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. 2026 Apr 5;44:e02562. doi: 10.1016/j.idcr.2026.e02562

Fatal Pasteurella multocida pneumonia and bacteremia in a patient with chronic obstructive pulmonary disease: A case report with autopsy findings

Tai Okusaki a,⁎, Masahiko Nimiya a, Natsuko Sumimoto a, Naohide Oue b, Yoshikazu Awaya a
PMCID: PMC13090549  PMID: 42004146

Abstract

Pasteurella multocida (P. multocida) is a well-recognized pathogen responsible for skin and soft tissue infections following animal bites or scratches. Notably, it can also cause severe systemic infections in the absence of direct trauma, particularly in immunocompromised individuals. Herein, we report the case of a 75-year-old man with chronic obstructive pulmonary disease who presented with fever and rapidly progressive respiratory failure. Based on clinical, radiological, and microbiological findings, he was diagnosed with P. multocida pneumonia and bacteremia. Despite appropriate antibiotic therapy, the patient died 32 h after admission. Autopsy revealed diffuse bronchopneumonia and multiorgan dysfunction secondary to septic shock. This case highlights the importance of considering P. multocida infection in patients with underlying comorbidities and potential animal exposure, even in the absence of direct trauma.

Keywords: Pasteurella multocida, Pneumonia, Bacteremia, No Direct Animal Contact, Chronic Obstructive Pulmonary Disease, Autopsy

Introduction

Pasteurella multocida (P. multocida) is a zoonotic, Gram-negative bacterium commonly found in animals such as dogs and cats [1]. While P. multocida is well-known for causing localized skin and soft tissue infections following direct animal contact, such as bites, scratches, licking, and kissing, systemic infections can also occur in the absence of direct animal contact [2]. Such infections are particularly associated with patients with severe comorbidities and are often linked to poor clinical outcomes [3], [4]. Herein, we report a case, including rare autopsy findings, of fulminant P. multocida pneumonia resulting in fatal bacteremia and septic shock in a patient with chronic obstructive pulmonary disease (COPD).

Case

A 75-year-old man presented to the emergency department of our hospital with worsening dyspnea over 2 days. Four years earlier, he had undergone partial resection of the right upper lobe, which revealed pleomorphic carcinoma of the right upper lobe, stage IA3 (pT1cN0M0). His medical history included hypertension and type 2 diabetes mellitus, for which he was receiving treatment at another hospital. Although severe emphysema had been previously identified on computed tomography (CT), and he had been diagnosed with COPD, he had not used any inhaled medications. The patient had a 45-pack-year smoking history, having smoked from age 20–65. He owned a 10-year-old cat and had previously owned two others but denied any recent cat scratches or bites.

On presentation, the patient’s temperature was 38.5 °C; blood pressure, 91/59 mmHg; and heart rate, 107 bpm. He exhibited labored breathing at 30 breaths/min, and oxygen saturation was 93% while receiving 3 L/min of oxygen via a nasal cannula. Physical examination revealed hypertrophy of the sternocleidomastoid muscles, supraclavicular retractions, attenuated breath sounds, and coarse crackles in the right lung. Heart sounds were regular without murmurs, and no peripheral edema was noted. Arterial blood gas analysis under 3 L/min of oxygen revealed pH 7.345, PaO2 65.8 mmHg, PaCO2 29.2 mmHg, HCO3– 15.5 mmol/L, and lactate 8.8 mmol/L, indicating hypoxemia and lactic acidosis with respiratory compensation. A complete blood count revealed a white blood cell count of 3700/μL (93.2% neutrophils), hemoglobin of 13.6 g/dL, and platelet count of 135,000/μL. Biochemical assays showed total bilirubin 1.4 mg/dL, creatinine 1.79 mg/dL, and C-reactive protein 22 mg/dL. Chest radiography demonstrated extensive consolidation in the right upper lung field, extending from reticular and infiltrative shadows observed 1 year earlier (Fig. 1A-1, B-1). CT imaging revealed widespread consolidation throughout the right upper lobe with retained airway secretions (Fig. 1B-2, B-3). Notably, 1 year earlier, localized consolidation had been present in the same region adjacent to the surgical staple line (Fig. 1A-2, A-3).

Fig. 1.

Fig. 1

Chest X-ray and computed tomography (CT) findings 1 year prior to admission (A) and on the day of admission (B). (A-1) Reticular and infiltrative shadows are visible in the right upper lung field. (A-2, A-3) Consolidations are present in the posterior aspect of the right upper lobe, adjacent to the surgical staple line (white arrowheads). (B-1) On presentation, chest X-ray shows extensive infiltrative shadows in the upper and middle lung fields. (B-2, B-3) CT images demonstrate consolidations occupying nearly the entire right upper lobe. At both time points, high-attenuation material consistent with retained secretions is visible in the trachea and bilateral main bronchi. Severe emphysematous changes are consistently noted on both CT scans.

Based on these findings, the patient was diagnosed with septic shock secondary to community-acquired pneumonia in the setting of COPD. Empirical antibiotic therapy with ampicillin/sulbactam (ABPC/SBT) and vasopressor support with norepinephrine was initiated. On the second hospital day, both sputum and blood cultures obtained at admission grew P. multocida, which was susceptible to ABPC/SBT. Despite appropriate antibiotic therapy and supportive management, the patient's respiratory status progressively deteriorated, necessitating noninvasive positive-pressure ventilation. In accordance with the patient's wishes, endotracheal intubation was not performed, and comfort-focused care was continued. The patient died 32 h after admission.

An autopsy was performed 9 h postmortem at the family's request to determine the cause of death. No skin lesions suggestive of cat scratches or bites were found. The right lung weighed 920 g and was loosely adherent to the chest wall with fibrotic tissue. The right upper lobe was firm, and mucus plugs were present within the upper bronchi (Fig. 2A). The left lung weighed 370 g and showed no circumscribed lesions. Microscopically, diffuse bronchopneumonia was evident in the right upper lobe, without evidence of recurrent carcinoma (Fig. 2B, C). Cultures from swab specimens obtained from the cut surfaces of the right lung also grew P. multocida. Cardiac examination revealed a heart weight of 490 g and a left ventricular wall thickness of 2 cm. Both kidneys showed indistinct corticomedullary junctions, consistent with acute tubular necrosis secondary to septic shock. These autopsy findings confirmed septic shock secondary to P. multocida pneumonia with associated multiorgan dysfunction as the cause of death.

Fig. 2.

Fig. 2

Autopsy findings of the right lung. (A) Gross examination reveals marked volume loss in the entire upper lobe and mucus plugs occupying the upper lobe bronchus (white arrowheads). Emphysematous bullae are also observed beneath thickened pleura. (B) Low-power microscopic view of the right upper lobe (HE, ×10) demonstrates diffuse inflammatory cell infiltration. No evidence of recurrent lung carcinoma is observed. (C) High-power microscopic view (HE, ×400) shows dense neutrophilic infiltration filling the alveolar spaces, consistent with bacterial bronchopneumonia.

Discussion

P. multocida is a facultative anaerobic, Gram-negative coccobacillus and a well-recognized zoonotic pathogen that colonizes the pharynx of 70–90% of cats and 20–50% of dogs [1]. Human infections with P. multocida typically result from direct animal contact through bites or scratches; however, transmission via exposure to animal respiratory secretions or aerosols has also been documented [2]. A case series reported that 34 of 79 P. multocida cases (43%) occurred without a history of direct animal bites or scratches [5]. Similarly, in our case, no bite or scratch injuries were identified upon examination or autopsy, suggesting that transmission likely occurred through indirect contact with the cat’s respiratory secretions or saliva.

Patient comorbidities significantly affect clinical outcomes. A case series revealed that major comorbidities, including COPD, diabetes mellitus, and malignancy, were associated with increased mortality in patients with P. multocida bacteremia [3]. Furthermore, a single-institution retrospective study reported that patients with P. multocida infection who did not have direct contact with animals tended to have serious comorbidities, required hospitalization and intensive care more frequently, and had higher mortality rates [4]. Our patient, who had type 2 diabetes mellitus and severe COPD but no documented cat bites or scratches, developed fatal pneumonia with bacteremia and septic shock, exemplifying the clinical patterns described in these studies. This case highlights the importance of considering P. multocida infection in patients with pet exposure and chronic lung diseases, such as COPD, even in the absence of direct animal trauma.

P. multocida is typically susceptible to penicillin; therefore, beta-lactam antibiotics such as ABPC/SBT are recommended as the first-line treatment for systemic P. multocida infections [6]. Our empirical therapy for community-acquired pneumonia was appropriate considering the results of the drug susceptibility test. However, the poor clinical outcome of our patient was likely attributable to multiple comorbidities and bacteremia, both of which are established poor prognostic factors for invasive P. multocida infections [7].

Several case reports of P. multocida pneumonia have been published previously [8], [9], [10], [11], [12], [13], [14], and bacteremic pneumonia is documented as one of the most common clinical manifestations of P. multocida bacteremia in one comprehensive review [15]. Nevertheless, reports describing autopsy findings in fatal P. multocida infections are scarce, and only one prior case report has described the pathological features of P. multocida pneumonia [16]. Yamamoto et al. reported the case of a 57-year-old man with liver cirrhosis who died of septic shock secondary to P. multocida pneumonia. Microscopic examination of the patient’s lungs revealed diffuse alveolar infiltration by inflammatory macrophages and lymphocytes [16]. Although the pulmonary pathological findings of P. multocida pneumonia are generally nonspecific, as observed in our case, this lack of specific features emphasizes the diagnostic challenge based solely on clinical or radiographic findings and highlights the importance of obtaining a detailed patient history and appropriate microbiological specimens before initiating therapy. Our autopsy was also valuable for excluding locoregional lung cancer recurrence, confirming the cause of death, and demonstrating the systemic dissemination of P. multocida.

A case of chronic P. multocida infection mimicking non-tuberculous mycobacteriosis, presenting with persistent consolidation and bronchiectasis on imaging, has been reported [17]. In our case, chest CT performed 1 year prior to admission revealed localized consolidation in the right upper lobe adjacent to the surgical staple line. Although the etiology of this consolidation remains unclear, the subsequent development of acute pneumonia at the same anatomical site suggests the possibility of chronic P. multocida colonization, which subsequently progressed to acute fulminant pneumonia.

Author agreement

All authors have read and agreed to the submitted version of the manuscript.

CRediT authorship contribution statement

Tai Okusaki: Writing – original draft, Writing – review & editing, Visualization, Data curation, Conceptualization. Masahiko Nimiya: Writing – review & editing. Natsuko Sumimoto: Writing – review & editing. Naohide Oue: Writing – review & editing, Resources, Investigation. Yoshikazu Awaya: Writing – review & editing, Supervision.

Consent

Written informed consent for publication of this case was obtained from the patient’s family.

Ethics statement

As per institutional policy, this case report did not require IRB approval.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Declaration of Competing Interest

The authors declare no known competing financial or personal interests that could have influenced the work reported in this paper.

Acknowledgements

We thank Editage (www.editage.jp) for assistance with English language editing.

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