Bordetella hinzii is a species isolated in poultry with respiratory disease, and has occasionally been described in humans. We present the case of an 85-year-old woman with respiratory symptoms consisting of cough, expectoration and dyspnoea on moderate exertion of several days duration. Sputum culture was requested from her primary care centre. It was inoculated in blood agar, chocolate agar and MacConkey agar (Oxoid®). The sample quality was considered optimal after Gram staining, with abundant polymorphonuclear leukocytes and Gram negative bacilli found on examination. After 24h incubation at 35°C, profuse growth of two types of colonies was detected on all three media. Two colony morphologies were observed on the MacConkey agar: a pinkish, mucoid colony, and a second colourless colony. Identification performed using the MALDI-TOF–MS biotyper 3 system classified them as Klebsiella oxytoca and B. hinzii, the latter with an index of 2.241, which is considered optimal for genus and species. Molecular confirmation was carried out by sequencing 500 base pairs of the 16S rRNA gene1 and comparing the sequence obtained with those banked in GenBank, using the NCBI BLASTn algorithm. Ninety-nine percent homology with other existing B. hinzii strains was obtained, including B. hinzii strain LMG 13501.1 The antibiotic treatment prescribed in the emergency department at discharge was amoxicillin–clavulanate 2000/62.5mg every 12h. Antibiotic susceptibility testing performed using the WalkAway® system microdilution panel (Siemens) found sensitivity to the following antibiotics: amoxicillin–clavulanate (MIC≤8/4μg/ml), azithromycin (MIC=1.5μg/ml), piperacillin–tazobactam (MIC≤8μg/ml), gentamicin (MIC=4μg/ml) and levofloxacin (MIC≤1μg/ml); intermediate sensitivity to: ampicillin–amoxicillin (MIC=16μg/ml) and ciprofloxacin (MIC=2μg/ml), and resistance to cefuroxime (MIC>16μg/ml), tobramycin (MIC>8μg/ml) and trimetoprim–sulfametoxazol (MIC>4/76μg/ml). Since B. hinzii was first described in 1994,1 isolates have been reported in respiratory samples from three patients. In one patient with cystic fibrosis, B. hinzii was isolated sequentially in sputum for a period of 3 years,2 together with Staphylococcus aureus in all samples except two, where it was the only microorganism isolated. It was also isolated in the bronchoalveolar lavage of a patient with acquired immunodeficiency virus (HIV), together with Nocardia asteroides.3 In this case, there were symptoms of respiratory infection, as in our patient. The aetiological role of B. hinzii may be questioned in our case, as K. oxytoca was cultured in parallel in the respiratory sample, but in the literature it appears as the only microorganism isolated in culture that causes the disease.4B. hinzii also appears as a causal agent of bacteraemia in three cases described in the literature, with immunosuppression the common factor in two of them: one patient with myelodysplastic syndrome and another patient with HIV.4 Similarly, B. hinzii also appeared as a causal agent of chronic cholangitis in a transplant patient on immunosuppressant treatment,5 so it is considered that it may have a potentially pathogenic role in immunocompromised persons. There were no findings in our patient to suggest immunosuppression. As in some previous publications,2,3 our patient had no known avian exposure, suggesting that the organism was obtained from another unidentified source. B. hinzii is usually resistant to, or has intermediate resistance to ampicillin, cefuroxime, ceftriaxone, cefotaxime, ciprofloxacin and tobramycin, and is sensitive to imipenem, meropenem, gentamicin, amikacin and trimetoprim–sulfametoxazol, which was similar to the antimicrobial sensitivity of our isolate, except as regards trimetoprim–sulfametoxazol. Molecular identification using MALDI-TOF–MS and 16S sequencing, as was performed here, provides the correct microbiological diagnosis.6 The use of rapid techniques that increase the reliability and speed of identification of this microorganism could lead to clarifying its role as a coloniser and human pathogen.