History
A 3-month-old Katahdin-Dorper–cross ewe lamb was submitted for necropsy. The lamb, which was unvaccinated and housed on a small farm with 5 other lambs, died suddenly after a 1-day period of lethargy. The lamb had no history of previous illness.
Clinical and Gross Findings
The lamb weighed 26.1 kg (57.4 lb). The carcass was moderately autolyzed and in adequate nutritional status. There was approximately 10 mL of pink-tan foam emitting from the nares. Multifocal to coalescing petechiae and ecchymoses were evident in the sublingual connective tissue, esophageal mucosa, and parietal pleura. There was multifocal to coalescing necrosis and ulceration of the esophageal mucosa, with abundant associated fibrin exudate, erythema, and hemorrhage that extended from the pharynx caudally to just aboral to the level of the diaphragm (Figure 1). Pleural and peritoneal effusion (volume, approx 25 mL) and pericardial effusion (volume, 10 mL) were present. The lungs were bright red and glistening, and wet and rubbery on palpation. The epicardium was dark red and glistening. The liver was diffusely pale tan to yellow. The abomasal submucosa was expanded by gelatinous yellow-tinged edema. The remainder of the gross examination findings were unremarkable.
Photograph of the opened esophagus and lungs of a 3-month-old unvaccinated lamb that died suddenly after a 1-day period of lethargy. Notice the tan, friable fibrinonecrotic material lining the esophageal mucosa (asterisk). The fibrinonecrotic lesions are rimmed by hyperemia. The lungs are heavy, red, and wet and ooze fluid on cut section (white arrow), consistent with pulmonary edema.
Citation: Journal of the American Veterinary Medical Association 251, 4; 10.2460/javma.251.4.405
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page→
Histopathologic and Microbiological Findings
Microscopic examination of sections of the esophagus revealed severe, multisegmental, necrotizing, ulcerative, and fibrinosuppurative esophagitis with microvascular thrombi, lamina proprial edema, and myriad intralesional bacteria (Figure 2). Multifocally, the esophageal epithelium and its basal lamina were completely absent and replaced by amorphous granular eosinophilic necrotic cellular debris and degenerate neutrophils. This necrotic material was covered by a pseudomembrane of compacted beaded fibrillar pale eosinophilic fibrin admixed with numerous small bacterial bacilli. In the lamina propria underlying the regions of necrosis, there were small blood vessels that had their lumina occluded by fibrin. The esophageal lamina propria was diffusely expanded by edema.
Photomicrographs of a section of the esophagus from the lamb in Figure 1. A—Segmental necrotizing ulcerative esophagitis (asterisk) is present with adjacent intact epithelium (black arrow) and intralesional bacterial colonies (white arrows). The vasculature within the subepithelial connective tissue is congested. H&E stain; bar = 100 μm. B—Higher-magnification view of the section in panel A. Notice the multifocal fibrinous thrombi in small, superficial, subepithelial blood vessels (arrowheads). There are overlying bacterial colonies (white arrow), and a focus of epithelial necrosis (asterisk). H&E stain; bar = 45 μm. C—Another higher-magnification view of the section in panel A. Bacterial colonies (white arrows) are subjacent to areas of necrotizing and ulcerative esophagitis (asterisk) with adjacent intact epithelium (black arrow). H&E stain; bar = 55 μm.
Citation: Journal of the American Veterinary Medical Association 251, 4; 10.2460/javma.251.4.405
Within the lungs, the alveoli and small bronchioles were diffusely filled with homogeneous, eosinophilic edema fluid; there was mild expansion of alveolar, interlobular, and pleural interstitia with pale eosinophilic edema fluid. Randomly distributed throughout the examined sections of lung tissue were small colonies of small bacilli and fibrinous exudate that filled the lumina and distended the diameter of alveolar capillaries and rare small pulmonary arterioles. There were rare individualized neutrophils or macrophages in association with these bacterial colonies. Similar foci of small bacterial colonies were randomly distributed in the splenic small vasculature, cardiac coronary arteries, hepatic sinusoids, and the interstitium adjacent to the thyroid gland; there was also very mild inflammatory response in these organs.
Splenic and pulmonary tissue samples collected at the time of necropsy underwent bacterial culture on enriched sheep blood agar. Bibersteinia trehalosi was the primary pathogen isolated from those samples.
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: diffuse systemic bacterial embolization and severe ulcerative and necrotizing esophagitis and pharyngitis with intralesional bacterial bacilli.
Case summary: systemic bibersteiniosis (caused by B trehalosi) in a ewe lamb.
Comments
Given the lamb's history and findings obtained during gross postmortem examination, an acute septicemic bacterial infection with B trehalosi was suspected. Bibersteinia trehalosi, a gram-negative bacillus, is a commensal organism of the mucosa of the ruminant upper respiratory tract.1 Bibersteinia trehalosi infection is characterized by a septicemic process that results in acute to peracute respiratory tract disease.1 As for the lamb of the present report, peracute bacteremia can result in acute interstitial pneumonia, with small colonies of bacteria and little inflammatory cell infiltrate.
Bibersteinia trehalosi was originally classified as Pasturella haemolytica biotype T, because of the organisms' ability to ferment trehalose, but was renamed after phylogenetic studies were performed in 2007.2 Bibersteinia trehalosi causes systemic bibersteiniosis (formerly systemic pasteurellosis2) in both wild and domestic sheep.1 Systemic bibersteiniosis develops in weaned sheep between 5 and 12 months of age and can cause sudden death without any respiratory signs.3 Often clinical disease develops after changes in management practices, such as a change in diet or housing. The exact mechanism of disease development is unknown, but stress and immunocompromise are potential contributors.3 The morbidity rate in an infected flock is typically low with only a few animals becoming ill. There is evidence that leukotoxin production by B trehalosi is required for the organism's virulence.4 Among sheep species, bighorn sheep appear to have a higher incidence of pneumonia attributable to infection with members of the family Pasteurellaceae; B trehalosi features prominently as a cause of respiratory tract disease in bighorn sheep lambs, as in the case described in the present report.4,5
A comparative study6 has been done to evaluate the pathogenicity of B trehalosi in calves because it is a commonly isolated organism in cases of bovine pneumonia. Results of the study were inconclusive, and B trehalosi is currently considered to be a secondary pathogen.6 In addition to respiratory tract disease, there has been a single case of subcutaneous botryomycosis (pyogranulomatous cellulitis) of the submandibular region in a 3-year-old steer, and another single case of acute fatal necrotizing hepatitis in a 9-year-old cow.7,8 Although its importance as a respiratory pathogen of cattle is unclear, B trehalosi should be a strong differential diagnosis for sudden death or respiratory tract disease in sheep, especially domestic lambs and bighorn sheep, as well as a rare cause of suppurative to pyogranulomatous lesions throughout the body of cows.
References
1. Quinn PJ. Pasteurella species, Mannheimia haemolytica and Bibersteinia trehalosi. In: Quinn PJ, Markey BK, Leonard FC, et al, eds. Veterinary microbiology and microbial disease. 2nd ed. Hoboken, NJ: John Wiley and Sons, 2011; 300–306.
2. Blackall PJ, Bojesen AM, Christensen H, et al. Reclassification of [Pasteurella] trehalosi as Bibersteinia trehalose. Int J Syst Evol Microbiol 2007; 57: 666–74.
3. Suàrez-Güémes F, Collins MT, Whiteman CE. Experimental reproduction of septicemic pasteurellosis in feedlot lambs: bacteriologic and pathologic examinations. Am J Vet Res 1985; 46: 193–201.
4. Dassanayake RP, Shanthalingam S, Subramaniam R, et al. Role of Bibersteinia trehalosi, respiratory syncytial virus, and parainfluenza-3 virus in bighorn sheep pneumonia. Vet Microbiol 2013; 162: 166–72.
5. Miller DS, Weiser GC, Ward ACS, et al. Pasteurellaceae isolated from bighorn sheep (Ovis canadensis) from Idaho, Oregon, and Wyoming. Am J Vet Res 2012; 73: 1024–1028.
6. Hanthorn CJ, Dewell RD, Cooper VL, et al. Randomized clinical trial to evaluate the pathogenicity of Bibersteinia trehalosi in respiratory disease among calves. BMC Vet Res 2014; 10: 89.
7. Watson PJ, Scholes SFE. Bibersteinia trehalosi necrotising hepatitis associated with sudden death in an adult cow. Vet Rec 2010; 167: 100–102.
8. Spagnoli S, Reilly TJ, Calcutt MJ, et al. Subcutaneous botryomycosis due to Bibersteinia trehalosi in a Texas Longhorn steer. Vet Pathol 2012; 49: 775–8.
