| Etiology: |
|
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 cuase 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 (Histophilosis : Introduction). When pulmonary abscessation occurs, generally in association with chronic pneumonia,
Arcanobacterium
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 due to 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 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 following 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 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. Fever (104-106°F [40-41°C]); 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 the formation of pulmonary abscesses. |
Lesions:
|
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
somnus
infection of the lungs results in purulent bronchopneumonia that may be followed by septicemia and infection of multiple organs. Occasionally,
H
somni
is associated with extensive pleuritis. |
|
Pulmonary abscessation can occur as the pneumonia becomes chronic. Abscesses develop in ~3 wk but do not become encapsulated until 4 wk.
Arcanobacterium
pyogenes
is frequently cultured from these abscesses. |
| |
| Diagnosis: |
| Generally, neither serologic testing nor direct bacterial detection are performed, and diagnosis relies on 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 postmortem. If possible, specimens for culture
should be collected from animals that have not been treated with antibiotics to permit determination of antimicrobial sensitivity patterns. |
| |
| Treatment: |
| Early recognition by trained personnel skilled at detecting the early symptoms of disease and treatment with antibiotics are essential for successful therapy. Antibiotics effective against the 3 gram-negative bacteria most often involved in BRD should be selected. Responses to treatment should be monitored and periodic culture and sensitivity should be performed to aid in the selection of antibiotics. Long-acting antibiotics have been specifically developed for treating
bacterial pneumonia in cattle. It is important that antibiotic therapy extend beyond apparent recovery to avoid relapses. Mass medication in feed or water is of limited value because sick animals do not eat or drink enough to achieve inhibitory blood levels of the antibiotic, and many of these oral antibiotics are poorly absorbed in ruminants. NSAID have been shown to be a beneficial ancillary therapy in treating bacterial pneumonia. If pulmonary abscessation has occurred, it is
difficult to achieve resolution with antimicrobials and culling of the animal should be considered. |
| |
| Control: |
| General principles of control are discussed under enzootic pneumonia of calves and shipping fever pneumonia (
Enzootic Pneumonia of Calves and Shipping Fever Pneumonia: Overview). 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. 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 that they are effective in control of BRD. |
| |
