. Clinical Classification of Pneumonias 1n Cattle

R. E. Pierson, D. V. M.; Robert A. Kainer, D. V.M., M.S.

College of Veterinary Medicine and Biomedical Sciences, Colorado State University , Fort Collins, CO 80523.

More beef cattle develop and subsequently die from prominent interlobular septa and a thick pleura that is respiratory diseases than from all other causes. In cattle supplied by branches of the bronchial artery. 3 Each lung is under close confinement respiratory diseases cause 75% of composed of thousands of lobules which contain the the illnesses and 64% of the deaths. 1 Pneumonias constitute terminal parts of the bronchial tree. Within each lobule, 75% of the diagnoses of respiratory diseases. primary bronchioles branch into secondary bronchioles Epizootics of respiratory disease are recognized by cattle which, in turn, branch into terminal bronchioles. The lining owners who request and expect accurate diagnosis, but epithelium becomes lower and the number of ciliated cells veterinarians experience difficulties making definitive and goblet cells fewer in distal progression through these diagnoses because of the similarity of signs in sick cattle and airways. Goblet cells are not present in the simple cuboidal the many viral and bacterial pathogens recovered at epithelium of the terminal bronchioles. Smooth muscle also necropsy. decreases progressively in the bronchiolar walls. Most-of the Since a specific clinical diagnosis may be difficult to make terminal bronchioles branch into alveolar ducts. 3 Rarely, a in the field, the purpose of this paper is to simplify diagnoses terminal bronchiole may continue into a very short by recommending a classification of pneumonias based on respiratory bronchiole. Alveolar ducts receive alveolar sacs pathogenesis where major signs in each pneumonia are and alveoli (Figure 3). different and distinguishable. A complex of blood vessels ramifies throughout the To clarify this classification, each pneumonia will be lobule. The branches of the pulmonary artery break-up into discussed in relationship to etiology, pathogenesis, a thick meshwork of capillaries surrounding the alveolar pathology, and clinical signs. sacs and alveoli (Figure 3). When pasteurellas are the pathogens for pneumonia, their endotoxins can cause Review of Anatomy and Physiology of the Lung thromboses in the capillary plexus and in pulmonary blood and lymphatic vessels resulting in ischemic necrosis of parts To more fully comprehend the pathogenesis of of lobules or many lobules (Figures 2 and 4). pneumonias, a brief review of the anatomy and physiology There are two sets of interconnecting lymphatic vessels in of the bovine· lung is indicated. the abundant connective tissue of the bovine lung-a pleural The lung is situated within the thoracic cavity on an plexus and a deep (peribronchovascular and septal) plexus. oblique angle so that the dorsal border of the lobes slopes dorsocaudad (Figure I). When cattle stand, the trachea slopes caudoventrad from the larynx into the thoracic inlet, then remains level to the bifurcation where the primary bronchi slope dorsocaudad toward the caudal lobes. When exudate is present in the lung, it gravitates into the cranioventral parts of the lung (Figures 2, 13 and 17). Although the trachea bifurcates medial to the middle lobe of the right lung, the first or apical bronchus emerges from the right side of the trachea at the level of the third rib and passes laterad to enter and ventilate the cranial lobe. 2 In exudative pneumonia, therefore, auscultation of the right cranial lobe for abnormal lung sounds is necessary. The basic structural feature of the lung is the lobule Figure I: Black and white drawing of anatomical position (Figure 3) which is clearly defined in the bovine organ by of respiratory system.

NOVEMBER, 1980 73 The most distal branches are the juxta-alveolar lymphatic caused by a sequential interaction of stressors, viruses, and vessels in the connective tissue adjacent to peripheral bacteria. Stressors include weaning, transportation, alveolar walls. Lymphatic vessels do not occur within processing, and exposure to changeable weather. Viral interalveolar septa.4 Lymph drains toward tracheobronchial agents include infectious bovine rhinotracheitis, para­ or caudal mediastinal lymph nodes. Septal lymphatic influenza-3 viruses and possibly others. Pathogenic agents vessels, which carry lymph toward the pleural plexus, are are various Pasteurella spp., Mycoplasma spp., and particularly prominent when dilated with fibrinous exudate Hemophilus spp. as a consequence of bronchial pneumonia (Figure 17). 2. Pathogenesis of Bronchial Pneumonia. Jensen2 and The main function of the lung is the exchange of oxygen others propos.ed the following hypothesis for the and carbon dioxide between air and blood across the pathogenesis of shipping fever: ( I) Chilling of the mucous alveolar-capillary membrane. This delicate membrane has membranes of the head and/ or infections in combination an absorptive surface 25-30 times that of the body surface with viruses cause tissue changes that predispose the and is constantly exposed to irritants and potential nasopharynx to colonization by pasteurellas and the pathogens. Diffusion of oxygen across the air /blood barrier development· of rhinitis. In early inflammation, ciliary is less efficient in the bovine lung than it is in the lungs of action is increased, but later it decreases. (2) Pathogens, most mammals. When pneumonia is developing, the lobule especially pasteurellas and possibly mycoplasmas, transfer is the primary target for injury; consequently, the interface from the nasopharynx to the lungs: (a) by gravitational for transfer of gases between the air and blood can be drainage of infected nasal secretions along the tracheal floor damaged or completely destroyed. If many lobules are into ventral bronchi; and; (b) by inhalation of infective damaged, the animal compensates either by breathing faster droplets. Because of higher ventilation and gravitational and deeper or by increasing the heart rate and force to push settling, both fluids and droplets inoculate the cranial the blood through a damaged alveolar capillary bed. (apical), middle (cardiac), and lower parts of the caudal Prolonged pneumonia leads to hypoxia and right heart (diaphragmatic) lobes and compromise the function of the failure. lobules (Figure 2). (3) Pasteurella spp. and possibly Other functions of the lung are compromised during Mycoplasma spp. colonize the ventral parts of the lungs and inflammation of the organ. Alterations in the regulation of produce pneumonia. ( 4) Pasteurella endotoxin causes body temperature, acid/ base balance, blood pressure (due clotting and thrombosis in lymphatic vessels, capillaries, and to decrease in converting enzyme which catalyzes to veins. The ischemia results in necrosis (Figures 2 and 4). (5) activation of angiotensin I to angiotensin II), the production Necrotic tissue may sequester an abscess (Figure 4). (6) of histamine, prostaglandins E and F, serotonin, Death results from hypoxemia, endotoxemia, pulmonary norepinephrine and bradykinin exert subtle to profound necrosis, shock, and heart failure. systemic changes. 5 3. Pathology of Bronchial Pneumonia. Figure 5 illustrates the sequential pathogenesis of lobular necrosis in Classification of Pneumonias the same section of lung. Figure 4-1 is a transverse section of a middle lobe with beginning bronchial pneumonia, showing Pneumonias can be classified according to: (I) exudate consisting of plasma protein rich in fibrin which has morphology (lobular, lobar); (2) character of exudate gravitated into the ventral respiratory bronchioles and (catarrhal, fibrinous, suppurative); (3) histologic changes alveolar sacs resulting in consolidation of the lobules. (edema, emphysema); (4) etiology (viral, pasteurellas, Lobules are in different stages of pneumonia from aspiration); (5) radiology; and (6) disease (shipping fever, hyperemia (stage I) to red and grey hepatization (stage II and enzootic calf pneumonia). None of these classifications III). Figure 4-2 is a more advanced bronchial pneumonia satisfies all requirements and each may contribute to the with all ventral lobules consolidated. The interlobular confusion. lymphatic vessels are dilatated and contain fibrin clots, a A classification that will aid clinical skills is based on the result of Pq_steurella endotoxins. In Figure 4-3 the route of the entry of the pathogen (pathogenesis) and pneumonia is more advanced with early infarction caused by includes three types of pneumonia: bronchial, interstitial, u thrombus in a large puimonary vein. The resulting necrotic and metastatic. Ninety percent or more of the pneumonias in tissue involves many lobules,- and the affected tissues are cattle fit into this classification. seen as pale brown surrounded by a grey line (leukocytes and In a recent survey into the causes of death of feedlot bacteria). Figure 4-4 demonstrates coagulative necrosis and yearlings, 6 over 83% of the pneumonias were bronchial, 12% early sequestration. Sections 4-5 and 4-6 are more advanced. interstitial, and 4% metastatic. They depict fibrosis of interlobular tissue with connective A. Bronchial Pneumonia. Shipping fever is an example of tissue forming capsules around foci of necrosis and bronchial pneumonia. Although the exact etiology and abscesses. pathogenesis have not been fully established, some facts 4. Clinical Signs of Bronchial Pneumonia. From the about shipping fever are presented below. onset of shipping fever, before pneumonia is present and I. Etiology of Bronchial Pneumonia. Shipping fever is until recovery or death of the animal, depression is a major

74 THE BOVINE PRACTITIONER- No. 15 clinical sign. Depression, characterized by lowered head emphysema, interstitial edema, hyperplasia of alveolar (Figure 5) and ears, separation from the other animals and a epithelium, and hyaline membrane development. The certain reluctance to move, is probably a result of the enlarged, firm, red-purple lungs fail to collapse. Affected Pasteurel/a endotoxins. Other signs include anorexia, lobules and lobes are red-purple rather than the salmon-pink pyrexia, shallow abdominal breathing, and suppressed of normal lobules. The caudal lobes are more commonly cough due to pleuritis. In more advanced. cases, there is affected than other lobes. A small amount of fluid exudes dehydration, dry muzzle, and occasional profuse diarrhea. from the cut surface of the lung, and the bronchial mucous Upon auscultation of the lung, referred bronchial sounds are membranes are congested and sometimes hemorrhagic. heard. Discharge from the nose is minimal. Death results Neither suppuration nor pleuritis occurs (Figure IO). from hypoxemia, endotoxemia, pulmonary necrosis, shock, 3. Pathogenesis of ARDS. Since several specific and heart failure. Complications of bronchial pneumonia syndromes are included in this classification, the include multilobular and even lobar necrosis, abscessation pathogenesis differs. For more details refer to recent of lobules, adhesions, bronchiectasis, cor pulmonale and a publications. 7, 8, 9, 10 permanently unthrifty animal. 4. Clinical Signs of Interstitial Pneumonia (ARDS). B. Interstitial Pneumonia. Interstitial pneumonia is less The term "acute respiratory distress" describes the general common than bronchial pneumonia. It includes several attitude of an animal suffering from interstitial pneumonia. distinct entities, and confusion arises from terminoiogy. In Affected cattle stand with heads extended, nostrils dilated, feedlot cattle intestitial pneumonia has been referred to as mouths open, and tongues protruded. Respirations are atypical intestitial pneumonia and pulmonary accelerated and labored; the pulse is rapid and weak; and the adenomatosis; in pastured cattle as acute pulmonary temperature is normal or slightly elevated. Any exertion emphysema or fog fever; in housed cattle as bovine farmer's may cause death (Figures 8 and 9). lung; and in recently weaned calves as pulmonary C. Metastatic Pneumonia with Hemoptysis. emphysema. Acute respiratory distress syndrome (ARDS) I. Causes. Causes include: phlebitis, endocarditis, and has been recommended as a term inclusive for this group of thrombosis associated with diseases such as metritis and pneumonias. 7 mastritis. In feedlot cattle, caudal vena caval thrombosis I. Etiology. All causes of interstitial pneumonia secondary to the rumenitis-liver abscess complex is the most (ARDS) are not known, but two conjectured causes­ common cause. 11 dietary tryptophan and hyper-sensitivity-are gaining 2. Pathogenesis - Caudal Vena Caval Trombosis acceptance. Recently a bovine respiratory syncytial (BRS) (Figures 11 and 12). Pathogenesis starts with a rumenitis virus has been identified as a possible cause. 5 associated with a sudden change in feed from roughage to Since several distinct entities fit into this classification, concentrate. Fusabaterium necrophorum, a rumen they will be discussed separately under their common names. inhabitant, gains entrance through the portal vein and a. Acute bovine pulmonary emphysema (ABPE), fog showers the liver with abscess-forming bacteria (Figure 11). fever. ABPE occurs principally in adult cattle shortly after a If an abscess develops adjacent to the caudal vena cava or a change from dry to lush pasture in the autumn. The disease is large hepatic vein, vasculitis and, subsequently, a caval caused by the ingestion of grass containing the amino acid, thrombus develop. Septic emboli detach from the thrombus L-tryptophan, which is converted by the ruminal and lodge in and occlude pulmonary vessels, weakening microorganisms to the highly toxic compound, 3-methyl­ their walls and leading to saccular aneurysms. Blood indole3 (Figure 6). pressure ruptures the saccule and opens adjacent bronchi b. Atypical interstitial pneumonia (pulmonary (Figure 16). Extavasated blood dissects the tunica adenomatosis, farmer's lung). This group of syndromes adventitia, forms hematomas, pours into a bronchus, and is performs as an allergic respiratory disease which develops expelled from the larynx. Death is a result of exsanguination after exposure to moldy hay or silage, containing the spores and pulmonary incapacitation. and metabolic products of Mycopolyspori faeni and other 3. Pathology. The erosion of hepatic abscesses into the thermophilic actinomycetes. Feedlot cattle may become caudal vena cava often result in septic' pulmonary sensitized to the fungus ingested from the feed bunks (Figure em bolization. 12 Affected lungs contain regions of 7). Later they become re-exposed to the fungus and then pneumonia and multiple abscesses. Lungs with ruptured develop an allergic reaction. 7 aneurysms are large, firm, and fail to collapse. One or more c. Pulmonary emphysema of recently weaned calves. aneurysms with clotted blood surround the ruptured The etiology of this syndrome may be multiple and complex aneurysm and fill bronchi, bronchioles and alveolar sacs with features similar to bronchopneumonia. 6 One possible with blood (Figure 12 and 16). cause for this is the BRS virus. The cause may also be a 4. Clinical Signs of Metastatic Pneumonia and hypersensitivity reaction due to preconditioning. Hemoptysis. Since signs of metastatic pneumonia may 2. Pathology of Interstitial Pneumonia (ARDS). resemble either bronchial pneumonia or acute respiratory Interstitial pneumonia usually involves both lungs with distress, it may be difficult to diagnose. Sudden elevation of combinations of the following changes: alveolar temperature followed by rapid, shallow breathing may

NOVEMBER, 1980 75 suggest showering of the lung with septic emboli, especially causes combinations of edema, emphysema, hyaline if the history indicates associated metritis, mastitis, or membranes, and hyperplasia of alveolar septal cells, all of similar problems. Hemoptysis (bright foamy blood around which incapacitate the lobule (Figure 15). This reaction is nose and mouth), respiratory distress with head and neck more acute than in bronchial pneumonia, and is extended, groaning on expiration, pale membranes, characterized clinically by acute respiratory distress with generalized weakness, and pulmonary rales over a large area extended head and open mouth breathing (Figure 14). during auscultation are signs suggestive of a ruptured Response to treatment is discouraging. pulmonary aneurysm associated with metastatic pneumonia Metastatic pneumonia, frequent sequel to caudal vena (Figure 12). caval thrombosis, may predispose the lung to pulmonary embolic aneurysms. Rupture of an aneurysm results in Summary hemoptysis and fatal exsanguination. Unless hemoptysis is present, metastatic pneumonia may be difficult to diagnose. Clients expect and whenever possible deserve a diagnosis Treatment, if started early, may prevent the aneurysm. of their animal's disease. However, in cases of respiratory disease, diagnosis may be extremely difficult. If pneumonia References is present, a careful evaluation of the history and major I. Jensen, R., et al.: Diseases of yearling feedlot cattle in Colorado. clinical signs may allow the veterinarian to classify JAVMA 169:497-499, Sept. I, 1976. - 2. Hare, W. C. C.: Ruminant pneumonia into one of three different types: bronchial, respiratory system. In Getty, R. (ed): "Sisson and Grossman's The interstitial, or metastatic. With this classification, the Anatomy of the Domestic Animals". Philadelphia: Saundes, pp 916-936. - diagnosis is specific, the prognosis accurate, and the 3. McLaughlin, R. F., Tyler, W. S., and Canada, R. 0.: A study of the treatment regime likely to succeed. subgross pulmonary anatomy in various mammals. Am J Anat 108: 149- 168, 1969. - 4. Galina, M. A.: Lymph System of the Bovine Lung. Bronchial pneumonia, the most common type, is Dissertation. Colorado State University, Fort Collins, CO, 1977. - frequently a result of viral and bacterial pathogens inhaled 5. Banks, W. J .: Applied Veterinary Histology. In press, 1980. - into the lung where they colonize the mucous membrane and 6. Jensen, R., et al.: Shipping fever pneumonia in yearling feedlot cattle. produce exudate which fills the incapacitated lobules JAVMA 169:500-506, Sept. I, 1976. - 7. Breeze, R. G., et al.: A (Figures 13 and 17). Endotoxins, produced by bacteria such reappraisal of atypical interstitial pneumonia in cattle. The Bov Proc 13:75- 81, Nov. 1978. - 8. Jensen, R., et al. : Atypical interstitial pneumonia in as Pasteurella spp, cause vasculitis and thromboses of yearling feedlot cattle. J AV MA 169:507-5 l 0, Sept. I, 1976. - lymphatic vessels, capillaries and veins resulting in lobular 9. Holzhouer, C. : Pinkengriep. Bovine respiratory syncytial virus as a necrosis and abscesses (Figure 4). Major signs of bronchial cause of atypical interstitial pneumonia in young cattle. - 10. Hibbs, C. pneumonia include depression characterized by lowered M.: Pulmonary emphysema in newly weaned calves . Proc. AABP I Ith head and ears, pyrexia, coughing, and shallow breathing Annual convention, pp. 125-128, Dec. 1978. - 11. Jensen, R., et al.: Ruptured pulmonary aneurysms in yearling feedlot cattle. JAVMA 169:, (Figures 5 and 14). Beginning cases respond to therapy. Sept. I, 1976. - 12. Rebhun, W. C., Rendano, V. T., Dill, S. G., et al.: Interstitial pneumonia is often due to hypersensitivity Caudal vana caval thrombosis in four cattle with acute dyspnea. J AVMA reactions, dietary causes, or viruses. The reaction in the lung 176: 1366-1369, 1980.

(SEE MEDICAL ILLUSTRATIONS NEXT THREE PAGES)

76 THE BOVINE PRACTITIONER- No. 15 List of Illustrations Figure 2: Schematic drawing of lung with consolidation and thrombosis of pulmonary vein. Figure 3: Schematic drawing of normal bovine lobule. Figure 4: Schematic drawing showing pathogenesis of lobular necrosis and lung abscesses. Figure 5: Drawing of calf with "shipping fever" llGINHINGCOHSOLIOAflOM 3 (bronchial pneumonia). ltlO AHO OIIA~ HE•ATllATION Figure 6: Pathogenesis of acute bovine pulmonary emphysema. Figure 7: Causes and pathogenesis of acute respiratory distress syndrome. Figure 8: Calf with acute alveolar emphysema. Figure 9: Cow with acute alveolar emphysema. Figure IO: Lung and section of lung with atypical 4 interstitial pneumonia (Al P) . 6 EAIIIL\'AISCfSS,OflMATIOH Figure I I: Pathogenesis of septic pulmonary embolism. Figure 12: Pathogenesis of hemoptysis. PATHOGENESIS OF BRONCHIAL PNEUMONIA (SHIPPING FEVER) •

NORMAL LUNG

PATHOGENESIS OF_ ACUTE BOVINE • PULMONARY EMPHYSEMA

2. Ingestion of plants containing amino acid ltryptophanl 3 . .Tryptophen converted to a~methyl lndol1t hi rumen ' 4'.° Metao olltes of 3 - MI absorbed Into blood. st_ream

5. Edema - Dyspnea - Interstitial Emphysema • PORTION OF NORMAL PULMONARY LOBULE

NOVEMBER, 1980 77 CAUSES & PATHOGENESIS OF ACUTE RESPIRATORY DISTRESS SYNDROME ATYPICAL INTERSTIAL PNEUMONIA IAIPI

• ► '111>,,,. 1. HYPERSENSITIVITY REACTION a. moldy hay • spores of mlcropolyspora faenl b. preconditioning of calves • 2. VIRUS a . .bovine respiratory syncytlal virus (BRS)

ACUTE ALVEOLAR EMPHYSEMA OF CALVES

PATHOGENES IS OF SE PTIC PUI MCNARY EM BO LISM (METASTATIC PNEUMON IA)

• PATH OGENESIS OF HEMOPTYSIS ACUTE BOVINE PULMONARY EMPHYSEMA

RUPTURED ANEURYSM

0 ~\ i _':~oo- ,.,ouSE CTION OF LUNG •. 11 ...... ,. ..

78 THE BOVINE PRACTITIONER- No. 15 NORMAL BOVINE LUNG BRONCHI AL PNE UMONIA !SH IPPING FEV ER I

BRONCHIAL PNEUMONIA

Figure 13 : Normal bovine lung and bovine lung with bronchial pneumonia. Figure 14: Clinical attitude of bovine with bronchial and interstitial pneumonia. Figure 15: Schematic drawing of lobule with interstitial pneumonia. Figure 16: Schematic drawing of lobule with blood filled alveoli from a ruptured aneurysm. Figure 17: Schematic drawing of lobule showing flooding of alveoli with exudate with bronchial pneumonia.

BRONCHIAL PNEUMONIA DEPRESSION - TOXEMIA

METASTATIC PNEUMONIA WITH RUPTURED PULMONARY ANEURYSM

INTERSTITIAL PNEUMONIA ACUTE RESPIRATORY DISTRESS

METASTATIC PNEU MONIA !with Rupt ured Pulmonary Aneurysm! HEMOPTYSIS

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