Patients with severe asthma demonstrate increased susceptibility to infections, requiring enhanced preventive strategies, including immunization and hygiene measures. Zoonoses are diseases transmitted between animals and humans via bacteria, viruses, fungi, or parasites, spreading through direct contact, vectors, or contaminated environments [1].
Close human–pet contact in household settings, particularly high-risk behaviors involving oral–oral mucosal exposure, constitutes an emerging route of zoonotic transmission in susceptible individuals. Canine oral secretions represent a potential source of severe respiratory infections in patients with chronic respiratory diseases [2]. These zoonotic infections often present with subacute progression and may escape early diagnosis without meticulous exposure history. We report a case of Pasteurella canis pneumonia in a patient with severe asthma receiving tezepelumab.
A 57-year-old female smoker (20 pack-years), employed in food services, cohabited with two dogs. She had a diagnosis of severe asthma with a high T2 phenotype, nonatopic eosinophilic type. She experienced occasional episodes of bronchospasm during childhood; however, a persistent form of the disease became evident at 35 years of age, characterized by frequent exacerbations requiring maintenance therapy. Recent pulmonary function tests showed an FEV1/FVC ratio of 0.61 and a postbronchodilator FEV1 of 1.71L (73% predicted). The patient exhibited persistent airflow limitation consistent with severe asthma with fixed obstruction, without meeting diagnostic criteria for chronic obstructive pulmonary disease. She had been receiving tezepelumab for the previous 8 months, along with high-dose triple inhaled therapy. Over the last year, she required three short courses of oral corticosteroids for asthma exacerbations, without chronic systemic corticosteroid use.
She presented with a 4-week history of progressive dyspnea and mucopurulent sputum. Physical examination revealed SpO2 95% on room air with diffuse wheezing. Given the subacute course and refractoriness to conventional treatment, high-resolution computed tomography (HRCT) of the chest was performed to evaluate alternative diagnoses or complications. HRCT showed right-sided ground-glass opacities involving the middle and lower lobes (Fig. 1), mild centrilobular emphysema in the upper lobes, and small right apical paraseptal bullae, without evidence of bronchiectasis or other significant structural abnormalities. Bronchoscopy yielded P. canis on culture. On targeted history-taking, the patient reported daily mouth-to-mouth contact with her dogs.
Treatment with oral levofloxacin (500mg/day for 10 days) was initiated according to antimicrobial susceptibility testing. The patient achieved complete clinical recovery with resolution of respiratory symptoms. Follow-up chest HRCT at 3 months (Fig. 1) demonstrated complete resolution of the ground-glass opacities.
The patient was receiving tezepelumab, a monoclonal antibody targeting thymic stromal lymphopoietin signaling. Pooled data from randomized clinical trials, meta-analyses, and pharmacovigilance programs indicate that tezepelumab does not increase the risk of pneumonia or other serious infections in patients with severe asthma compared with placebo [3]. However, in real-world clinical practice, additional factors such as concomitant corticosteroid use, smoking, or respiratory comorbidities may modulate infection risk.
P. canis infection remains exceptionally rare in humans, with transmission occurring primarily through close contact with domestic animals, particularly dogs [4]. Smoking cessation counseling remains essential to reduce the risk of respiratory infections and optimize asthma control in this population. To our knowledge, this is the first reported case of P. canis pneumonia occurring during biologic therapy for severe asthma. This case highlights two critical clinical implications: (1) reinforcement of hygienic measures during follow-up visits for patients with asthma who have household pets and (2) systematic evaluation of zoonotic exposures before attributing clinical deterioration to biologic refractoriness.
Authors’ contributionsAPT, AGO, and EMM wrote the manuscript draft and approved the final manuscript.
Declaration of generative AI and AI-assisted technologies in the writing processNo generative artificial intelligence tools were used in the preparation of this manuscript.
FundingNone declared.
Conflicts of interestAPT declares no conflicts of interest related to this manuscript. AGO declares no conflicts of interest related to this manuscript. EMM declares no conflicts of interest related to this manuscript.







