeruginosa penetrates the epithelium of the external auditory canal and invades the underlying soft tissue, cartilage, and cortical bone. Infection may then occur in the soft tissue of the retromandibular and parotid spaces, the mastoid air cells, and the temporal bones. When the temporal bones become infected and necrotic, infection can spread to the base of the skull leading to inflammation and even necrosis of the ipsilateral seventh, ninth, tenth, eleventh, and twelfth cranial nerves.

Patients with skull base osteomyelitis usually present with pain and discharge from the affected ear. Hearing loss may or may not be present. On examination, the external auditory canal usually appears swollen and inflamed with a purulent discharge. Adjacent structures such as the pinna, periauricular and retromandibular areas, and the mastoid tip may also show signs of inflammation. The tympanic membrane, which may be either intact or perforated, is often hidden by the swelling and the granulation tissue. Cranial nerve palsies appear later in the course. Trismus may occur from infection of the temporomandibular joint.

Prompt diagnosis and treatment of this infection is essential. (See "Malignant (necrotizing) external otitis".)

Otitis media — P. aeruginosa is the most commonly isolated organism from the middle and external ears of patients with chronic suppurative otitis media. Otitis media due to P. aeruginosa can also occur in infants less than six weeks of age. The presence of this pathogen should be suspected when patients with otitis media fail to respond to usual antibiotic therapy. Neonates with otitis media due to P. aeruginosa often have misleading symptoms such as cough, rhinorrhea, diarrhea, and difficulty in feeding, whereas older children with P. aeruginosa ear infections usually have signs and symptoms typical of otitis media. (See "Chronic suppurative otitis media (CSOM): Clinical features and diagnosis".)

The treatment of chronic suppurative otitis media is discussed elsewhere. (See "Chronic suppurative otitis media (CSOM): Treatment, complications, and prevention".)

Acute otitis media can also occur in the presence of tympanostomy tubes [15]. Piperacillin-tazobactam coated tympanostomy tubes were noted to be resistant to P. aeruginosa biofilm formation in one study [16].

Perichondritis — P. aeruginosa perichondritis of the helix or tragus of the ear can occur after trauma, surgery, or burns. Cases have also been described after ear piercing [17] and acupuncture [18].

In a systematic review of 29 case reports or small clusters of infectious complications following transcartilaginous ear piercing, 87 percent were caused by P. aeruginosa [19]. In one cluster of cases involving patients who underwent ear piercing at a commercial kiosk, P. aeruginosa was recovered from a disinfectant bottle and nearby sink; molecular subtyping confirmed a match with the isolates from infected patients [20]. The use of an open piercing gun as opposed to a sterile straight needle may predispose to an increased risk of infection secondary to shearing trauma of the perichondrium with the former methods [21]. Exposure of the wound to fresh water or hot tubs immediately after the procedure may additionally increase the risk of infection [22].

Affected patients usually have a markedly swollen, red, and tender pinna. Infection may progress rapidly to produce necrosis of the cartilage.

Prompt therapy with antibiotics that have activity against P. aeruginosa is important (table 1), as perichondritis can result in permanent ear deformity [23,24]. In the systematic review of post-piercing infections noted above, delays of longer than five days before seeking treatment were associated with hospitalization, and perichondritis of the scapha (ie, the hollow part of the helix) versus the helix itself was associated with resultant ear deformity (100 versus 43 percent) [19].

Oral ciprofloxacin has been shown to be effective if the infecting strain is susceptible [25]. Infections may require prolonged antimicrobial therapy plus incision and drainage, as the cartilaginous portion of the ear has a poor blood supply. Abscesses, when present, should be drained promptly and cultured to both reduce the risk of pressure-induced cartilage damage and to provide a microbiological diagnosis and sensitivity results. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)

URINARY TRACT INFECTIONS

Epidemiology — Urinary tract infections (UTIs) caused by P. aeruginosa are typically hospital-acquired. Community-acquired P. aeruginosa is less common and generally occurs in patients with some predisposing factor.

Hospital acquired — P. aeruginosa is the third most common pathogen to cause hospital-acquired UTIs, after Escherichia coli and Enterococcus spp. Most such UTIs occur in patients with impaired host defenses and in those who have had recent urinary tract instrumentation and/or chronic indwelling urinary catheters. (See "Catheter-associated urinary tract infection in adults".)

Most strains of P. aeruginosa causing catheter-associated UTIs produce biofilms. A microbiologic study of P. aeruginosa isolates recovered from patients with indwelling urinary catheters found 20 of 26 (77 percent) were biofilm producers [26]. The majority of the isolates were multidrug resistant (69 percent); gentamicin resistance correlated with increased biofilm production. The association of gentamicin resistance and biofilm production could partly explain the increased prevalence of gentamicin-resistant infections encountered in this clinical setting.

Other identified risk factors for hospital-acquired P. aeruginosa UTI include male sex, longer hospitalization prior to UTI, and prior use of penicillins, third-generation cephalosporins, carbapenems, aminoglycosides, and vancomycin [27].

Other outbreaks of P. aeruginosa infection of the urinary tract have also occurred from contaminated urologic equipment or facilities including:

●Urodynamic equipment [28,29]

●A cystoscopy room via an unsealed drain [30]

●A urology unit with a contaminated sink, scope, and bedside table [31]

Community-acquired — Community-acquired UTIs due to P. aeruginosa usually develop in patients with:

●Urinary tract obstruction

●Chronic prostatitis

●Prolonged courses of antibiotic therapy

●Recurrent infections

In women, colonization of the vaginal introitus may rarely serve as a reservoir for community-acquired P. aeruginosa UTIs [32]. P. aeruginosa rarely causes UTIs in otherwise healthy school children.

Clinical features — The clinical manifestations of P. aeruginosa UTIs are similar to infections caused by other pathogens. Typical signs and symptoms include dysuria, frequency, urgency, suprapubic pain, and/or hematuria with cystitis and fever, chills, and flank pain in addition to patients with pyelonephritis. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents", section on 'Clinical manifestations'.)

However, certain features may be more common in patients with UTIs due to P. aeruginosa. For example, ulcerations in the mucosa of the bladder, ureters, and renal pelvis may rarely occur in severe infections due to P. aeruginosa. When ulcerations develop, obstruction or bleeding can result. Also, patients with UTIs due to P. aeruginosa may rarely have green urine. However, green urine has many other causes, including foods containing coloring agents and various medications [33-35].

Additionally, involvement of the urinary tract may occur from either ascending infection or hematogenous spread from a distant source of primary infection. In cases of hematogenous spread, renal infarcts may occur from bacterial invasion of medium and small-sized blood vessels.

Diagnosis — The diagnosis of P. aeruginosa UTI is similar to that for UTIs caused by other organisms. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents", section on 'Diagnostic approach'.)

For patients with a chronic indwelling bladder catheter, the isolation of P. aeruginosa from the urine is not diagnostic of a UTI, since bacteriuria and even pyuria in the absence of overt infection are common in such settings. The presence of consistent symptoms should determine whether infection is present and antibiotics should be administered.

Treatment — The management of P. aeruginosa UTI (ie, bacteriuria accompanied by symptoms consistent with UTI) involves antibiotic administration as well as correction of obstruction and removal of an indwelling catheter, if present. When P. aeruginosa UTI occurs in a patient with a chronic indwelling bladder catheter, eradication of the organism is usually impossible without catheter removal. If needed, the catheter should be replaced at the outset of antibiotic therapy. (See "Catheter-associated urinary tract infection in adults", section on 'Treatment'.)

The approach to empiric antimicrobial treatment of acute simple cystitis and acute complicated UTI is discussed in detail elsewhere. (See "Acute simple cystitis in adult and adolescent females" and "Acute simple cystitis in adult and adolescent males" and "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)

Once P. aeruginosa has been identified as the cause, the antimicrobial regimen can be tailored to the susceptibility of the isolate. Any antipseudomonal antibiotic to which the isolate is susceptible should be effective (table 1).

●For patients with acute simple cystitis due to P. aeruginosa, fosfomycin may be an active option depending on regional susceptibility [36,37]. Fosfomycin susceptibilities may need to be specifically requested. However, emergent fosfomycin resistance during treatment is a potential concern based on a simulation study [38].

●An oral fluoroquinolone, such as ciprofloxacin can be used for acute simple cystitis and for acute complicated P. aeruginosa UTI provided the isolate is susceptible and the patient is a suitable candidate for oral therapy.

Other options for antipseudomonal therapy are parenteral (table 1). Resistant isolates may only be susceptible to novel antimicrobial agents, such as ceftolozane-tazobactam [39], ceftazidime-avibactam [40], and plazomicin [41]. Options for resistant P. aeruginosa isolates are discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)

The duration of treatment for P. aeruginosa UTI is the same as for UTIs caused by other organisms. (See "Acute simple cystitis in adult and adolescent females", section on 'Alternative antimicrobial options' and "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents", section on 'Duration'.)

three to five days for simple cystitis, two to three weeks for pyelonephritis, and longer pending clinical resolution for intrarenal and perinephric abscesses. When cystitis is complicated by sepsis or bacteremia, the optimal duration is uncertain. In the absence of urinary obstruction, foreign bodies (such as stones or catheters), or abscess, antibiotic therapy can be discontinued after clinical and laboratory signs and symptoms of infection have resolved. This generally takes longer than five days.

The value of chronic suppressive therapy to prevent recurrence following a curative course of antibiotics for P. aeruginosa UTI is often limited by the lack of effective oral agents with significant antipseudomonal activity. Although ciprofloxacin generally has good in vitro activity against P. aeruginosa, this agent often rapidly induces the development of resistance when used for suppression. Methenamine salt administered in combination with ascorbic acid has been used by some for chronic suppression of UTI due to drug resistant organisms, but we do not endorse this practice since the long-term efficacy of this agent is poor [42]. (See "Recurrent simple cystitis in women", section on 'Methenamine'.)

GASTROINTESTINAL INFECTIONS — Although uncommon, particular gastrointestinal tract infections with P. aeruginosa have been described.

Clinical syndromes

Post ERCP — P. aeruginosa cholangitis and bacteremia following endoscopic retrograde cholangiopancreatography (ERCP) have been described, with the same strain or serotype found in the blood of patients and the implicated endoscope [43-46]. The source of these infections has been traced to inadequate decontamination or cleaning of the endoscope, contamination with nonsterile rinse water following decontamination, or inadequate drying of the endoscope.

Septic complications following ERCP are discussed elsewhere. (See "Infectious adverse events related to endoscopic retrograde cholangiopancreatography (ERCP)".)

Typhlitis — Typhlitis, or neutropenic enterocolitis of the cecum or surrounding gut, is most commonly seen in patients with chemotherapy-induced neutropenia. Although such infections are polymicrobial, P. aeruginosa has been detected from the blood in some patients at the time of presentation with this syndrome [47,48].

Typhlitis has been most commonly described in children with leukemia but may also occur in adults with leukemia and in patients with neutropenia from chemotherapy used for treatment of solid tumors.

Patients with typhlitis present with the sudden onset of fever with abdominal pain (particularly in the right-lower quadrant) and distention. Because diarrhea and fever are common toxicities associated with high dose chemotherapy, it is likely that many cases of typhlitis go unrecognized. Computed tomography and/or ultrasonography should be performed in all neutropenic patients with right-lower-quadrant signs to permit prompt diagnosis and treatment [47]. Typhlitis should be suspected in any immunocompromised patient presenting with right lower quadrant pain and compatible radiographic findings.

Most patients can be treated conservatively with intravenous fluids and antibiotics, although surgery may be necessary if complications arise [49]. Antibiotics with activity against P. aeruginosa are discussed elsewhere (table 1). (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)

Typhlitis is discussed in greater detail separately. (See "Neutropenic enterocolitis (typhlitis)".)

Enteritis due to P. aeruginosa (Shanghai fever) — Enteritis due to P. aeruginosa (Shanghai fever) may mimic the clinical features of typhoid fever and produce fever, splenomegaly, diarrhea, and even "rose spots" [50]. Cases have mainly been reported in infants and children from Taiwan and China. The clinical course can be severe. In a series of 27 children from Taiwan with febrile diarrhea, sepsis, and P. aeruginosa isolated from a clinical specimen (blood or other sample), 23 had necrotizing enteritis, nine had bowel perforation requiring surgery, seven had seizures in the setting of hyponatremia, and two had meningitis [51].

Given the few reported cases, treatment of this entity has not been extensively studied. The general principles of antipseudomonal therapy are likely to apply. These and specific antibiotics with activity against P. aeruginosa are discussed elsewhere (table 1). (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections".)

CENTRAL NERVOUS SYSTEM INFECTIONS — Meningitis or suppurative brain abscesses due to P. aeruginosa are rare. Most patients with central nervous system (CNS) infections caused by P. aeruginosa have serious underlying diseases or have had recent trauma, neurosurgical procedures, or burns [52-55].

In a retrospective case series, P. aeruginosa was the second most common etiologic agent in uremic hemodialysis patients with bacterial meningitis [52]. In a study of 544 episodes of spontaneous acute bacterial meningitis, gram-negative bacilli were identified as the causative agent in 40 (7 percent), and P. aeruginosa was the second most common gram-negative pathogen [53]. Clinical factors independently associated with P. aeruginosa included advanced age, history of cancer, hospital-acquired infection, urinary tract infection as a distant focus of infection, absence of rash, hypotension, and a high cerebrospinal fluid white-cell count. The in-hospital mortality rate was 53 percent.

Clinical features and diagnosis of P. aeruginosa CNS infections are similar to those for infections caused by other gram-negative pathogens. (See "Health care-associated meningitis and ventriculitis in adults: Clinical features and diagnosis", section on 'Diagnosis'.)

Empiric therapy of gram-negative bacillary meningitis is discussed elsewhere. (See "Health care-associated meningitis and ventriculitis in adults: Treatment and prognosis", section on 'Systemic antimicrobial therapy'.)

Once P. aeruginosa is identified as the causative agent and susceptibility testing returns, we use a single antipseudomonal agent to which the isolate is susceptible and that has good CSF penetration, preferably ceftazidime or cefepime. For CNS infections due to multidrug-resistant isolates, ceftolozane-tazobactam may be an option [56]. There is no clear evidence that combination therapy offers additional benefit in directed therapy of P. aeruginosa infections. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Role of combination antimicrobial therapy'.)

We treat for at least 21 days, although therapy should be individualized. Repeat CSF analysis and culture should confirm clearance of the organism. Treatment of drug resistant organisms should be done in consultation with an expert in treating such infections and may include alternative agents such as colistin and local (eg, intrathecal) therapy. (See "Health care-associated meningitis and ventriculitis in adults: Treatment and prognosis", section on 'Intrathecal and intraventricular therapy'.)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

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SUMMARY AND RECOMMENDATIONS

●Clinical significance of Pseudomonas aeruginosa – P. aeruginosa can cause severe hospital-acquired infections (especially in immunocompromised hosts), is often antibiotic resistant, and is often associated with a high mortality rate. (See 'Introduction' above.)

●Eye infections – P. aeruginosa can cause both minor and vision-threatening infections of the eye. These infections include dacryocystitis, blepharoconjunctivitis, and orbital cellulitis. The pathogen can also be directly introduced into the cornea, anterior chamber, or vitreous via trauma or surgery. P. aeruginosa has been implicated in some cases of ophthalmia neonatorum and scleral abscesses. Hematogenous infection of the vitreous occurs rarely in patients with P. aeruginosa bacteremia. (See 'Eye infections' above.)

•Corneal infections due to P. aeruginosa – These usually result from minor trauma to the cornea and are frequently associated with contact lens use. Clinical signs are usually localized to the eye; fever and other systemic manifestations are generally absent. Diagnosis is made by Gram stain and culture of corneal scrapings. Treatment usually consists of topical and systemic antipseudomonal agents. (See 'Corneal and conjunctival infections' above.)

•Endophthalmitis – Endophthalmitis can occur in the setting of perforated corneal ulcers, following penetrating ocular injuries, following eye surgery, and from hematogenous spread. The course of pseudomonal endophthalmitis is typically fulminant, developing over hours. Patients virtually always have intense ocular pain accompanied by decreased visual acuity. The diagnosis is made clinically and confirmed with vitreal cultures. Therapy of P. aeruginosa endophthalmitis frequently includes vitrectomy and intravitreal antibiotics. (See 'Endophthalmitis' above and "Bacterial endophthalmitis".)

●Ear infections – P. aeruginosa causes four types of ear infection: simple otitis externa (ie, "swimmer's ear"), malignant external otitis, otitis media, and perichondritis. (See 'Ear infections' above.)

•Otitis externa – P. aeruginosa is the most common cause of external otitis, accounting for more than 70 percent of all cases. Otitis externa due to P. aeruginosa is common in swimmers and in residents of tropical or humid climates. (See 'Otitis externa' above.)

In some patients, particularly elderly patients with diabetes mellitus, otitis externa may progress to a more severe and even life-threatening illness. Skull base osteomyelitis (also known as malignant external otitis) occurs when P. aeruginosa penetrates the epithelium of the external auditory canal and invades the underlying soft tissue, cartilage, and cortical bone. (See 'Skull base osteomyelitis' above and "Malignant (necrotizing) external otitis".)

•Otitis media – P. aeruginosa is the most commonly isolated organism from the middle and external ears of patients with chronic suppurative otitis media. Otitis media due to P. aeruginosa can also occur in infants less than six weeks of age. The presence of this pathogen should be suspected when patients with otitis media fail to respond to usual antibiotic therapy. (See 'Otitis media' above.)

●Other types of infections – Other sites of infection discussed in this topic include urinary tract infections (UTIs), gastrointestinal infections, and central nervous infections.

•UTIs – UTIs caused by P. aeruginosa are typically hospital-acquired or associated with urinary tract obstruction, chronic prostatitis, prolonged courses of antibiotic therapy, or recurrent infections. Management involves antibiotic administration (table 1) as well as surgically correcting any obstruction and removing an indwelling catheter. (See 'Urinary tract infections' above and "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)

•Gastrointestinal infections – P. aeruginosa can cause bacteremia following endoscopic retrograde cholangiopancreatography and typhlitis in patients with chemotherapy-induced neutropenia. (See 'Gastrointestinal infections' above.)

•Central nervous system infections – Meningitis or suppurative brain abscesses due to P. aeruginosa can occur, especially in patients with serious underlying diseases or recent trauma or neurosurgical procedures. (See 'Central nervous system infections' above.)