Delayed diagnosis of fatal pneumonic canine plague: clinical and pathologic features in two naturally infected Colorado dogs.

BACKGROUND: Plague caused by Yersinia pestis is a highly infectious and potentially fatal zoonotic disease that can be spread by wild and domestic animals. In endemic areas of the northern hemisphere plague typically cycles from March to October, when flea vectors are active. Clinical forms of disease include bubonic, septicemic, and pneumonic plague. All clinical forms are uncommon in dogs and the pneumonic form is exceedingly rare. CASE PRESENTATION: Two mixed breed young-adult male domestic dogs presented to Colorado veterinarians with fever and vague signs that progressed to hemoptysis within 24 h. Case 1 presented in June 2014, while Case 2 occurred in December 2017. Thoracic radiography of Case 1 and 2 revealed right dorsal and right accessory lobe consolidation, respectively. In Case 1 initial differential diagnoses included pulmonary contusion due to trauma or diphacinone toxicosis. Case 1 was euthanized ~ 24 h post presentation due to progressive dyspnea and hemoptysis. Plague was confirmed 9 days later, after the dog's owner was hospitalized with pneumonia. Case 2 was treated as foreign body/aspiration pneumonia and underwent lung lobectomy at a veterinary teaching hospital. Case 2 was euthanized after 5 days of hospitalization when bacterial culture of the excised lobe yielded Yersinia pestis. Both dogs had severe diffuse necrohemorrhagic and suppurative pneumonia at post mortem examination. CONCLUSIONS: Both dogs were misdiagnosed due to the atypical lobar presentation of an extremely rare form of plague in a species that infrequently succumbs to clinical disease. Presentation outside of the typical transmission period of plague was also a factor leading to delayed diagnosis in Case 2. Erroneous identification by automated bacterial identification systems was problematic in both cases. In endemic areas, plague should be ruled out early in febrile dogs with acute respiratory signs, hemoptysis, lobar or diffuse pathology, and potential for exposure, regardless of season. Seasonal and geographic distributions of plague may shift with climate change, so vigilance by primary care veterinarians is warranted. Timely submission of samples to a veterinary diagnostic laboratory could expedite accurate diagnosis and reduce potential for human and domestic animal exposure.

Fatal hemoptysis after bronchoscopic biopsy in a dog.

An 8-year-old 24.6 kg mixed breed dog underwent bronchoscopy for evaluation of a persistent progressive cough. Bronchoscopy documented a markedly thick and irregular, cobblestone appearance of the mucosa. A bronchoscopic biopsy was obtained; immediately after the biopsy, a large amount of hemorrhage poured from the endotracheal tube. Multiple efforts to control the hemorrhage were unsuccessful and the dog suffered a cardiopulmonary arrest and could not be revived. A necropsy was performed, which was significant for pallor, evidence of prior heartworm disease, prominent bronchial arteries, and erosion of the submucosal vessels at the site of the biopsy. The cause of death was hemorrhage associated with transbronchial biopsy of an enlarged bronchial artery associated with heartworm disease. This report describes a rare complication of a routine diagnostic procedure.

Severe acute pulmonary haemorrhage and haemoptysis in ten dogs following eastern brown snake (Pseudonaja textilis) envenomation: Clinical signs, treatment and outcomes.

This report describes a series of ten cases of fulminant pulmonary haemorrhage in dogs following envenomation by the eastern brown snake (Pseudonaja textilis) in south eastern Queensland, Australia. All cases were presented for veterinary treatment during 2011-2018 at a specialist veterinary emergency centre. Each case received prompt antivenom treatment and supportive care. Pulmonary haemorrhage was diagnosed based on clinical examination; overt haemoptysis; thoracic radiographic demonstration of a diffuse alveolar pattern; and, the presence of venom induced consumptive coagulopathy. The median elapsed time from hospital admission to onset of haemoptysis was 2 h (range 0-18 h). In 80% (8/10) of cases endotracheal intubation was required, whilst 20% (2/10) were successfully treated with mask oxygen supplementation alone, and 40% (4/10) received mechanical ventilation; but only 25% (1/4) of these survived to hospital discharge. Fresh frozen canine plasma was administered to 70% (7/10) of cases and 43% (3/7) of these survived. Of the total number of cases presented for treatment, 30% (3/10) survived to hospital discharge, 60% (6/10) were euthanised due to poor prognosis and 10% (1/10) died from cardiac arrest. Initial serum brown snake venom antigen levels were retrospectively measured from frozen serum samples by venom specific sandwich ELISA in two dogs at 154 ng/mL (survived) and 3607 ng/mL (euthanised); no free venom was detected post-antivenom. Dogs that survived were discharged from hospital without apparent complications. Pulmonary haemorrhage is an uncommon event following envenomation by P. textilis in dogs and has not been described in similarly envenomed humans. This case series highlights the potential for fulminant and fatal pulmonary haemorrhage in dogs following eastern brown snake envenomation.

Acute Hypoxemic Respiratory Failure With Hemoptysis in a Dog Exposed to Copper Sulfate Powder.

A 2-year-old male mongrel dog was presented because of the onset of dry cough. About 16 hours before, the dog had been exposed to the pesticide that the owner was spraying in the vineyard. Approximately 3 hours later an acute respiratory failure, with a rapid evolution, began. Hemoptysis and regenerative normocytic normochromic anemia arose within hours, and a pulmonary hemorrhage was diagnosed. Pulmonary hemorrhage fast led to pneumonia, as evidenced by the serial CXR findings and the developing of leukocytosis. The hypothesis that we believe more likely is that the dog inhaled an amount of copper sulfate powder enough to determine respiratory tree damage, extending from the trachea to the pulmonary alveoli. Oxygen supplementation, antibiotics, antioxidant, and gastroprotective medications had been administered. After 4 days of hospitalization the dog was discharged. After a follow-up of more than 2 years later, the dog is still alive and in good health. To the authors knowledge no evidences of acute pulmonary involvement after copper sulfate inhalation exist in any species. This report is a contribution to the knowledge of copper poisoning, scarcely mentioned both in human and veterinary literature, and which has never been described in companion animals.

Intermittent Haemoptysis due to an Aortobronchial Fistula in a Warmblood Mare.

A 7-year-old warmblood mare showed sudden onset of mild intermittent haemoptysis. Clinical examination revealed no significant abnormalities. Haematological examination showed mild anaemia, hypoalbuminaemia and neutrophilia. Coagulation tests were normal. Endoscopic examination revealed unilateral pulmonary haemorrhage with blood clots in the bronchi and trachea. Treatment with antibiotics was started and the horse was given stable rest. Two weeks later, the horse was found dead with blood and frothy sputum leaking from the nostrils. Post-mortem examination revealed a large thoracic aortic aneurysm communicating with a pseudoaneurysm that had formed a fistula into a right bronchial branch. Microscopical examination of the aneurysm showed extensive medial fibrosis with prominent degeneration, fragmentation and mineralization of the elastic fibres and deposition of mucoid material in the tunica media. The pseudoaneurysm was lined by collagen bundles admixed with fibroblasts and a small amount of adipose tissue. Aortobronchial fistula is a rare condition in man that is usually associated with primary aortic pathology, most often aneurysms. To the authors' knowledge this is the first case of a fatal aortobronchial fistula in a horse or any other animal species.

Severe haemoptysis associated with seizures in a dog.

CASE HISTORY: A 7-year-old, sterilised male German Shepherd dog was presented with a history of three episodes of severe haemoptysis and associated dyspnoea within a 3-week period. A generalised tonic-clonic seizure was witnessed preceding the third episode. CLINICAL FINDINGS: Thoracic radiographs revealed a severe bilateral alveolar lung pattern of the caudodorsal lung fields; extension into the left cranial lung lobe was present but pulmonary vessels were within normal size limits. Frank blood was the only abnormality present at bronchoscopy. A coagulation profile, parasitological screening, thoracic and brain computed tomography (CT), and cerebrospinal fluid (CSF) cytological analysis did not identify any abnormalities. DIAGNOSIS: Haemoptysis due to either severe neurogenic pulmonary oedema or rupture of the pulmonary capillaries secondary to seizures was considered a possible diagnosis. The primary generalised seizures were attributed to late-onset idiopathic epilepsy diagnosed by exclusion of other causes. CLINICAL RELEVANCE: This is the first known case report describing severe haemoptysis associated with seizures in a dog.

Clinical signs, clinicopathological findings, etiology, and outcome associated with hemoptysis in dogs: 36 cases (1990-1999).

Hemoptysis, the expectoration of blood or bloody mucus from the respiratory tract at or below the larynx, was retrospectively evaluated in 36 dogs. Cough, tachypnea, and dyspnea were common historical and physical examination signs. Anemia was documented in 11 dogs, but was severe in only one dog. Other clinicopathological findings reflected the underlying diseases. All thoracic radiographs obtained were abnormal; alveolar and interstitial patterns were most common. Diseases predisposing to hemoptysis included bacterial bronchopneumonia (n=7), neoplasia (n=5), trauma (n=5), immune-mediated thrombocytopenia (n=4), heartworm disease (n=4), rodenticide poisoning (n=3), lung-lobe torsion (n=1), left-sided congestive heart failure (n=1), pulmonary hypertension (n=1), and foreign-body pneumonia (n=1). Four additional dogs had more than one underlying disease process. Nine dogs were either euthanized or died in the hospital during the initial visit. While at least half of the 27 dogs discharged went on to completely recover, five dogs discharged were known to have either died or been euthanized as a result of their disease in <6 months.

Serum creatine kinase activities in dogs with dirofilariasis.

Total serum creatine kinase (CK) and its isozyme activities were determined in dogs with dirofilariasis. Before heartworm removal, total CK and isozyme activities in dogs of the mild group were not different from those in dogs of the heartworm-free group. BB activity was higher in dogs of the hemoptysis group. Dogs of the ascites group displayed a mild increase in MM activity. In dogs of the caval syndrome (CS) group, total CK and MM activities were highest among the heartworm-free and heartworm-infected dogs, and MM isozyme accounted for most (75%) of total CK activity. MB and BB activities were also higher. However, there were no significant differences in CK activities between the surviving and non-surviving cases. In dogs with pulmonary heartworm disease (mild and ascites groups), MM activity correlated significantly with the number of heartworms (r = 0.45), hematocrit value (Ht, r = -0.40), serum alanine aminotransferase (ALT, r = 0.42) and lactate dehydrogenase (LDH, r = 0.46) activities, mean pulmonary arterial pressure (r = 0.64) and total pulmonary resistance (r = 0.50). In dogs with CS, MM activity did not correlate with any parameter, but BB activity correlated with the number of heartworms at the right atrium (r = 0.61), Ht (r = -0.53), ALT (r = 0.80), LDH (r = 0.73) and serum urea nitrogen (r = 0.47). At 1 week after heartworm removal, BB and MM activity decreased in dogs of the hemoptysis and ascites groups, respectively. In dogs of the CS group, total CK and MM isozyme activities decreased markedly (P less than 0.01) regardless of their prognosis.

Efficacy of furosemide in the treatment of exercise-induced pulmonary hemorrhage in Thoroughbred racehorses.

The repeatability of endoscopic observations of exercise-induced pulmonary hemorrhage (EIPH) and the efficacy of furosemide as a prophylactic treatment of horses with EIPH were studied in Thoroughbred race horses after consecutive breezes (at or near maximum speed, approx 16 m/s). Of 56 horses examined greater than or equal to 2 times, 21 (38%) had identical EIPH scores, whereas 26 (46%) and 9 (16%) had scores that differed by greater than or equal to 1 grade. In 56 nontreated horses, there was good agreement between 2 consecutive observations (K = 0.59, Z = 4.54, P less than 0.001). Similar comparisons after placebo (saline solution) treatment of 21 horses yielded fair to good agreement, whereas poorer agreement was seen after furosemide treatment of 23 horses. Comparison of average and maximum EIPH scores of 44 horses with a minimum of 4 observations (2 nontreated, 1 saline-treated, and 1 furosemide-treated) indicated that although furosemide did not stop EIPH, it did reduce the EIPH score in 28 (64%) horses.

Percutaneous lung biopsy in the horse.

Percutaneous lung biopsies with a cutting needle (Vim Tru Cut) were obtained from 20 horses. The procedure was performed in standing horses under a local anesthesia without sedation. All lung tissue specimens were suitable for histologic examinations and contained both pulmonary parenchyma and large airways. The only complication was hemoptysis in 2 (10%) horses which required no therapy. All horses were subsequently killed, and no gross abnormalities were present at the biopsy site.

Pulmonary tuberculosis in a sulfur-crested cockatoo.

An adult, female sulfur-crested cockatoo (Kakatoe sp) was examined because of dyspnea associated with hemoptysis. On radiographic examination there was a large cystic pulmonary mass that, on aspiration, was found to contain thick sanguineous fluid. Ziehl-Neelsen staining of aspirate smears revealed numerous acid-fast organisms. Gross necropsy and microscopic findings suggested a diagnosis of tuberculosis, with primary focus of infection in the pulmonary tissues. Bacteriologic isolation and typing confirmed a diagnosis of tuberculosis and established Mycobacterium avium as the etiologic agent.