11-year-old, female spayed, dachshund, canine After two weeks of boarding at the referring veterinarian, the dog became acutely lethargic, tachypneic, and had two episodes of vomiting. Evaluation at the veterinary clinic that day revealed pyrexia (temperature: 106.9 oF), mild coughing, and mucoid nasal discharge. Thoracic radiographs were unremarkable. The dog was administered a fluid bolus and then later received Lasix and supplemental oxygen. Although the temperature decreased to 101.8 oF, clinical signs of dyspnea and tachypnea progressed, and the dog developed epistaxis, hemorrhagic discharge from the mouth, as well as bloody diarrhea/melena. The temperature dropped to 95.4 oF the next morning and the dog died.

Gross Description:  

The pleural cavity contained approximately 125 mL of dark red slightly turbid fluid. The lungs were diffusely dark red, heavy, and firm with failure to collapse and generalized consolidation/hepatization. Scattered throughout all lobes were pinpoint to 0.1 cm diameter hard white bony spicules. The pulmonary parenchyma exuded copious serosanguinous to hemorrhagic fluid on cut surface and sections from all lobes sank 10% formalin.

There was generalized venous congestion of the splanchnic vasculature. Few paintbrush hemorrhages were multifocally dispersed along the serosa of the descending colon. The mucosa of the stomach, duodenum, and orad jejunum were mottled tan-red and the luminal contents consisted of abundant partially digested blood and mucus.

Histopathologic Description:

Lung: Multiple sections of lung are examined and similarly affected. Approximately 25-60% of the pulmonary parenchyma is disrupted by coagulative to lytic necrosis characterized by loss of tissue architecture with replacement by coalescing lakes of hemorrhage admixed with a dense inflammatory exudate. Airways are often occupied by high numbers of erythrocytes, toxic neutrophils, and foamy macrophages enmeshed in eosinophilic proteinaceous edema fluid and fibrillar fibrin. Scattered extracellular and intrahistiocytic short basophilic bacilli are occasionally observed within alveolar spaces, bronchioles, and bronchial lumina. The respiratory epithelium is often attenuated with cellular swelling, rounding, and loss of cilia (degeneration) or hypereosinophilia and pyknosis with luminal sloughing and exposure of a denuded basement membrane (necrosis). There is a paucity of bronchial associated lymphoid tissue. Pulmonary capillaries are occasionally distorted by luminal fibrin thrombi, and larger vasculature is multifocally variably obscured by deposition of hyalinized fibrin within the vessel wall (fibrinoid vascular necrosis). Other vessels are congested, lined by plump reactive endothelium, and surrounded by perivascular edema.

Alveolar septa multifocally contain low numbers of hematopoietic precursor cells (extramedullary hematopoiesis). Few small trabeculae of bone are randomly dispersed throughout the parenchyma. Rarely adjacent to larger airways are small clusters of histiocytes that contain finely granular black intracytoplasmic pigment. Histiocytes are intermingled with lymphocytes and fewer plasma cells.

Sections of the stomach, small intestine, and colon (slides not submitted) are diffusely hyperemic with marked transmural vascular congestion. Increased numbers of lymphocytes and plasma cells expand the gastrointestinal mucosa and there is occasional leukocyte exocytosis. Low numbers of neutrophils are intermingled within the superficial gastric mucosa.

Special staining of the lung reveals gram-negative bacilli within airways.

Morphologic Diagnosis:  

1. Severe diffuse acute necrohemorrhagic and fibrinosuppurative pneumonia with numerous gram-negative bacilli
2. Multifocal heterotopic bone
3. Minimal multifocal pneumoconiosis

Stomach (not submitted):
1. Mild multifocal chronic neutrophilic and lymphoplasmacytic gastritis
2. Marked mural congestion

Small intestine, colon (not submitted):
1. Mild to moderate diffuse chronic lymphoplasmacytic enterocolitis
2. Marked mural congestion

Lab Results:  

Aerobic culture of the lung postmortem yielded heavy growth of Escherichia coli (E. coli) and a second isolate of Streptococcus minor. Antimicrobial susceptibility testing results indicated that the E. coli isolate was sensitive to amikacin, cephalexin, enrofloxacin, imipenum, marbofloxacin, tetracycline, tobramycin, and trimethoprim/sulfamethoxazole.


E-coli-associated pneumonia

Contributor Comment:  

In dogs, bacterial pneumonia is most often attributed to opportunistic pathogens that occur as commensals of the normal microflora. Diagnosis therefore warrants an investigation for a predisposing cause that resulted in impairment of the pulmonary defense mechanism. Possible primary causes include viral infection (distemper, adenovirus-2, parainfluenza) or immunosuppression.5,6,8,12 Aside from Bordetella bronchiseptica, which can be a primary pathogen, common opportunistic bacterial isolates include Streptococcus spp, E coli, Pasteurella multocida, and Klebsiella pneumoniae. Mixed bacterial infections are not infrequent. 5,6,8,12

E. coliE. coli is often isolated in cases of aspiration pneumonia, and lesions are typically unilateral, necrotizing, and sometimes reveal the presence of foreign material within airways.5 A predisposing factor to either aspiration pneumonia (i.e. dysphagia, regurgitation, megaesophagus) or bacterial pneumonia was not identified in this dog. Affected animals with either bacterial and/or aspiration pneumonia are susceptible to subsequent bacteremia, disseminated intravascular coagulation, and diffuse alveolar damage, which manifests clinically as acute respiratory distress syndrome (ARDS).5

Alternatively, mucosal barrier dysfunction in the gut can lead to bacterial translocation and hematogenous spread of the organism to the lungs.5,7 Evaluation of the gastrointestinal tract in the present case revealed changes compatible with chronic inflammatory bowel disease. No definitive foci of ulcers/erosions were identified, however the presence of neutrophils identified within the gastric mucosa could suggest mucosal barrier disruption.

Characterization and virulence typing of the E. coli isolate was unfortunately not pursued in this case. Previous reports of E. coli-associated hemorrhagic pneumonia in dogs have yielded isolates with an O serotype (specifically O4 and O6).2,7,11 In a case series describing the disease in four dogs, Handt et al. identified the presence of the following virulence factors in all E. coli isolates: cytotoxic necrotizing factor 1 (CNF1), alpha hemolysin, and the adhesin factor papG allele III.6 Both CNF1 and alpha hemolysin cause hemorrhage, necrosis, and edema 11,12 and are commonly produced by extraintestinal strains of pathogenic E. coli. 4,7,12 In another case report, the bacterial isolate was found to lack alpha hemolysin and instead possess fimbrial antigen K88.2

Extraintestinal pathogenic E. coli (ExPEC) harbor virulence factors not present in strains of commensal E. coli.11 ExPEC are implicated in several human and animal disease conditions, including urinary tract infections, meningitis, septicemia, and pneumonia.4,7,10 Review of the literature sometimes refers to these strains as necrotoxic or necrotoxogenic E. coli.2,7 The pathogenesis of ExPEC involves bacterial adherence to the mucosal surface of the host epithelial cell, which is mediated by their adhesin encoded by papG. Colonization ensues, and there is initiation of the immune response via molecular triggers (i.e. TLR4) and subsequent production of proinflammatory cytokines.11,12 While mechanisms of infection are uncertain, it has been hypothesized that animal affected by ExPEC may be immunocompromised secondary to stress, possibly induced by shipping or shelter overcrowding. These animals could be then be infected through inhalation following exposure to their own microflora or fecal contamination from a subclinical animal or human.7,11

It is worth noting that in both of these studies,2,7 all dogs had a recent history of travel and were reportedly healthy prior to the development of peracute, fulminant, respiratory disease. Sudden death occurred in two dogs, while the remaining animals (including the current case) died within 24 hours following the onset of clinical signs. Clinical findings frequently included tachypnea, dyspnea, lethargy, and inappetance; when available, clinicopathologic abnormalities typically showed neutropenia with left shift. 2,7 A retrospective study specifically investigating hemoptysis determined that bacterial pneumonia was the most common underlying cause.1 Consumption of expectorated blood from the respiratory tract was considered the most likely cause for melena in the present cause, however unidentified gastrointestinal ulcers cannot be ruled out.

JPC Diagnosis:  

Lung: Pneumonia, interstitial, fibrinosuppurative, necrotizing, and hemorrhagic, diffuse, severe with multifocal necrotizing vasculitis

Conference Comment:  

The contributor has given an outstanding review of extraintestinal E. coli infection in the dog. A second pathogen was isolated from the lung in this animal, a minor population of non-speciated streptococci was also identified.

Within the last decade, several outbreaks of necrohemorrhagic pneumonia have been reported in confined dogs as a result of infection with Streptococcus equi var. zooepidemicus, a common commensal bacterium and opportunistic pathogen of horses.3,9,10 One of these outbreaks affected over 1000 shelter dogs in less than one year.9 Other smaller outbreaks affected animals within shelters and in one case, a university research colony.10 Prior to this, it had been identified as a sporadic pathogen in dogs.10

In these outbreaks, infected dogs presented with respiratory signs of coughing, mucoid or hemorrhagic nasal discharge, and dyspnea, with some dying within 24-48 hours of clinical signs. At autopsy, pleural cavities often contained hemorrhage, and the predominant clinical signs were a necrotizing and fibrinous bronchopneumonia affecting all lobes and extending to the pleura. Numerous cocci are present within the cytoplasm of neutrophils, macrophages, or free within alveoli.10

While the pathogenesis of this disease is yet unknown, the potential for exotoxins of S. equi var. zooepidemicus has been postulated to cause an exuberant inflammatory response, such as may be seen in S. equi var. equi infection in horses and S. pyogenes, incriminated in toxic shock in humans. During the rapid clinical course of this condition, there is a marked elevation in a

number of proinflammatory cytokines including IL-6, tumor necrosis factor, and interleukin-8 in the blood of infected animals. In these cases, S. zooepidemicus is routinely cultured from nasopharyngeal swabs or as a pure culture from affected lung tissue, and other common respiratory pathogens are seldom present. However, efforts to infect healthy dogs with cultures of S. zooepidemicus alone have not borne fruit, suggested as yet unexplained factors or co-pathogens in full-blown infection.

The moderator discussed the concept of diffuse alveolar phase, as well as the three phases of septal injury -exudative, proliferative (2-3 days later with type II pneumocyte hyperplasia) and repair (in which fibrosis may be seen in severe cases). Participants discussed the difficulty in this slide in differentiating hyaline membranes from necrotic alveolar walls or smooth muscle, as well as the remarkable amount of necrosis in the lung that apparently occurred within 24 hours in this animal.


1. Bailiff NL, Norris CR. Clinical signs, clinicopathological findings, etiology, and outcome associated with hemoptysis in dogs: 36 cases (1990-1999). J Am Anim Hosp Assoc. 2002;38:125-133.
2. Breitschwerdt EB, DebRoy C, Mexas AM, et al. Isolation of necrotoxigenic Escherichia coli from a dog with hemorrhagic pneumonia. J Am Vet Med Assoc. 2005;226:2016-2019.
3. Byun JW, Yoon SS, Woo GH, Jung BY, Joo YS. An outbreak of fatal hemorrhagic pneumonia caused by Streptococcus equi subsp. zooepidemicus in shelter dogs. J Vet. Sci. 2009:10(3):269-271.
4. Caprioli A, Falbo, Ruggeri RM, et al. Cytotoxic necrotizing factor production by hemolytic strains of Escherischia coli causing extraintestinal infections. J Clin Micro. 1987:25:146-149.
5. Caswell JL, Williams KJ. Respiratory System. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol. 2. 6th ed. St. Louis, MI: Elsevier; 2016: 564-569, 635-640.
6. Cohn, LA, Diseases of the Pulmonary Parenchyma. In: Ettinger SJ, Feldman EC, Cote E. Textbook of Veterinary Internal Medicine. Vol. 2. 8th ed. Philadelphia, PA: WB Saunders Company; 2017:1113-1117.
7. Handt LK, Stoffregen DA, Prescott JS, et al. Clinical and microbiologic characterization of hemorrhagic pneumonia due to extraintestinal pathogenic Escherichia coli in four young dogs. Comp Med. 2003;53:663-670.
8. Lopez A, Martinson SA, Respiratory System, Mediastinum, and Pleurae. In: Zachary JM, ed. Pathologic Basis of Veterinary Disease. Vol. 6th ed. St. Louis, MI: Elsevier; 2017:546-547.
9. Pesavento PA, Hurley KF, Bannasch MJ, Artiushin S, Timoney JF. A Clonal Outbreak of Acute Fatal Hemorrhagic Pneumonia in Intensively Housed (Shelter) Dogs Caused by Streptococcus equi subsp. zooepidemicus. Vet Pathol. 2008:45:51-53.
10. Priestnall SL, Mitchell JA, Walker CA, Eries K, Brownlie J. New and emerging pathogens in canine infectous respiratory disease. Vet Pathol2014:51(2)492-504.
11. Sura R, Van Kruiningen HJ, DebRoy C, et al. Extraintestinal pathogenic Escherichia coli-induced acute necrotizing pneumonia in cats. Zoonoses Public Health. 2007;54:307-313. 12. Zachary JF, Mechanisms of Microbial Infections. In: Zachary JM, ed. Pathologic Basis of Veterinary Disease. Vol. 2. 6th ed. St. Louis, MI: Elsevier; 2017:151-153.

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02-1. Lung, dog.

02-2. Lung, dog.

02-3. Lung, dog.

02-4. Lung, dog.

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