Corynebacterium propinquum (C. propinquum) is a bacterium found in the normal flora of the skin and mucous membranes that mainly colonizes the oropharyngeal region of the upper respiratory tract.1 Some rare cases of opportunistic respiratory infection by C. propinquum, often associated with immunosuppression or underlying lung disease, have been reported.2,3

We report a case of respiratory infection in a 75-year-old man, former smoker of 60 pack-years, diagnosed with chronic obstructive pulmonary disease (COPD) GOLD IV, treated with bronchodilators and high-dose inhaled corticosteroids, with a history of frequent exacerbations requiring antibiotics and systemic corticosteroids. The patient was hospitalized with a 1-week history of fever, increased dyspnea, and cough with purulent expectoration. Empirical treatment with levofloxacin began in the emergency room and samples were collected for microbiological analysis, including sputum for standard culture and urine for pneumococcal and Legionella spp. antigen testing, in view of initially suspected pneumonia. Rhonchi and wheezing were heard in both lung fields on physical examination. Clinical laboratory testing showed 17,040leukocytes/mm3 (92% neutrophils) and blood biochemistry results were normal. Lung function tests revealed FVC: 1.6l (52%), FEV1: 0.63l (27%) and FEV1/FVC 39%. No infiltrates were seen on chest X-ray.

The sputum Gram stain showed fewer than 10 epithelial cells and more than 25 polymorphonuclear leukocytes/100× field, and Gram positive bacilli with morphology suggestive of Corynebacterium spp. (10/1000× field). Culture was negative at 24h, so it was reincubated. At 48h, there was abundant growth of creamy, round, whitish, catalase-positive colonies. C. propinquum was identified using the API® Coryne system (bioMérieux), and subsequently confirmed by mass spectrometry (MALDI-TOF) and 16S rRNA gene sequencing. The disk diffusion method was used for antibiotic sensitivity testing, showing the isolate to be sensitive to penicillin, ampicillin, ciprofloxacin, tetracycline, cefotaxime, vancomycin and rifampicin, and resistant to erythromycin and clindamycin.

One of the main problems in establishing the etiological diagnosis of respiratory infections is the fact that the microorganisms that cause most respiratory infections often occur in the upper airways as part of the normal flora or as colonizers. Thus, to determine the clinical significance of these microorganisms, the quality of the respiratory specimen must first be evaluated by Gram stain. In this evaluation, generally performed in sputum, epithelial cells, suggestive of oropharyngeal contamination, and polymorphonuclear leukocytes, indicative of a pulmonary focus, are quantified. In our case, the Gram stain report suggested that the specimen was representative of a lower respiratory tract sample, so the cause of the exacerbation, in the absence of other causes, could be attributed to C. propinquum infection. The patient progressed well with clinical respiratory improvement, confirmed with a subsequent negative culture.

Since C. propinquum was first described in 1993, very few clinically significant cases have been published. Most authors report it as an opportunistic pathogen and an emerging infection in both the respiratory tract and other sites.4 As mentioned, C. propinquum respiratory infection is rare, and has been documented mainly in hospitalized, immunosuppressed patients, and in patients with underlying respiratory disease, such as COPD or bronchiectasis, receiving wide-spectrum antibiotics.5

The few cases reported in the literature agree on the importance of the Gram stain for establishing the pathogenic role of C. propinquum, particularly in immunosuppressed or hospitalized patients who have received previous antibiotic treatment.2,3,5

Although C. propinquum is generally sensitive to vancomycin, multiresistant strains do exist,6 so antibiotic sensitivity testing is recommended for prescribing the appropriate treatment.

In our opinion, although few cases have been published, C. propinquum can behave as an emerging pathogen. It can be responsible for COPD exacerbations, particularly if the patient presents predisposing factors, and the strain is isolated from a lower respiratory tract sputum sample.