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Bacterial Pneumonia in Cattle

By John Campbell, DVM, DVSc, Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan

Mannheimia haemolytica–associated Bovine Respiratory Disease


Mannheimia haemolytica serotype 1 is the bacterium most frequently isolated from the lungs of cattle with BRD. Although less frequently cultured, Pasteurella multocida is also an important cause of bacterial pneumonia. Histophilus somni is being increasingly recognized as an important pathogen in BRD; these bacteria are normal inhabitants of the nasopharynx of cattle (see Histophilosis). When pulmonary abscessation occurs, generally in association with chronic pneumonia, Trueperella pyogenes is frequently isolated.

Under normal conditions, M haemolytica remains confined to the upper respiratory tract, in particular the tonsillar crypts, and is difficult to culture from healthy cattle. After stress or viral infection, the replication rate of M haemolytica in the upper respiratory tract increases rapidly, as does the likelihood of culturing the bacterium. The increased bacterial growth rate in the upper respiratory tract, followed by inhalation and colonization of the lungs, may occur because of suppression of the host’s defense mechanism related to environmental stressors or viral infections. It is during this log phase of growth of the organism in the lungs that virulence factors are elaborated by M haemolytica, such as an exotoxin that has been referred to as leukotoxin. The interaction between the virulence factors of the bacteria and host defenses results in tissue damage with characteristic necrosis, thrombosis, and exudation, and in the development of pneumonia. The pathogenesis of pneumonia caused by P multocida is poorly understood. This organism may opportunistically colonize lungs with chronically damaged respiratory defenses, such as occurs with enzootic calf pneumonia or existing lung lesions of feedlot cattle, and cause a purulent bronchopneumonia. H somni may invade the lung and cause pneumonia after damage to the respiratory defenses. This organism is capable of systemic spread from the lung to the brain, myocardium, synovium, and pleural and pericardial surfaces; often, death can occur later in the feeding period (40–60 days after arrival) from involvement of these additional organ systems.

Clinical Findings:

Clinical signs of bacterial pneumonia are often preceded by signs of viral infection of the respiratory tract. With the onset of bacterial pneumonia, clinical signs increase in severity and are characterized by depression and toxemia. A combination of clinical signs of depression and fever (104°–106°F [40°–41°C]), without any signs attributable to other body systems, are the classic components of a case definition for early cases of BRD. Serous to mucopurulent nasal discharge; moist cough; and a rapid, shallow respiratory rate may be noted. Auscultation of the cranioventral lung field reveals increased bronchial sounds, crackles, and wheezes. In severe cases, pleurisy may develop, characterized by an irregular breathing pattern and grunting on expiration. The animal will become unthrifty in appearance if the pneumonia becomes chronic, which is usually associated with formation of pulmonary abscesses.


M haemolytica causes a severe, acute, hemorrhagic fibrinonecrotic pneumonia. The pneumonia has a bronchopneumonic pattern. Grossly, there are extensive reddish black to grayish brown cranioventral regions of consolidation with gelatinous thickening of interlobular septa and fibrinous pleuritis. There are extensive thromboses, foci of lung necrosis, and limited evidence of bronchitis and bronchiolitis.

P multocida is associated with a less fulminating fibrinous to fibrinopurulent bronchopneumonia. In contrast to M haemolytica, P multocida is associated with only small amounts of fibrin exudation, some thromboses, limited lung necrosis, and suppurative bronchitis and bronchiolitis.

H somni infection of the lungs results in purulent bronchopneumonia that may be followed by septicemia and infection of multiple organs. H somni is associated with extensive fibrinous pleuritis in feedlot calves.

Pulmonary abscessation can occur as the pneumonia becomes chronic. Abscesses develop in ~3 wk but do not become encapsulated until 4 wk. T pyogenes is frequently cultured from these abscesses.


Generally, neither serologic testing nor direct bacterial detection are performed, and diagnosis relies on gross necropsy findings and bacterial culture. Because the bacteria involved are normal inhabitants of the upper respiratory tract, the specificity of culture can be increased by collecting antemortem specimens from the lower respiratory tract by tracheal swab, transtracheal wash, or bronchoalveolar lavage. Lung specimens can be collected for culture at necropsy. If possible, specimens for culture should be collected from animals that have not been treated with antibiotics to permit determination of antimicrobial sensitivity patterns. A multiplex PCR has been used to identify a number of bacterial agents implicated with bovine respiratory disease, including M hemolytica.


Early recognition by trained personnel skilled at detecting the early clinical signs of disease followed by treatment with antibiotics is essential for successful therapy. Treatment protocols should be established so the producer has a standardized approach to identifying and treating cases. Long-acting antimicrobials such as tulathromycin, tilmicosin, florfenicol, and enrofloxacin have label claims to treat BRD and are commonly used as first- or second-line treatment options in feedlot calves. These long-acting antimicrobials allow the feedlot producer to avoid commingling sick animals in a hospital pen, and treated animals can return directly to the home pen. NSAIDs have been shown to be a beneficial ancillary therapy in controlling fever in cases of BRD, but data are lacking in terms of effect on relapse and mortality outcomes. If selection for treatment is late and pulmonary abscessation has occurred, it is difficult to achieve resolution with antimicrobials, and use of a convalescent pen or culling of the animal should be considered.


General principles of control are discussed under Enzootic Pneumonia of Calves and Shipping Fever Pneumonia. The value of M haemolytica and P multocida bacterins is questionable, and some reports indicate they may even exacerbate the disease. Newer vaccines, which include live culture and subunit vaccines (leukotoxin), show much more promise for disease prevention and may reduce morbidity in high-risk feedlot calves given one dose of vaccine on arrival by as much as 25%; however, trials have not been consistent in all risk categories of feedlot cattle. Ideally, vaccination should be done 3 wk before transport to the feedlot and can be repeated on arrival. In dairy calves, vaccination of the dam may be of benefit by providing passive immunity to the calf. H somni bacterins are available, and there is some evidence they are effective in control of BRD in feedlot calves even when only one dose is given on arrival.

Mycoplasmal Pneumonia

Mycoplasma bovis is an emerging cause of respiratory disease and arthritis in feedlot cattle and in young dairy and veal calves. Experimental infections usually result in inapparent to mild signs of respiratory disease, but virulent strains have been identified that cause severe lung disease in calves. However, this does not preclude a synergistic role for mycoplasmas in conjunction with viruses and bacteria in BRD. Mycoplasmas can be isolated from the respiratory tract of nonpneumonic calves, but the frequency of isolation is greater in those with respiratory tract disease. M bovis has been associated with otitis media in young calves and a syndrome involving chronic pneumonia and polyarthritis in feedlot cattle. These cattle invariably have a pneumonic lesion, and 40%–60% may also develop a polyarthritis and tenosynovitis that causes severe chronic lameness. The condition results in a chronic disease that does not respond to antimicrobial therapy. A significant proportion of these animals are euthanized because of the chronic nature of the disease. Lesions include chronic bronchopneumonia with caseous and coagulative necrosis. In severe cases, >80% of the lung tissue may be involved. Culture of these organisms requires special media and conditions; growth of the organisms may take up to a week. PCR tests are now available that can detect the mycoplasma within hours, thus greatly speeding up diagnosis. Immunohistochemical tests can also be done on fixed tissue that link the mycoplasma antigen directly with the lung lesion. Vaccines are commercially available for M bovis, but their efficacy has not been demonstrated conclusively.

Chlamydial Pneumonia

Chlamydial agents have been implicated in a number of diseases of cattle, including pneumonia. Clinical signs and lesions of bronchopneumonia have been produced by experimental infections. A synergism between Chlamydia and Mannheimia haemolytica has been demonstrated experimentally. Because this pathogen is infrequently tested for, its overall importance remains undetermined. The organism can be tested for by staining sections of lung lesions with Gimenez stain or by fluorescent antibody. Isolation requires inoculation of yolk sacs of embryonating chicks. Chlamydial agents are sensitive to tetracyclines. (See also Chlamydiosis.)