Research Summary - 3
The Pathologist's Approach to Diagnosing the Diversity of Cardiopulmonary Phenotypes Encountered in the Feedlot
| Date/Time: |
9/13/2025
11:00
|
| Author: |
Greta M Krafsur |
| Clinic: |
University of Nebraska-Great Plains Veterinary Educational Center |
| City, State, ZIP: |
Clay Center, NE 68933 |
G.M. Krafsur, DVM, DACVP, MSc, PhD Candidate
1
;
1University of Nebraska-Great Plains Veterinary Educational Center
Introduction:
Feedlot pulmonary hypertension (PH) frequently progressing to congestive heart failure (CHF) represents a significant health challenge to the cattle industry. Often the condition is misconstrued as primary respiratory disease with cor pulmonale, infectious myocarditis (Histophilus somni), acute interstitial pneumonia (AIP), ionophore intoxication, neoplasia, hardware disease and even bloat, among others. There is a considerable overlap in clinical manifestations between the various etiologies underlying bovine heart failure although each has a unique gross and histomorphologic cardiopulmonary phenotype, emphasizing the value of postmortem examination and histomorphologic interpretation for proper classification. Likely the magnitude of feedlot PH and CHF remain underestimated. Although bovine respiratory disease (BRD) underlies the greatest number of illnesses and deaths in the feedlot, the trajectory for bovine PH and CHF remains constant if not growing with a tendency to cluster among herds with high performing Angus influence genetics, accounting for up to 7% of death losses. The objective of this work was to compare and contrast gross and histomorphologic attributes of the "alphabet soup" of these important cardiopulmonary disease challenges in the feedlot, discuss genetic tools used by the pathologist to assist in situations with clustering of cases and utilization of machine learning to provide more robust assessment of cardiac fibrosis and adiposity in feedlot PH and CHF.
Materials and methods:
Cardiopulmonary tissues excised from cases of feedlot cattle that died or were euthanized with a clinical diagnoses of pulmonary hypertension, heart failure, acute interstitial pneumonia, monensin intoxication, animals found dead with globose hearts, chronic passive congestion, ascites and or acute pulmonary artery dissection together with cattle enrolled in longitudinal studies assessing the evolution of pulmonary hypertension throughout the production cycle were compared. Gross lesions were recorded and photodocumented. Routine formalin-fixed cardiopulmonary tissues were stained with routine H&E and modified elastic trichrome for brightfield microscopic interpretation. When deemed appropriate, fresh lung was submitted for culture and molecular diagnostics to rule out concomitant bacterial and viral pneumonia and ear notches or myocardial tissue was submitted for genotyping. Digital whole slide scanning (100X) was performed on modified elastic trichrome stained full thickness left and right ventricular explants from feedlot cattle enrolled in longitudinal field studies for future HALO quantitative image analysis.
Results:
There was considerable overlap in clinical presentation among cattle with congenital cardiac anomalies, chronic pneumonia, pulmonary hypertension and congestive heart failure. Predictably alterations in cardiac morphology transitioning from right ventricular adaptive to maladaptive hypertrophy with eccentric dilation, septal shift and left ventricular septal compression were invariably present with these phenotypes. Enlargement of the right auricular appendage/atrium, dilation of the main pulmonary artery and acute pulmonary artery dissection were more varied among these cases. Hypoxia-induced perturbations arising from chronic parenchymal lung disease, congenital cardiac anomalies with hemodynamic significance and feedlot pulmonary hypertension target the pulmonary vasculature and not the alveolar-capillary membrane, hence acute or chronic fulminant pulmonary edema was not observed with these conditions. Monensin intoxication giving rise to acute or chronic left ventricular failure was associated with loss of integrity to the alveolar capillary membrane and acute pulmonary edema. Pulmonary vascular remodeling with attendant pulmonary hypertension and right ventricular enlargement were not present. Likewise, injury to the alveolar-capillary membrane, flooding of the alveoli with proteinaceous edema fluid and subsequent hyaline membranes were observed with acute interstitial pneumonia. The perturbations underlying injury to the alveolar capillary membrane associated with acute interstitial pneumonia remain poorly understood however the process did not target the pulmonary vasculature and hence pulmonary hypertension was not part of the process. Likewise, cardiac lesions observed with monensin intoxication did not parallel those seen with feedlot pulmonary hypertension and congestive heart failure. Rather variable replacement and more commonly interstitial and perivascular fibrosis characterized cardiac lesions associated with feedlot pulmonary hypertension and congestive heart failure. The genetic regions associated with the condition were highly expressed in feeding organizations exhibiting a clustering of cases.
Significance:
Although there exists considerable overlap in clinical manifestations associated with the constellation of cardiopulmonary disease challenges facing the cattle feeding industry, there is considerable disparity in gross and histomorphologic attributes indicating that feedlot pulmonary hypertension and congestive heart failure is a syndrome unique from other disease challenges. While the pathologic mechanisms remain unknown, the putative genetic regions associated with disease may provide a tool for making informed breeding and disease management decisions.
