Hemorrhagic tracheitis syndrome is an emerging condition of nursery pigs and less commonly in growing pigs characterized by tracheal hemorrhage and edema (Figure A) accompanied by variable degrees of necrohemorrhagic, fibrinonecrotizing or suppurative inflammation. Although the syndrome is increasingly recognized during diagnostic investigations, its etiology remains poorly understood, and no definitive causative agent has been established. Recent observations suggest that respiratory pathogens capable of damaging the tracheal epithelium may contribute to lesion development, particularly swine influenza virus and Mycoplasma hyopneumoniae. A recent publication has identified SIV within affected tracheas by PCR and IHC.
Swine influenza virus is a well-recognized cause of acute respiratory disease and can induce epithelial necrosis and inflammation throughout the respiratory tract, including the trachea. Likewise, M. hyopneumoniae colonizes the ciliated respiratory epithelium, causing ciliostasis, epithelial dysfunction and chronic airway inflammation. Through these mechanisms, both pathogens may compromise tracheal integrity and predispose affected pigs to the development of hemorrhagic tracheal lesions.
To explore this potential association, a retrospective review of the University of Minnesota Veterinary Diagnostic Laboratory database was performed. Between 2014 and 2026, 422 nursery/growing pig cases exhibiting tracheitis were identified. Among these, 139 cases (32.9%) were positive for SIV by PCR in lung tissue. Of the remaining 283 SIV-negative cases, 118 (41.7%) were positive for M. hyopneumoniae. Consequently, 165 cases (39.1%) were negative for both pathogens.
The lesions observed encompassed a spectrum ranging from acute fibrinonecrotizing and necrohemorrhagic tracheitis (Figure B, C) to more chronic inflammatory changes characterized by lymphocytic inflammation (Figure D, E), ciliary loss and squamous metaplasia. No clear relationship was identified between lesion type and the infectious agent detected. Additionally, comparable lesions were present in cases in which neither SIV nor Mycoplasma hyopneumoniae was identified, suggesting that HTS is likely a multifactorial condition and that additional etiologic factors may be involved.
Collectively, 257 of 422 cases (60.9%) exhibited evidence of infection with either SIV or M. hyopneumoniae. While these retrospective observations do not establish a causal relationship, they suggest that both pathogens may represent important contributors to the development of HTS. Given their known tropism for the respiratory epithelium and their capacity to induce epithelial injury and inflammation, further investigation is warranted to determine whether these agents play a direct role in lesion development. Prospective studies incorporating tracheal pathogen detection (by RT-qPCR, IHC and or ISH), lesion characterization, and experimental infection models will be necessary to clarify the pathogenesis of HTS and the contribution of these respiratory pathogens.
This article was written by By Carlos Lopez Figueroa for the National Hog Farmer.