Pseudomonas aeruginosa, an opportunistic Gram-negative bacterium long feared in human hospitals, is increasingly recognized as a cause of chronic, recurrent, and treatment-refractory infections in dogs and cats. A comprehensive review published in Frontiers in Bacteriology by Inês Chambino, Juliana Menezes, and Adriana Belas of Lusófona University in Lisbon synthesizes current knowledge on the epidemiology, virulence traits, biofilm-associated persistence, and antimicrobial resistance of P. aeruginosa in companion animals, and argues that pets may participate in the maintenance and dissemination of clinically important lineages. The authors emphasize that the bacterium’s pathogenic success rests on a broad virulence repertoire—adhesion factors, extracellular enzymes, exotoxins, multiple secretion systems, quorum sensing regulation, and a marked capacity for biofilm formation—combined with intrinsic resistance and the ability to acquire additional resistance determinants, frequently producing multidrug-resistant (MDR) phenotypes.
In companion animals, P. aeruginosa is associated with a wide range of clinical syndromes, primarily affecting dogs, with reported prevalence ranging from approximately 2.0 to 40.9 percent depending on the study, sample type, and population. In cats, prevalence is generally lower, from 0.8 to 25.0 percent, with higher rates observed in chronic or recurrent infections. The authors caution that these variations likely reflect heterogeneity among studies, including differences in animal populations, health status, sample size, breed distribution, and diagnostic approaches. Infections are typically opportunistic, occurring in the presence of underlying conditions, disruption of host barriers, immunosuppression, or prior antimicrobial exposure. While P. aeruginosa is the most frequently isolated Pseudomonas species from companion animals, other species such as P. fluorescens have occasionally been reported, and P. luteola and P. aestus have been associated with pyogranulomatous panniculitis and chronic rhinitis in cats, respectively.
Otitis externa represents the most frequent and clinically significant presentation in dogs and a major therapeutic challenge in veterinary practice. Canine otitis externa affects approximately 20 to 29 percent of dogs presented to veterinary practices in some populations, and while it is typically initiated by primary factors such as allergic dermatitis, endocrine disorders, or ectoparasites, P. aeruginosa frequently emerges as a secondary pathogen in chronic or recurrent cases, accounting for approximately 28 to 37 percent of such infections. Anatomical features, including excessive hair in the ear canal and pendulous pinnae, may increase humidity and reduce ventilation, creating conditions favorable for microbial proliferation. The bacterium’s ability to adhere to ear canal epithelium, produce proteases and toxins, and form robust biofilms promotes persistence and reduces susceptibility to both host immune responses and antimicrobial therapy. Clinically, infections are characterized by purulent exudate, malodour, pain, and inflammation, often accompanied by epithelial hyperplasia and canal stenosis in advanced cases.
Urinary tract infections, although less commonly reported, are an important manifestation, particularly in complicated or recurrent cases. Reported prevalences range from 3.3 to 13.1 percent in dogs and from 1.3 to 25 percent in cats. These infections are commonly associated with predisposing factors such as urinary catheterisation, urolithiasis, anatomical abnormalities, and prior antimicrobial therapy, while in cats, underlying chronic conditions including chronic kidney disease, hyperthyroidism, and diabetes mellitus further increase susceptibility. P. aeruginosa urinary infections are often persistent and prone to recurrence, largely due to intrinsic resistance mechanisms and the capacity to form biofilms on uroepithelial surfaces and indwelling medical devices. Ocular disease is equally concerning: P. aeruginosa is a well-known cause of severe ulcerative keratitis in dogs, accounting for approximately 15.5 to 19.5 percent of cases. These infections are typically acute, rapidly progressive, and potentially vision-threatening, driven by proteases, exotoxins, and other virulence factors that mediate rapid tissue destruction, with brachycephalic breeds showing a higher incidence and severity likely due to anatomical and functional alterations of periocular structures.
The virulence of P. aeruginosa is mediated by pili and flagella that promote initial colonisation of epithelial surfaces, lipopolysaccharides in the outer membrane that provide intrinsic resistance and modulate host immune responses, and toxins delivered via type I, II, III, IV, and VI secretion systems. During early infection, adhesion structures promote colonisation when host defences are compromised, as in inflamed ear canals or damaged corneal tissue. As infection becomes established, extracellular enzymes and toxins—including exotoxin S, exotoxin A, elastases, and phospholipases—contribute to tissue damage, inflammation, and disruption of host barriers. The type III secretion system is predominantly important for pathogenicity: ExoS is associated with an invasive phenotype that interferes with host cell signaling and cytoskeletal organisation, whereas ExoU is a potent phospholipase linked to the cytotoxic phenotype, rapid cell lysis, extensive epithelial damage, and more severe disease. Most canine isolates exhibit ExoS-positive profiles, with smaller proportions ExoU-positive; strains carrying ExoU are often associated with multidrug resistance and high-risk lineages such as ST235.
Biofilm formation is one of the most important virulence factors of P. aeruginosa and is often responsible for antibiotic treatment failure. A biofilm is a structured community of microorganisms embedded within a self-produced matrix of exopolysaccharides, proteins, and extracellular DNA. The pel and psl gene clusters encode exopolysaccharides essential for biofilm architecture—pel is required for biofilm formation on solid surfaces, while psl mediates surface adhesion and microcolony development—and the ppyR gene positively regulates psl expression. Quorum sensing systems, particularly the transcriptional regulators LasR and RhlR, coordinate the transition from a motile, planktonic lifestyle to a sessile, biofilm-associated state and control biofilm maturation, exoenzyme and toxin production, and persistence. Within biofilms, bacterial cells are embedded in a protective matrix that limits antimicrobial penetration and reduces susceptibility to host immune defenses, acting as a reservoir for ongoing or recurrent infection. Biofilms also facilitate horizontal gene transfer and the accumulation of resistance determinants, creating a highly resilient pathogenic system that underpins persistence in clinical settings.
Antimicrobial resistance poses substantial diagnostic and therapeutic challenges. The World Health Organization has designated P. aeruginosa a high-priority bacterium requiring urgent development of new antimicrobial therapies, and it is a member of the ESKAPE group of pathogens recognized for their ability to evade antimicrobial treatment. The bacterium demonstrates extensive intrinsic resistance to multiple antimicrobial classes, including ampicillin and amoxicillin with their β-lactamase inhibitor combinations, third-generation cephalosporins such as cefotaxime and ceftriaxone, the carbapenem ertapenem, chloramphenicol, trimethoprim, and tetracycline derivatives including tigecycline. These mechanisms are primarily associated with low outer membrane permeability combined with constitutive or inducible expression of multidrug efflux pumps. Beyond intrinsic resistance, P. aeruginosa frequently acquires additional resistance through chromosomal mutations and horizontal gene transfer mediated by mobile genetic elements, particularly integrons. Several class D oxacillinases, including OXA-50, OXA-395, OXA-486, and OXA-488, are part of the chromosomal resistome, although these intrinsic enzymes exhibit only weak carbapenem-hydrolysing activity and do not on their own confer clinically significant carbapenem resistance.
Carbapenem-resistant P. aeruginosa strains have become especially concerning. Studies in companion animals have reported resistance rates ranging from 2.1 to 74.1 percent for meropenem and 6.7 to 77.6 percent for imipenem. Carbapenem resistance is most frequently associated with the production of metallo-β-lactamases, particularly Verona Integron-encoded (VIM) and New Delhi (NDM)-type enzymes, with occasional reports of Imipenemase (IMP)-type carbapenemases. The emergence of NDM-producing isolates in dogs and cats is of particular concern due to their association with MDR phenotypes and their relevance in a One Health context. Nonetheless, carbapenem resistance is not solely mediated by carbapenemase production; in many cases it is more commonly associated with non-enzymatic mechanisms, including loss or modification of the OprD porin and overexpression of efflux pumps. In some cases, extensively drug-resistant phenotypes have been identified, with isolates exhibiting resistance to nearly all available antimicrobial classes and carrying multiple resistance genes, frequently associated with persistent infection, treatment failure, and increased risk of recurrence.
The circulation of internationally recognized high-risk clones in companion animals raises concern from both clinical and One Health perspectives. ST235 is currently the most clearly documented and clinically significant lineage, widely recognized in human medicine as a successful epidemic clone with a marked capacity to accumulate resistance determinants, including carbapenemase genes; it has been identified in companion-animal isolates in Japan. Recent genomic studies of canine otitis from the United Kingdom have also reported ST111 and ST244, two high-risk clones well known in human healthcare-associated infections, and in Algeria, a cluster of carbapenem-resistant ST244 cases was reported in dogs and cats. In Greece, an extensively drug-resistant feline isolate carrying blaNDM-1 was characterized. A particularly illustrative example of interconnectedness was reported in the United States, where two canine cases of carbapenemase-producing P. aeruginosa in a veterinary hospital were linked to a contemporaneous human outbreak strain associated with contaminated over-the-counter artificial tears. The authors conclude that companion animals are not merely incidental hosts but may act as reservoirs of clinically important lineages relevant to both veterinary medicine and the wider One Health context.
Disinfectant tolerance adds a further layer of difficulty. Prolonged exposure to chlorhexidine, one of the most widely used antiseptics in human and veterinary medicine, can drive the evolution of P. aeruginosa populations with increased tolerance and reduced susceptibility to clinically relevant antibiotics, including β-lactams and aminoglycosides, due mainly to genetic and phenotypic changes affecting efflux systems and membrane permeability. Complementary findings have demonstrated that P. aeruginosa can also develop enhanced tolerance to chlorhexidine following adaptation to other biocides, such as octenidine, under both laboratory and simulated clinical conditions. The mexAB-oprM, mexCD-oprJ, and mexEF-oprN efflux operons play a pivotal role in mediating tolerance and adaptive resistance to a wide range of biocidal compounds, and their highly conserved genes and regulators can be transmitted horizontally, including via bacteriophage-mediated mechanisms. Despite growing knowledge, important gaps remain: most resistance data come from in vitro susceptibility surveys, robust clinical trials comparing treatment protocols are scarce, and current One Health evidence is based largely on case reports and small genomic studies. Future work should integrate genomic surveillance, clinical data, environmental studies, and experimental models to better define pathogenesis, transmission, and treatment outcomes across animal and human health.
Subject of Research: Virulence and antimicrobial resistance mechanisms of Pseudomonas aeruginosa in companion animals
Article Title: Virulence and antimicrobial resistance mechanisms in Pseudomonas aeruginosa in dogs and cats: a review
Article References: Chambino, I., Menezes, J., & Belas, A. (2026). Virulence and antimicrobial resistance mechanisms in Pseudomonas aeruginosa in dogs and cats: a review. Frontiers in Bacteriology, 5, Article 1891783. https://doi.org/10.3389/fbrio.2026.1891783
Image Credits: AI Generated
DOI: 10.3389/fbrio.2026.1891783
Keywords: Pseudomonas aeruginosa, companion animals, dogs, cats, antimicrobial resistance, biofilm, otitis externa, multidrug resistance, One Health, high-risk clones, virulence factors, veterinary medicine
Cite Scienmag News
Kristina Jarvis. (October 24, 2026). Dogs and Cats Harbor Drug-Resistant Pseudomonas aeruginosa Lineages of Human Concern, Review Finds. Scienmag. https://scienmag.com/dogs-and-cats-harbor-drug-resistant-pseudomonas-aeruginosa-lineages-of-human-concern-review-finds/
Kristina Jarvis. "Dogs and Cats Harbor Drug-Resistant Pseudomonas aeruginosa Lineages of Human Concern, Review Finds." Scienmag, 24 October 2026, https://scienmag.com/dogs-and-cats-harbor-drug-resistant-pseudomonas-aeruginosa-lineages-of-human-concern-review-finds/. Accessed 24 October 2026.
Kristina Jarvis. "Dogs and Cats Harbor Drug-Resistant Pseudomonas aeruginosa Lineages of Human Concern, Review Finds." Scienmag. October 24, 2026. https://scienmag.com/dogs-and-cats-harbor-drug-resistant-pseudomonas-aeruginosa-lineages-of-human-concern-review-finds/

