Corrigendum to “Community-Acquired Cavitary Pseudomonas Pneumonia Linked to Use of a Home Humidifier”

[This corrects the article DOI: 10.1155/2017/5474916.].


Introduction
Pseudomonas aeruginosa is an opportunistic pathogen that usually causes pneumonia in patients with an underlying medical condition or a risk factor that predisposes them to infection [1]. However, several reports of severe P. aeruginosa pneumonia in previously healthy patients without apparent immunode ciency have been reported [1,2]. Only a few cases have been attributable to an identi able source [1,3,4]. In this case, we describe community-acquired pneumonia (CAP) in a previously healthy 30-year-old male who we believe acquired the P. aeruginosa infection from a home humidi er.

Case Presentation
A 30-year-old male with no past medical history presented to the emergency department reporting three weeks of progressively worsening cough producing yellow sputum, pleuritic right scapular pain, four days of fever (to 38.9°C), and one episode of night sweats. Additionally, he noted a ten-pound weight loss, which he attributed to decreased appetite. He denied hemoptysis, shortness of breath, diarrhea, or dysuria. e patient had recently completed a veday course of azithromycin and had been using benzonatate without relief.
In the two months prior to his presentation, he traveled through Japan, Cambodia, ailand, Laos, and Israel. He took antimalarial medications when appropriate and had received all required travel vaccinations prior to departing. Additionally, one month before presentation, he had attended Burning Man, an artistic gathering in the middle of the Black Rock Desert in Nevada. His ancée had traveled with him and was also experiencing a similar but less severe cough.
ey used a single-room humidi er nightly while sleeping. He had no history of recurrent or severe infections. He denied tobacco or alcohol use. He had a history of occasional marijuana use but denied any intravenous drug use. He worked as a teacher.
On physical exam, his blood pressure was 140/69 mmHg with a pulse rate of 84/min. His tympanic temperature was 36.5°C. His respiratory rate was 18/min, and oxygen saturation on room air was 99%. He was in no acute distress, and examination of his chest was clear to auscultation bilaterally.
Laboratory results showed a leukocytosis (WBC 11.3 × 10 3 /μL, 11.2%) without eosinophilia, an elevated venous blood lactate (3.3 mmol/L), and anemia (hemoglobin 12.9 g/dL). His initial chest x-ray was abnormal, so a CT chest with contrast was obtained, which demonstrated a 2.9 cm right upper lobe cavitary lesion (Figure 1(a)). A brief workup for immunode ciency was then performed. e patient had a negative 4th generation HIV antigen-antibody test as well as a negative HIV RNA PCR. His CD4 count was not measured, but quantitative immunoglobulin analysis was within normal limits (IgG 875 mg/dL, IgA 186 mg/dL, and IgM 76 mg/dL). Quantiferon TB Gold was negative.
Given his clinical stability, failure of outpatient antibiotics, and inability to produce an adequate sputum sample for Gram stain, the decision was made to proceed with bronchoscopy. Bronchoscopy showed di use in ammation with mild thick yellow secretions. Cultures of bronchoalveolar lavage, washings, and tissue culture performed during bronchoscopy resulted with heavy growth of P. aeruginosa (Figure 1(b)). No other pathogens were identi ed. Fungal culture showed no growth after four weeks. Blood cultures, three Kinyon smears of sputum, and urine Legionella antigen were also negative. Aspergillus galactomannan antigen and (1-3)-β-D-glucan assay (Fungitell) were negative. Histoplasma urine antigen, serum cryptococcal antigen, and serum coccidioides antigens were not detected. Echinococcus antibody was not detected. Once Gram-negative bacilli were identi ed on cultures, he was treated with ceftazidime (1g q8h IV). e dose was increased to 2g q8h IV after speciation, and sensitivities became available. On this regimen, his condition steadily improved. He was subsequently transitioned to oral cipro oxacin (750 mg BID for 14 days) and discharged with outpatient follow-up. He completed a 21-day antibiotic course in total.

A Search for the Source
e identi cation of P. aeruginosa as the etiologic agent of this otherwise healthy patient's chronic cough and CT chest ndings prompted a review of his history for possible exposures to contaminated water. According to the patient, he had three signi cant exposures to aerosolized water in the past few months: nightly use of a humidi er while sleeping, being sprayed with water at Burning Man, and swimming near a waterfall in Southeast Asia. We asked the patient's family to bring his ultrasonic cool-mist humidi er from home. It was noted to have a thin gray-green lm coating the plastic covering as well as standing water in the basin (Figure 1(c)). e patient was unsure when the unit had last been cleaned. We obtained cultures of the humidi er water and basin, which both returned positive for P. aeruginosa (Figure 1(d)). Humidi er and patient isolates had identical patterns of antibiotic sensitivities. We performed whole genome sequencing (PacBio RSII) on the isolates obtained from the humidi er basin and from the bronchoscopy tissue. We found the isolates to be identical (accessions: NTGC01000000-NTGD01000000).

Discussion
In this report, we present the case of a young man diagnosed with cavitating P. aeruginosa pneumonia. By comparing antibiotic resistance patterns and using whole genome sequencing, we were able to con rm that his home humidi er 2 Case Reports in Infectious Diseases was likely colonized with an identical P. aeruginosa isolate. e humidi er was removed from the patient's room and discarded, and he has not had any recurrence of P. aeruginosa pneumonia after several months of follow-up.
Our case highlights the fact that P. aeruginosa pneumonia in the community should prompt environmental investigations to identify possible sources of infection. e incidence of community-acquired P. aeruginosa pneumonia in otherwise healthy individuals is low. In one study, the P. aeruginosa pathogen was isolated in 0.4% of patients diagnosed with CAP [5]. A previous review of published cases of P. aeruginosa CAP in previously healthy adults using strict criteria showed only 12 cases [2]. As noted, isolated cases have been reported in which environmental sources including a home-humidifying device and a whirlpool spa have been identi ed.
We suspect that the patient described in this report acquired P. aeruginosa from the contaminated water in his humidi er. Maintenance of this patient's humidi er was inadequate; stagnation of tap water without sterilization of the machine likely permitted production of an increased bacterial load and bio lms. Home humidi ers, particularly cool-mist and ultrasonic units, like the one possessed by this patient, have been shown to aerosolize their contents [6]. When the uid in the reservoir of a humidi er becomes contaminated with bacteria, the aerosol may contain high concentrations of bacteria [7]. To obtain a broader perspective on the microbiology of single-room humidi ers, Hull et al. sequenced rRNA obtained from 26 home humidi ers [8]. e authors found that bacteria encountered were generally low in diversity and were dominated by the orders Sphingomonadales, Rhizobiales, and Burkholderiales. ese are all types of bacteria that can form bio lms and are commonly found in environmental water sources. Very few sequences of P. aeruginosa were found [8]. However, another study of respiratory devices in multiple medical settings found a surprisingly high (21% of 70 samples) rate of P. aeruginosa contamination [9].
Patients such as ours reinforce the possibility for a rare but potentially life-threatening adverse e ect of home humidi er use. Similar to the patient in this case, many other individuals fail to adequately clean their home humidi ers. According to a survey conducted by Consumer Reports, 40% of Americans rarely or never clean their humidi ers [10]. In accordance with the Centers for Disease Control and Prevention guidelines for the prevention of nosocomial pneumonia, room-air humidi ers that create aerosols should not be used unless they can be sterilized or subjected to daily disinfection and lled only with sterile water [11]. In addition to frequent disinfection of the device to avoid microbial colonization, performing periodic surveillance of the humidi er components to look for microbial growth would also be prudent. Finally, as whole genome sequencing is becoming a more readily available technology in the clinical space, it proved useful in con rming that the patient and environment isolates were identical [12].

Disclosure
is Whole Genome Shotgun project has been deposited at DDBJ/ENA/GenBank under the accession NTGC00000000 and NTGD00000000. e version described in this paper is version NTGC01000000 and NTGD01000000.

Conflicts of Interest
e authors declare that there are no con icts of interest regarding the publication of this article.