Person-to-Person transmission of Pseudomonas pneumonia in the community: documentation by pulsed-field electrophoresis.

ABSTRACT: Pseudomonas aeruginosa is a rare cause of community-acquired infection. The source of this organism has usually been inapparent or environmental (ie, contaminated humidifiers). We documented transmission of P aeruginosa leading to cavitary pneumonia and lung abscess from daughter to mother and confirmed the clonal identity of our two patients' isolates using pulsed-field electrophoresis.

**********

PNEUMONIA caused by Pseudomonas organisms occurs almost exclusively in hospitalized patients, particularly patients with critical illness and significant comorbidities. Community-acquired Pseudomonas pneumonia has been reported in healthy adults (1-4) but is rare. Some cases of community-acquired Pseudomonas pneumonia have been associated with home humidifiers as well as home whirlpools. (5,6) Contaminated anesthesia apparatus and mechanical ventilators, delivery room resuscitators and humidifiers, and health care workers all have been implicated in the transmission of Pseudomonas pneumonia in the hospital setting. (7-9) We report a case of Pseudomonas pneumonia acquired by person-to-person transmission in the community setting.

CASE REPORT

An 83-year-old white woman was admitted to the Jersey Shore Medical Center because of shortness of breath and productive cough. She also reported light-headedness, lethargy, hypersomnia, anorexia, and weight loss for a week.

The patient's medical history included asthma for 76 years for which she took montelukast (Singulair), nebulized albuterol, salmeterol inhaler (Serevent), theophylline (Theo-Dur), and budesonide inhaler (Pulmicort). A month before admission, prednisone (20 mg/day) had been added to the regimen. The patient had had no other medical illness except for community-acquired bacterial pneumonia in 1998.

On physical examination, the patient was a well-developed white woman in mild respiratory distress. Her temperature was 96.9[degrees]F, blood pressure 167/80 mm Hg, pulse rate 119/min, and respiratory rate 23/min. Diffuse expiratory wheezes were present bilaterally, but the remainder of the physical examination was unremarkable. Initial sputum culture grew Serratia marcescens, but initial chest radiograph was unremarkable except for some chronic changes related to asthma (Fig 1). The white blood cell count was 15,200/[mm.sup.3], hemoglobin value 15.3 g/dL, and serum glucose value 305 g/dL. She was treated with oral antibiotics and intravenous methylprednisolone (Solu-Medrol) in addition to theophylline, montelukast, salmeterol inhaler, albuterol, and ipratropium neubilizer with supplemental oxygen. One week later, the patient's symptoms had not improved, and repeated chest radiography revealed a right upper lobe infiltrate (Fig 2). Ceftriaxone (Rocephin) was administered. Symptoms persisted, and the antibioti c regimen was changed to ciprofloxacin. Symptoms worsened, and hemoptysis developed.

Four weeks after admission, the chest film revealed cavitary pneumonia (Fig 3). The patient had computed tomography (CT). of the chest (Fig 4) and diagnostic bronchoscopy. Culture of the bronchial brush and aspirate grew Pseudomonas aeruginosa sensitive to [beta]-lactams and aminoglycosides (Table). Treatment with tobramycin and piperacillin for 20 days produced no significant improvement. Piperacillin therapy was discontinued and ceftazidime, 2 g every 12 hours, was administered. CT-guided aspiration of the lung abscess again confirmed the presence of P aeruginosa, now sensitive only to tobramycin and imipenem (Table). The antibiotic regimen was changed, and the patient's condition significantly improved. After 27 days of inpatient treatment, the patient was discharged to a rehabilitation facility on intravenous antibiotics for 1 more week.

One month before admission, the patient's 52-year-old daughter had lived with the patient for approximately 1 month and had had multiple medical problems, including allergic bronchopulmonary aspergillosis, steroid-dependent asthma, invasive aspergillosis, and bronchiectasis. Four months before admission of the patient, the patient's daughter had had an episode of Pseudomonas pneumonia and had been discharged from the hospital after 2 months of antibiotic therapy. She was readmitted to the hospital approximately 1 month after our patient's hospital admission and was treated for hemoptysis due to invasive aspergillosis. At this time, she remained colonized with P aeruginosa, which over time had developed increased antibiotic resistance as shown by our patient's isolate (Table).

These findings led us to speculate that she had transmitted the resistant P aeruginosa to our patient. To test this hypothesis, genotypic testing was done on both patients' isolates to determine clonal relatedness using pulsed-field electrophoresis (BioRad Genepath System, Hercules, Calif). Organisms were grown overnight in a broth solution and standardized to a predetermined inoculum. Bacterial cells were embedded in an agarose plug, treated with lysozyme, and washed. After an overnight incubation in proteinase K, plugs were washed several times before the addition of a specific restriction enzyme, Spe 1. Plugs were digested overnight and then again subjected to a series of wash steps. Slices of the agarose plugs containing the chromosomal DNA fragments were inserted into the wells of an agarose gel, and the restriction fragments were resolved into a pattern of discrete bands, using a gel apparatus that switches the direction of current according to a predetermined pattern. At the completion of the electroph oretic separation and after staining with ethidium bromide, bands were visualized on a transilluminator. The DNA restriction patterns of both the isolates were identical, thus confirming clonality of the two isolates.

DISCUSSION

Community-acquired Pseudomonas pneumonia is well documented in immunocompromised hosts. (10,11) In one recent study, 68% of Pseudomonas infections associated with HTV infection were community acquired. (12) Pseudomonas remains extremely uncommon as a community-acquired pathogen in normal hosts or even in those with chronic obstructive pulmonary disease. We found no report of person-to-person transmission in the community setting.

Unlike other reported cases of community acquired Pseudomonas pneumonias, which resulted in severe septicemic illness and lobar consolidation, (1,12) our patient presented with the gradual onset of necrotizing cavitary pneumonia without evidence of bacteremia. Colonization of the oropharynx with P aeruginosa in acutely ill or debilitated patients may lead to pneumonia. (13) Although findings on our patient's initial chest x-ray film were normal, it is likely that colonization of the oropharynx with Pseudomonas had been present for weeks and predisposed to the development of pulmonary infection. The similarity of the organisms isolated from our patient and her daughter, confirmed by electrophoresis, support this hypothesis and provide compelling evidence of person-to-person transmission.

Transmission of P aeruginosa from person to person by direct inoculation from shared respiratory equipment has been documented. In our case, however, the mother and daughter lived together but never shared their inhalers or nebulizer equipment. It is also possible that transmission occurred when our patient visited her daughter in the hospital. It seems more likely, however, that the transmission occurred in the home environment based on the duration of exposure and temporal relationship to our patient's illness. Finally, it is conceivable that our patient, whose initial chest film was unremarkable acquired Pseudomonas infection in the hospital environment. This appears unlikely since there was no other case of Pseudomonas infection on our patient's unit around the time of her admission and up to development of her symptoms of chest infection. While pulmonary infection was likely to be facilitated by the coexistence of multiple factors including advanced age, asthma, steroid therapy, and newly diagnosed diabe tes mellitus, it seems most likely that infection with this particular organism was a result of person-to-person transmission.

TABLE Comparison of Pseudomonas aeruginosa Isolates *

                                 Patient's Specimens
Antibiotics              Bronchial Brush  CT-Guided Aspiration

Amikacin                        -                 32 I
Aztreonam                     16 I               >16 R
Chloramphenicol               >16 R              >16 R
Ceftriaxone                   >32 R              >32 R
Ceftazidime                   <8 S               >16 R
Carbenicillin                Resistant           Resistant
Cefotaxime                    >32 R              >32 R
Ciprofloxacin                 >2 R                >2 R
Gentamicin                    <4 S                >8 R
Mezlocillin                   64 S               >64 R
Piperacillin                  <16 S              >64 R
Ticarcillin/Clavulanate       64 S               >64 R
Tobramycin                    <4 S                <4 S

                             Daughter's Specimens
Antibiotics              First Admission  Readmission

Amikacin                        -            <16 S
Aztreonam                     16 I           >16 R
Chloramphenicol               >16 R          >16 R
Ceftriaxone                   >32 R          >32 R
Ceftazidime                   <8 S           >16 R
Carbenicillin                 Resistant     Resistant
Cefotaxime                    >32 R          >32 R
Ciprofloxacin                 >2 R           >2 R
Gentamicin                    <4 S            8 I
Mezlocillin                   64 S           >64 R
Piperacillin                  <16 S          >64 R
Ticarcillin/Clavulanate       64 S           >64 R
Tobramycin                    <4 S           <4 S

* I = Intermediate, R = resistant, S = sensitive.

References

(1.) Hoogwerf BJ, Khan MY: Community-acquired bacteremic Pseudomonas pneumonia in a healthy adult. Am Rev Respir Dis 1981; 123:132-134

(2.) Quirk JA, Beaman MH, Blake M: Community-acquired Pseudomonas pneumonia in a normal host complicated by metastatic panophthalmitis and cutaneous pustules. Aust N Z J Med 1990; 20:254-256

(3.) Fishman H, Eaton B, Lipson A, et al: Primary Pseudomonas pneumonia in a previously healthy man. South Med J 1983; 76:260-262

(4.) Govan J, Reiss-Levy E, Bader L, et al: Pseudomonas pneumonia with bacteremia. Med J Aust 1977; 1:627-628

(5.) Harris AA, Goodman L, Levin S: Community acquired Pseudomonas aeruginosa associated with the use of a home humidifier. West J Med 1984; 141:521-523

(6.) Rose HD, Franson TR, Seth NK, et al: Pseudomonas pneumonia associated with the use of a home whirlpool spa. JAMA 1983; 250:2027-2029

(7.) Olds JW, Kirch AL, Eberle BJ, et al: Pseudomonas aeruginosa respiratory tract infection acquired from contaminated anesthesia machine. Am Rev Respir Dis 1972; 105:629-632

(8.) Fierer J, Taylor PM, Gezon HM: Pseudomonas aeruginosa epidemic traced to delivery room resuscitators. N Engl J Med 1967; 276:991-996

(9.) Foca M, Jakob K, Whittier S, et al: Endemic Pseudomonas aeruginosa infection in a neonatal intensive care unit. N Engl J Med 2000; 343:695-700

(10.) Chatzininkolaou I, Abi-Said D, Bodey GP, et al: Recent experience with Pseudomonas aeruginosa bacteremia in patients with cancer: retrospective analysis of 245 episodes. Arch Intern Med 2000; 160:501-509

(11.) Dropulic LK, Leslie JM, Eldered LJ, et al: Clinical manifestations and risk factors of Pseudomonas aeruginosa infection in patients with AIDS. J Infect Dis 1995; 171:930-937

(12.) Iannini PB, Claffey T, Quintiliani R: Bacteremic Pseudomonas pneumonia. JAMA 1974; 230:558-561

(13.) Levsion ME, Kaye D: Pneumonia caused by gram-negative bacilli: an overview. Rev Infect Dis 1985; 7:656-665

RELATED ARTICLE: KEY POINTS

* Pseudomonas aeruginosa should be considered in the differential diagnosis of cavitary pneumonia.

* In an era of increasingly complex home medical care, pathogens usually associated with nosocomial infection, such as P aeruginosa, may become important agents of community-acquired infection.

* Molecular techniques such as pulsed-field electrophoresis can help to answer epidemiologic questions and increase our understanding of infectious diseases and their transmission.

From the Department of Medicine, Division of Infectious Disease, and the Department of Pathology (Microbiology Laboratory), Jersey Shore Medical center, Neptune, NJ.

Reprint requests to Elliot Frank, MD, Jersey Shore Medical center, Department of Medicine, 1945 Route 33, Neptune, NJ 07754.