Six yearling white-tailed deer (Odocoileus virginianus), male and female.Over a period of 6-9 months 6 of 20 white-tailed deer confined to a small pasture developed weight loss, increased respiratory rate, intermittent nasal discharge, and labored breathing, with coughing upon forced exercise. The six affected deer were isolated in a sick pen and treated orally with antibiotics. In spite of antibiotic treatment and ad lib feed, minimal improvement was noted and all 6 deer were euthanized and examined.

Gross Description:  

Deer were thin, in poor body condition with minimal fat stores. Lesions were similar in all deer and varied only in degree of severity. Pulmonary lesions consisted of red to purple discoloration and atelectasis of cranial lung lobes with variable involvement of middle and caudal lung lobes. Discolored and atelectatic lung was sharply demarcated from less affected lung which generally remained pink and inflated. Affected lung was firm and on cut surface airways oozed purulent exudate. 

Affected lung did not float in formalin. Tracheal mucosa was diffusely reddened and contained intraluminal mucopurulent exudate. Tracheobronchial and mediastinal lymph nodes were moderately enlarged and edematous.

Histopathologic Description:

Submitted sections of lung are from different animals and differ slightly in degree of involvement and severity. Multifocally, bronchi and bronchioles are variably filled with large numbers of degenerate and non-degenerate neutrophils, small amounts of fibrin, and detached epithelial cells. In the most severely affected airways, epithelium is characterized by multifocal areas of degeneration and necrosis with attenuation of remaining epithelial cells. Moderate numbers of neutrophils are seen within airway epithelium. Affected airways and vessels are surrounded by variable cuffs of lymphocytes, plasma cells and macrophages. The most pronounced lymphoid cuffs contain lymphoid follicles. In the remainder of affected lung alveolar interstitium is congested and alveoli contain neutrophils, erythrocytes and small amounts of fibrin with alveoli near bronchi/bronchioles being most severely affected. Interlobular regions are expanded by clear space due to edema and there are multifocal, mild infiltrates of neutrophils with the pleura.

Morphologic Diagnosis:  

Lung, broncho-pneumonia, fibrinosuppurative, multifo-cal to focally extensive, acute to subacute, moderate, with multifocal airway epithelial necrosis and interlobular edema

Lab Results:  

Bacteriologic culture of fresh lung from all deer yielded heavy, pure growth of Pasteurella multocida.


Pasteurella multocida, deer

Contributor Comment:  

Pasteurella organisms are nonmotile, nonsporeforming, aerobic, fermentative, gram-negative coccobacilli. Pasteurella spp. are distributed worldwide and are a common etiology of diseases in cattle, bison, water buffalo, sheep, goats, domestic and wild birds, rabbits, laboratory animals and marine mammals.(2,4,5,7) Pasteurella multocida is a common commensal organisms of the tonsil and nasopharynx in healthy ruminants.(2) Transition from infection to disease may be facilitated by stressors such as social changes, or changes in feed or management.(2)

P. multocida has traditionally been classified into 5 capsular groups (A,B,D,E and F). Worldwide, serogroup A isolates are major causes of bovine respiratory disease. Serogroups A, and to a lesser extent D, cause fowl cholera in birds. Serogroups B and E are associated with hemorrhagic septicemia in cattle and water buffaloes in tropical regions of Africa and Asia. Serogroups B and E are rarely isolated from cattle in North America. In pigs, atrophic rhinitis and pneumonia are associated with toxigenic strains of serogroups D and A, respectively. Serogroup F strains are predominately isolated from diseased poultry.(4)

Pasteurellosis has been recorded in many species of deer including axis, black-tailed deer, mule deer, fallow, red, roe, sambar, reindeer, elk and white-tailed deer.(4,5,7) Disease generally presents as either hemorrhagic septicemia or pneumonia. Hemorrhagic septicemia has been responsible for outbreaks with high mortality in elk and fallow deer.(4,5) The pneumonic form, as seen in this case, is characterized by fibrinosuppurative bronchopneumonia, with or without necrosis and hemorrhage. 

While Mannheimia haemolytica (formerly P. haemolytica) can cause severe, acute fibrinonecrotic pneumonia and is an important component of the bovine respiratory disease complex, P. multocida is associated with less fulminating fibrinous to fibrinopurulent bronchopneumonia with limited lung necrosis.(2)

JPC Diagnosis:  

Lung: Bronchopneumonia, suppurative, chronic-active, diffuse, severe with intralobular edema and emphysema.

Conference Comment:  

This case nicely characterizes bronchopneumonia in a deer and allowed conference participants to discuss the neutrophil-rich, bronchial and bronchiolar-centric nature of the disease process. Though all agreed that the extensive bronchopneumonia was most consistent with an infectious (most likely bacterial) etiology, most participants determined that infectious organisms were difficult, if not impossible, to visualize by routine histologic examination. Gram stains did not aid in identifying organisms. Additional histologic features discussed included type II pneumocyte hyperplasia, segmental atelectasis, and prominent bronchus associated lymphoid tissue (BALT) hyperplasia, a finding that varied in severity between slides. Despite the slide variation, the presence of BALT hyperplasia along with the bronchial and bronchiolar-centric inflammatory process lead conference participants to include Mycoplasma bovis as the main differential diagnosis. However, most agreed that the lack of well-differentiated nodules of necrosis made this diagnosis less likely. Another differential diagnosis discussed included Mannheimia hemolytica. However, oat cells, fibrin rich exudate, and extensive necrosis, characteristic histologic features of M. hemolytica, were not present in this case. Additionally, bacterial aggregates are often easy to visualize in pneumonic mannheimiosis. The typical gross findings of M. hemolytica and P. multocida were compared as well. The classic gross postmortem findings of M. hemolytica including fibrin, hemorrhage, necrosis, and pleuritis with extensive marbling (due interlobular edema) particularly affecting the cranioventral lung regions were key features discussed in making the distinction between M. hemolytica and P. multocida. Other bacterial agents of respiratory disease in ruminants include Histophilus, somni, Trueperella (formerly Arcanobacterium) pyogenes, and Bibersteinia trehalosi

Compared to M. hemolytica, bacterial patho-genicity is reduced in P. multocida infection resulting in a slower onset of disease with absence of necrosis, vasculitis and exudation of abundant fibrin. In P. multocida, injury to cells of the respiratory system results from infiltration of inflammatory cells and release of their mediators and enzymes.(9) In contrast, M. haemolytica causes injury by release of bacterial toxins, such as leukotoxin, in addition to the effects of inflammatory mediators released from leukocytes, which results in a more necrotizing and fibrinous lesion. The leukotoxin, which is a member of the RTX group of toxins, is M. hemolyticas most important virulence factor, and can be directly toxic to cells as well as enhances the overall acute inflammatory response through activation of leukocytes and the complement system. Additionally, M. haemolytica has other virulence determinants such as polysaccharide in the capsule which can facilitate bacterial adherence and colonization, and inhibit their phagocytosis.(9) Environmental stressors and concurrent viral infection with agents such as bovine respiratory syncytial virus, bovine viral diarrhea, and infectious bovine rhinotracheitis virus result in increased susceptibility to infection by the bacterial agents. 

P. multocida hemorrhagic septicemia is a reportable condition which occurs in cattle and water buffalo in Asia and Africa, and uncommonly in wild ruminants in the United States as previously mentioned by the contributor.(4,5) In this condition, the bacteria disseminate hematogenously to multiple organs resulting in congestion and hemorrhages in the respiratory, gastrointestinal and urinary tracts.(1) It is a high mortality condition with death being rapid,(6) and infection is thought to occur by inhalation or ingestion. Natural infections also occur in goats, but this species is considered more resistant to the infection.(8)


1. Annas S, Zamri-Saad M, Jesse FF, Zunita Z. Comparative clinicopathological changes in buffalo and cattle following infection by Pasteurella multocida B:2. Microb Pathog. 2015;88:94-102.

2. Confer AW: Update on bacterial pathogenesis in BRD. Anim Health Res Rev. 2009;10:145-148.

3. Dabo SM, Taylor JD, Confer AW: Pasteurella multocida and bovine respiratory disease. Anim Health Res Rev. 2008;8:129-150.

4. Eriksen L, Aalbaek B, Leifsson PS, Basse A, Christiansen T, Eriksen E, Rimler RB: Hemorrhagic septicemia in fallow deer (Dama dama) caused by Pasteurella multocida multocida. J Zoo Wild Med. 1999;30:285-292.

5. Franson JC, Smith BL: Septicemic pasteurellosis in elk (Cervus elaphus) on the United States National Elk Refuge, Wyoming. J Wild Dis. 1988; 24:715-717.

6. Lopez A. Respiratory system, mediastinum and pleurae. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby Elsevier; 2012:500-520.

7. Mackintosh C, Haigh JC, Griffin F: Bacterial diseases of farmed deer and bison. Rev Sci Tech Off Int Epiz. 2002;21:249-263.

8. Shafarin MS, Zamri-Saad M, Khairani BS, Saharee AA. Pathological Changes in the Respiratory Tract of Goats infected by Pasteurella multocida B:2. J Comp Path. 2009;140:194-197.

9. Zachary JF. Mechanisms of microbial infections. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby Elsevier; 2012:170-180

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2-1. Lung

2-2. Lung

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