The clinical isolate was cultured from a sputum sample of a 30-year-old HIV negative male suffering from an exacerbation of bronchiectasis in September 2015. He was referred to our institute for evaluation of cough with sputum production and repeated episodes of sneezing and nasal discharge for the last 15 years and breathlessness for the past one year. His clinical course was characterised by progressive exertional dyspnoea along with wheezing. A week prior to presentation, he experienced low-grade intermittent fever along with chills and rigors, which prompted the referral. Based on his symptomatic and radiological profile, he had received anti-tuberculous therapy for nine months three years back without relief. He was never a smoker with no history of exposure to environmental smoke, biomass fuel smoke or toxic fumes. General physical examination revealed presence of digital clubbing. There was no evidence of pallor, cyanosis or lymphadenopathy. He was afebrile with a respiratory rate of 18 per minute and oxygen saturation of 94% on oxygen @ 2 L/min. On auscultation, vesicular breath sounds were audible bilaterally along with coarse creptations over all areas of the lung. The total leucocyte count was 17.9 × 103 cells/ mm3, with neutrophilic predominance. Spirometry was suggestive of severe restriction with no response to bronchodilators. Chest radiograph showed multiple ring like shadows in bilateral lower zones. High resolution computed tomography of the thorax revealed multiple dilated bronchi with classical signet ring sign and string of pearls appearance in bilateral lower lobes and right middle lobe, suggestive of cystic bronchiectasis. The patient was admitted to the ward and a sputum sample was sent to the aerobic culture laboratory. Empirical treatment with intravenous infusion of piperacillin-tazobactam 4.5 gm QID and oral azithromycin 500 mg OD was started. On direct microscopic examination of sputum, the sample had 15-20 pus cells and 0-5 epithelial cells/ low power field. Plenty of gram negative bacilli were observed under the oil immersion objective. The sample was processed by semi-quantitative method using a calibrated loop after treatment with N-acetyl cysteine. It was cultured on sheep blood agar and MacConkey agar plates. The plates were incubated overnight at 37 ° C in ambient air and 5% CO2 for Blood agar plates. More than 105 cfu/ ml non-hemolytic, 2 mm in diameter, greyish, translucent, moist, low convex colonies on Blood agar and non-lactose fermenting colonies in MacConkey agar, were isolated which were identified as P. monteilii. Since significant counts of a single type of organism were isolated from a good quality sputum specimen, it was considered pathogenic. Antimicrobial susceptibility for piperacillin, cefepime, ceftazidime, meropenem, ciprofloxacin, levofloxacin, gentamicin and amikacin was tested using Kirby Bauer's disk diffusion method; for colistin E-test was used (MIC of 2 mcg/ml). Pseudomonas aeruginosa ATCC 27853 strain was used as control. The organism was found to be susceptible to all tested antimicrobials []. Treatment with piperacillin-tazobactam was continued. Surveillance samples - nasal and pharyngeal swabs, urine and stool specimens were collected on day 1 and day 8 of admission as part of a separate study. None of these samples grew pathogenic organisms. The patient’s symptoms settled, total leucocyte count returned to normal (9.4 × 103 cells/ mm3), and sputum culture was negative before he was discharged after eight days of hospital stay. A brief summary of his stay in the hospital has been depicted in the timeline (Additional file ). On discharge, the patient was shifted to oral piperacillin-tazobactam, which was continued for a further 7 days. On follow up, P. monteilii has not been cultured from clinical samples from this patient since. Surveillance cultures from the hospital environment in the month of September 2015 did not grow any P. monteilii. The two environmental isolates were cultured one each from a bed railing in the Intensive Care Unit in February 2016, and from a bedside table in the ward in March 2016. Both tested susceptible to all antimicrobials (colistin MIC 1.5 mcg/ml). We did not identify any related clinical isolates in that time period. Though the isolates had identical antibiograms, typing by Random amplification of polymorphic DNA (RAPD) using the ERIC2 primer found 35–57% homology between the strains in UPGMA generated dice coefficients, indicating no clonal relationship. This was expected since the patient acquired the infection prior to admission and the isolates were recovered months apart. The discriminatory power of this primer is unknown for P. monteilii. However, RAPD being affected by differences in factors other than antimicrobial susceptibility, is a more sensitive method for identifying heterogeneity [].