Viral respiratory diseases

An overview of the more commonly encountered viral diseases of the dog and cat is presented. The reader is acquainted with the principles of antiviral therapy and the drugs that have been studied for use in animal viral respiratory diseases. An update on vaccination principles and guidelines is provided.     

Canine respiratory viruses

Acute contagious respiratory disease (kennel cough) is commonly described in dogs worldwide. The disease appears to be multifactorial and a number of viral and bacterial pathogens have been reported as potential aetiological agents, including canine parainfluenza virus, canine adenovirus and Bordetella bronchiseptica, as well as mycoplasmas, Streptococcus equi subsp. zooepidemicus, canine herpesvirus and reovirus-1,-2 and -3. Enhancement of pathogenicity by multiple infections can result in more severe clinical forms. In addition, acute respiratory diseases associated with infection by influenza A virus, and group I and II coronaviruses, have been described recently in dogs. Host species shifts and tropism changes are likely responsible for the onset of these new pathogens. The importance of the viral agents in the kennel cough complex is discussed.     

Experimental reproduction of respiratory tract disease with bovine respiratory syncytial virus

An experiment was conducted to reproduce respiratory tract disease with bovine respiratory syncytial virus (BRSV) in one-month-old, colostrum-fed calves. The hypothesized role of viral hypersensitivity and persistent infection in the pathogenesis of BRSV pneumonia was also investigated. For BRSV inoculation a field isolate of BRSV, at the fifth passage level in cell culture, was administered by a combined respiratory tract route (intranasal and intratracheal) for four consecutive days. Four groups of calves were utilized as follows: Group I, 6 calves sham inoculated with uninfected tissue culture fluid and necropsied 21 days after the last inoculation; Group II, 6 calves inoculated with BRSV and necropsied at the time of maximal clinical response (4-6 days after the last inoculation); Group III, 6 calves inoculated with BRSV and necropsied at 21 days after the last inoculation; Group IV, 6 calves inoculated with BRSV, rechallenged with BRSV 10 days after initial exposure, and necropsied at 21 days after the initial inoculation. Clinical response was evaluated by daily monitoring of body temperature, heart rate, respiratory rate, arterial blood gas tensions, hematocrit, total protein, white blood cell count, and fibrinogen. Calves were necropsied and pulmonary surface lesions were quantitated by computer digitization. Viral pneumonia was reporduced in each principal group. Lesions were most extensive in Group II. Disease was not apparent in Group I (controls). Significant differences (p less than 0.05) in body temperature, heart rate, respiratory rate, arterial oxygen tension, and pneumonic surface area were demonstrated between control and infected calves. Results indicate that severe disease and lesions can be induced by BRSV in one-month-old calves that were colostrum-fed and seropositive to BRSV. BRSV rechallenge had minimal effect on disease progression. Based on clinical and pathological response, results did not support viral hypersensitivity or persistent infection as pathogenetic mechanisms of BRSV pneumonia.     

Evaluation of respiratory parameters at presentation as clinical indicators of the respiratory localization in dogs and cats with respiratory distress

Objective ? To describe clinical respiratory parameters in cats and dogs with respiratory distress and identify associations between respiratory signs at presentation and localization of the disease with particular evaluation between the synchrony of abdominal and chest wall movements as a clinical indicators for pleural space disease. Design ? Prospective observational clinical study. Setting ? Emergency service in a university veterinary teaching hospital. Animals ? Cats and dogs with respiratory distress presented to the emergency service between April 2008 and July 2009. Interventions ? None. Measurements and Main Results ? The following parameters were systematically determined at time of admission: respiratory rate, heart rate, temperature, type of breathing, movement of the thoracic and abdominal wall during inspiration, presence of stridor, presence and type of dyspnea, and results of thoracic auscultation. Abdominal and chest wall movement was categorized as synchronous, asynchronous, or inverse. Diagnostic test results, diagnosis, and outcome were subsequently recorded. Based on the final diagnoses, animals were assigned to 1 or more of the following groups regarding the anatomical localization of the respiratory distress: upper airways, lower airways, lung parenchyma, pleural space, thoracic wall, nonrespiratory causes, and normal animals. One hundred and seventy‐six animals (103 cats and 73 dogs) were evaluated. Inspiratory dyspnea was associated with upper airway disease in dogs and expiratory dyspnea with lower airway disease in cats. Respiratory noises were significantly associated and highly sensitive and specific for upper airway disease. An asynchronous or inverse breathing pattern and decreased lung auscultation results were significantly associated with pleural space disease in both dogs and cats (P<0.001). The combination is highly sensitive (99%) but not very specific (45%). Fast and shallow breathing was not associated with pleural space disease. Increased or moist pulmonary auscultation findings were associated with parenchymal lung disease. Conclusions ? Cats and dogs with pleural space disease can be identified by an asynchronous or inverse breathing pattern in combination with decreased lung sounds on auscultation.     

Ferret respiratory diseases.

Ferret behavior often brings them into close contact with potential respiratory pathogens and traumatic insults. Although respiratory disease accounts for a small percentage of cases, they are usually dramatic. Acute and chronic conditions occur, and many lesions are confined to the upper or lower respiratory tree but may not involve both. Pathogens such as influenza A account for a large percentage of upper respiratory infections and often mirror the "flu" season of humans. Traumatic insults to the head and chest are relatively common and account for many veterinary visits. Numerous diseases affecting the upper and lower respiratory systems are discussed, with suggestions for diagnostics and therapies.     

Reptile respiratory medicine.

Respiratory tract disease is commonly diagnosed in captive collections of reptiles and associated with high morbidity and mortality. Improper environmental conditions are often contributing factors for the development of respiratory disease in reptiles. A detailed knowledge of the unique reptilian respiratory morphology and function is essential to successfully diagnose and treat respiratory disease. A variety of noninfectious and infectious causes have been identified in the etiology of reptile respiratory disease. Knowledge of the pathophysiology of reptilian diseases is increasing, and with the availability of new therapeutic agents and advanced diagnostic techniques, the diagnosis and treatment of reptile respiratory tract disease has become more successful.     

Amphibian respiratory diseases.

This article describes the diseases that commonly affect the lungs, gills, and nasal passages of frogs, toads, and salamanders. Although these organs often are affected by systemic infections, only diseases that are limited to the respiratory system are discussed. Gills of aquatic amphibians commonly are affected by poor water quality, infestations by protozoa or trematodes, or infections by water molds. Nematodes in the genus Rhabias are significant pulmonary pathogens in frogs and toads. The nasal passages of frogs, toads, and salamanders may be parasitized by Bufolucilia fly larvae.     

Canine respiratory virus infections

The aetiology and pathogenesis of canine respiratory disease is complex. Current research has implicated a number of viruses in this important disease problem. Distemper virus, two adenoviruses (ICH virus and A26/61 virus), herpesvirus and reovirus have all been isolated from the respiratory tract of dogs and are all capable of causing respiratory lesions in experimental animals. The general features of each of these virus infections are discussed.
Résumé. L'étiologie et la pathogenèse des maladies respiratoires chez le chien est complexe. Une recherche en cours a impliqué un nombre de virus dans cette maladie qui pose un problème important. Le virus de la maladie du jeune âge chez le chien, les adénovirus twp (le virus ICH et le virus A 26/61), le virus de l'herpts et le réovirus ont été tous isolés des voies respiratoires de chiens et sont tous susceptibles de causer des lesions respiratoires chez des animaux expérimentaux. On discute des traits généraux de chacune de ces infections par virus.
Zusammenfassung. Die Ätiologie und Pathogenese von Hunde-Atmungskrankheiten ist komplex. Gegenwärtige Forschung hat eine Reihe von Viren mit diesem wichtigen Krankheitsproblem in Verbindung gebracht. Staupevirus, twp Adenovirus (ICH Virus und A26/61 Virus), Herpesvirus und Reovirus wurden alle vom Luftweg von Hunden isoliert und sind alle fähig Atemläsionen in Versuchstieren zu verursachen. Die allgemeinen Merkmale von diesen Virusinfektionen wurden erörtet.     

Bovine respiratory syncytial virus

The current knowledge is reviewed in regards to the importance of bovine respiratory syncytial virus in the bovine respiratory disease complex. The epidemiology, clinical disease, pathologic findings, pathogenesis, diagnosis, treatment, and prevention of this viral disease are discussed.     

Cellular defense of the avian respiratory system: effects of Pasteurella multocida on respiratory burst activity of avian respiratory tract phagocytes

The respiratory tract of healthy chickens contain few free-residing phagocytic cells. Intratracheal inoculation with Pasteurella multocida stimulated a significant (P less than 0.05) migration of cells to the lungs and air sacs of White Rock chickens within 2 hours after inoculation. We found the maximal number of avian respiratory tract phagocytes (22.9 +/- 14.0 x 10(6] at 8 hours after inoculation. Flow cytometric analysis of these cells revealed 2 populations on the basis of cell-size and cellular granularity. One of these was similar in size and granularity to those of blood heterophils. Only this population was capable of generating oxidative metabolites in response to phorbol myristate acetate. The ability of the heterophils to produce hydrogen peroxide, measured as the oxidation of intracellularly loaded 2',7'-dichlorofluorescein, decreased with time after inoculation. These results suggest that the migration of heterophils, which are capable of high levels of oxidative metabolism, to the lungs and air sacs may be an important defense mechanism of poultry against bacterial infections of the respiratory tract.     

Extensive mast cell degranulation in bovine respiratory syncytial virus-associated paroxystic respiratory distress syndrome

Bovine respiratory syncytial virus (BRSV) infection is an important cause of outbreaks of respiratory disease among calves. This virus commonly induces mild to severe respiratory signs but, in a substantial proportion of cases, is also reported to be associated with paroxystic respiratory distress syndrome (PRDS). The pathogenesis of this 'malignant' clinical form has not been fully elucidated. The present study aimed at determining whether mast cell (MC) degranulation plays a role in the physiopathologic cascade leading to the PRDS. Paired serum samples were taken in herds during outbreaks of severe respiratory diseases (acute sera) and 3 weeks after (convalescent sera). Based on seroconversion to BRSV and clinical picture, 67 pairs of sera were selected from calves with a BRSV-associated PRDS for circulating MC tryptase determination. A MC metachromatic score was measured in post-mortem lungs from animals died from a BRSV-associated PRDS (principals) and compared with reference scores obtained from healthy lungs (controls). Levels of tryptase were significantly higher in acute sera (26.6 +/- 12.4 microg/l) compared to convalescent sera (8.4 +/- 7.8 microg/l; P<0.001). Metachromatic scores yielded significantly different results between controls and principals (P<0.01), demonstrating a significant disappearance of metachromatic granules from lung MCs in principals. Taken together, these data demonstrate the presence of an extensive MC degranulation in BRSV-associated PRDS.     

Experimental bovine respiratory syncytial virus infection in conventional calves: ultrastructural respiratory lesions

The morphogenesis and repair of airway and alveolar injury induced by bovine respiratory syncytial virus (BRSV) was studied ultrastructurally in conventional calves to characterize pulmonary cell types susceptible to viral infection and cytopathologic changes associated with infection. Viral nucleocapsids and budding virions were present in tracheal and bronchial ciliated and nonciliated epithelial cells and mucous cells 3, 5, and 7 days after inoculation and in bronchiolar ciliated and nonciliated epithelial cells 5 days after inoculation. Mild interstitial pneumonia was observed 5 days after inoculation and was characterized by swelling of type 1 and type 2 alveolar epithelial cells, interstitial edema, and infiltration by lymphocytes and macrophages. Viral assembly and release in tracheal and bronchial epithelial cells was associated with loss of cilia from ciliated cells, formation of syncytial epithelial cells, swelling of mitochondria and endoplasmic reticulum, and cell necrosis. Neutrophils, lymphocytes, and macrophages were present in close association with the viral-infected and damaged epithelial cells. There was intercurrent hyperplasia of basal epithelial cells that, in association with other epithelial lesions, resulted in the loss of normal ciliated epithelium in these airways 5 and 7 days after inoculation. Regeneration of airway epithelium was largely completed by 10 days after inoculation, except in 1 of 4 calves that had failure of epithelial repair and that developed secondary bacterial pneumonia. Pulmonary ultrastructure in BRSV-inoculated calves 30 days after inoculation was indistinguishable from that in controls. The results demonstrated that BRSV can induce reversible alterations in airway epithelium, which may cause depression of mucociliary clearance and thereby enhance susceptibility to bacterial infection.     

Immunopathogenesis of porcine reproductive and respiratory syndrome in the respiratory tract of pigs

Porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) impairs local pulmonary immune responses by damaging the mucociliary transport system, impairing the function of porcine alveolar macrophages and inducing apoptosis of immune cells. An imbalance between pro- and anti-inflammatory cytokines, including tumour necrosis factor-α and interleukin-10, in PRRS may impair the immune response of the lung. Pulmonary macrophage subpopulations have a range of susceptibilities to different PRRSV strains and different capacities to express cytokines. Infection with PRRSV decreases the bactericidal activity of macrophages, which increases susceptibility to secondary bacterial infections. PRRSV infection is associated with an increase in concentrations of haptoglobin, which may interact with the virus receptor (CD163) and induce the synthesis of anti-inflammatory mediators. The balance between pro- and anti-inflammatory cytokines modulates the expression of CD163, which may affect the pathogenicity and replication of the virus in different tissues. With the emergence of highly pathogenic PRRSV, there is a need for more information on the immunopathogenesis of different strains of PRRS, particularly to develop more effective vaccines.