Brendan M. Corcoran, MVB, Dip Pharm, PhD, MRCVS
Hospital for Small Animals, The University of Edinburgh, Easterbush Veterinary Centre Roslin
Bacterial bronchopneumonia is invariably a consequence of another disease process or injury to the lung that allows the resident bacterial population of the respiratory system to proliferate. In other situations the entry of non-resident organisms into the respiratory system may precipitate the development of bronchopneumonia, but again, it is usually necessary for an initial lung insult to have been present.
The organisms typically located within the respiratory system, and that are then ready to proliferate under the right circumstances, are usually gram negative aerobes and include Pasturella, Klebsiella, Proteus spp. and E. Coli. Gram positive Staphylococcus and Streptococcus organisms can also be present. The presence of Pseudomonal agents, and anaerobic organisms such as Nocardia, Actinomyces, and Bacteroides spp are presumed to be invading organisms, while the exact role of Mycoplasma spp in pneumonia is not known. These organisms will proliferate when there is aspiration of food or stomach contents, if a primary (unchecked) primary respiratory infection is present and if there is long standing chronic respiratory disease, such as chronic bronchitis. The role of ageing, immunocompromise and systemic illness in the development of bronchopneumonia is well recognised in humans, but is not fully characterised in the dog and cat.
Diagnosis is achieved by considering all aspects of the clinical presentation and the results of all diagnostic tests. It is readily accepted that reliance on a single diagnostic test is unlikely to allow a diagnosis to be made.
The clinical history is important. The rapid development of coughing, tachypnoea, dyspnoea, orthopnoea, lethargy, anorexia, with or without pyrexia, in an otherwise healthy animal, would raise suspicion of bronchopneumonia, once there was no evidence of congestive heart failure or pleural effusion. Suspicion would be further raised if the patient had been vomiting or regurgitating, had a history of recent or chronic respiratory disease, gastrointestinal disease or had been in close association with other dogs (kenneled). Physical examination will give other diagnostic clues (depending on the severity and extent of disease). In particular, the exclusion of a cardiac explanation for the clinical presentation is crucial. The patient should be checked for evidence of abnormal respiratory pattern, including elevated respiratory rate (ignoring panting) and increased effort, audible respiratory sounds (rhonchi, crackles and wheezes), coughing that can be elicited on tracheal pinch or chest percussion and the presence of pyrexia. The alertness of the patient and hydration status should also be evaluated.
Ancillary diagnostic tests which can assist with diagnosis include thoracic radiography, blood gas analysis, airway sampling, bronchoscopy and cytological analysis of bronchial and broncho-alveolar lavage samples, and routine haematology and biochemistry profiles. Of these test radiography is the most widely used and it is often on the basis of radiographic findings that a tentative (not definitive) diagnosis can be made. Right and left lateral and ventro-dorsal projections should be obtained. The presence of alveolar density, with air bronchograms and a cranio-ventral distribution, is highly suggestive of bronchopneumonia, and in a severely compromised patient is reason enough to make a tentative diagnosis and institute intensive therapy. The main radiographic differential consideration is pulmonary oedema, but if there is no evidence of cardiac disease it would be reasonable to exclude this explanation. In certain parts of the world mycotic pneumonia would need to be considered. The collection of airway samples to confirm inflammation is present (neutrophils, macrophages) and to obtain material for culture and sensitivity testing, can be undertaken depending on the patient's clinical status. This can be achieved by trans-tracheal sampling in the compromised patient and by bronchoscopy in the less severely affected patient. Arterial blood gas analysis is the most sensitive way in assessing respiratory function and should be attempted in all cases. However, if the procedure itself (arterial sampling) is causing too much distress then a venous sample should be obtained. Blood gas analysis will allow estimation of the degree of ventilation-perfusion mismatch present. Bronchoscopy can be undertaken in those patients that will tolerate a general anaesthetic. Its main use is to allow visualisation of muco-purulent material in the airways and the accurate collection of samples from the bronchi, lower airways and alveoli. Lastly, routine haematology and biochemistry can be of benefit and should be carried out as a matter of course to assess overall health status. With respect to bacterial bronchopneumonia, these tests are rarely of diagnostic value except if there is a leucocytosis with a pronounced neutrophilia.
Management and Treatment
Antibacterial therapy is the mainstay of successful treatment of bacterial bronchopneumonia. As it is known that there is a high level of probability that gram negative aerobes are involved, then the selection of an antibacterial agent, with potent activity against such organisms, such as a fluoroquinolone, on a purely empirical basis would appear to be sound. Furthermore, if it is recognised that anaerobes can also be implicated, and that such organisms are notoriously difficult to culture, then empirical selection of an antibacterial agent to target such organisms would again be a sound judgment. In the authors' experience, it is the vigorous antibacterial therapy targeting the widest range of possible organisms that will give the best chance of success in severe fulminating bacterial bronchopneumonia cases. Coupled with these points is the necessity for the antibacterial agent to be able to penetrate well into lung tissue. The ability to localised intracellularly, such as in macrophages, is probably an advantage but probably not crucial. Using these guidelines, the antibacterials appropriate for treating bacterial bronchopneumonia include the potentiated sulphonamides, cephalosporins, fluoroquinolones, clindamycin and metronidazole. Antibiotic therapy should be continued until 2-3 weeks after resolution of clinical signs and in some instances should be administered for up to 8 weeks. If after prolonged multiple antibacterial therapy there is no resolution and the pathology has localised to a single lung lobe then lobectomy should be performed as it gives the best opportunity for total cure. Initially, administration of antibacterial agents is preferably by the intra-venous route, and at the top end of the recommend dose range. Subsequent maintenance therapy is given orally. Effective antibacterial therapy in severe pneumonic cases depends on rapid intervention, as serious or life-threatening deterioration in lung function can occur within hours. That tends to mean that empirical selection is likely in the majority of cases rather than on the basis of culture and sensitivity testing. Antibiotic selection can be amended in the light of what is cultured, but it should also be remembered that the organisms cultured are not necessarily the only organisms implicated. For example, anaerobic organisms can prove particularly difficult to culture, taking several weeks, and if antibacterial therapy has been instituted prior to sampling, then it is difficult to know if the true culprit organisms have been identified.
The other main consideration in the effective treatment of bronchopneumonia cases is adequate supportive care. This includes tending to the patients' dietary and fluid needs, maintaining warmth and comfort, periodically changing the patients' position to prevent positional atelectasis, and providing supplemental oxygen. Intravenous fluid therapy is required to maintain proper hydration, as the patient is likely to be adipsic and anorexic, but also as there will be fluid loss from the airway as a consequence of increased respiratory effort. The use of physiotherapy (coupage) will be beneficial, as it will allow thick viscid secretions to move rostrally and the material can then be removed by coughing.
The use of bronchodilators, such as the β-adrenoreceptor agonists and the methylxanthines, is controversial and are of doubtful benefit. The use of antitussives, such as codeine, should be avoided, as coughing is an important protective mechanism in pneumonia cases. Anti-inflammatory agents tend not to be used in treating bacterial bronchopneumonia, but may be of use in controlling pyrexia. In desperate situations, intravenous corticosteroids have been used in an attempt to salvage the situation, but there is no information as to their efficacy or the potential benefits of anti-inflammatory agent use in general. The administration of drugs by nebulisation is also of questionable value in that it is unlikely that the drug will get as far as the alveoli in a hypoventilating case. It can, however, be useful for delivery of toxic drugs, such as gentamycin (Pseudomonas infection).
1. Brownlie, SE (1990). A retrospective study of diagnoses in 109 cases of canine lower respiratory disease. JSAP, 31: 371-376, 1990.
2. Dye, JA, McKiernan, BC, Rozanski, EA et al (1996). Bronchopulmonary disease in the cat: historical, physical, radiographic, clinicopathologic, and pulmonary functional evaluation of 24 affected and 15 healthy cats. JVIM, 10: 385-400.
3. Hawkins, EC, De Nicola, DB, Kuehn, NF (1990). Bronchoalveolar lavage in the evaluation of pulmonary disease in the dog and cat. JVIM, 4: 267-274.
4. McKiernan, B Smith AR, Kissil, M (1984). Bacterial isolates form the lower trachea of clinically healthy dogs. JAAHA, 20: 139-142.
5. Thayer, GW, Robinson, SK (1984). Bacterial bronchopneumonia in the dog: a review of 42 cases. JAAHA, 20: 731-735.