Feedlot Cattle Pneumonias

Symposium on Bovine Respiratory Disease

Feedlot Cattle Pneumonias

Steven E. Wikse, D.V.M.*

Pneumonia has been called the megamalady of feedlot cattle, causing economic losses greater than all other feedlot diseases combined. 29 An Alberta feedlot disease survey involving 249,144 received cattle revealed respiratory diseases, including shipping fever and infectious bovine rhinotracheitis, to be responsible for approximately two thirds of the sickness and death. 11 In California25 (Table 1) and Colorado32 studies, each involving approximately 2000 necropsies of feedlot cattle, pneumonia was responsible for nearly one half of the deaths. Mortality losses are highly visible, but they are far exceeded by the financial costs of treatment, reduced daily weight gains, and reduced slaughter value of poor responders. 22 Feedlot pneumonia is such a great problem because of man's manipulation, through management practices, of a complex interaction between cattle, their environment, and ubiquitous infectious agents. Veterinarians have two major responsibilities concerning feedlot cattle pneumonias: (1) prevention, by client education and encouragement of prophylactic measures; and (2) accurate diagnosis and treatment of individual cases and control of outbreaks. To successfully accomplish these tasks, it is necessary to possess a working knowledge of the etiology, epidemiology, clinical signs, and gross pathology of feedlot cattle pneumonias. That information is presented in this article. Bovine pneumonias have been named and classified on many different criteria such as anatomy (lobar), exudate (fibrinous), etiology (viral), histopathology (interstitial), and clinical description (shipping fever). 35 These multiple names for what is often the same condition are sometimes confusing. The following discussion is based on a simplified arrangement, somewhat similar to a previously recommended classification, 48 that organizes the pneumonias into categories separated by differing epidemiologic factors, etiologies, clinical signs, and lesions (Table 2). This approach helps a clinician to make immediate, useful recommendations based on evaluation of field epidemiologic, clinical, and pathologic findings. *Diplomate, American College of Veterinary Pathologists; Associate Professor, Field Disease Investigation Unit, Department ofVeterinary Clinical Medicine and Surgery, Washington State University College of Veterinary Medicine, Pullman, Washington

Veterinary Clinics of North America: Food Animal Practice-Vol. 1, No. 2, July 1985

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290 Table 1.

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Relative Frequency of Various Fatal Respiratory Diseases of Feedlot Cattle NUMBER OF DEATHS

DISEASES

PROPORTION OF TOTAL DEATHS* FROM ALL CAUSES

MORTALITY RATEt

(%)

(%)

Broncho pneumon ia and fibrinous pneumon ia Atypical interstiti al pneumo nia Fibrinou s pleuritis and pleuropn eumonia Infectiou s bovine rhinotrac heitis Necrotic laryngiti s Hemopty sis Pulmona ry abscessa tion Larynge al edema Metastat ic pneumo nia Vermino us pneumon ia Tracheit is (nonspecific) Pulmona ry venous thrombo sis

681 177 55 51 8 4 3 3 3 1 1 1

31.5 8.2 2.5 2.4 0.4 0.2 0.1 0.1 0.1

0.57 0.15 0.05 0.04 0.01

Totals

988

45.7

0.82

Table reproduc ed with the permissi on of Dr. C. A. Hjerpe. which necropsi es were *A total of 2163 deaths was utilized, which excluded 345 deaths in . obtained not were s diagnose not perform ed and clinical January 22, 1972 tin 120,054 cattle (97,482 yearlings and 22,572 calves) received between and Decemb er 31, 1977, 110,430 of which were closed out.

SHIPP ING FEVER Shippi ng fever, an acute febrile respira tory infectio n of recentl y arrived host defeedlot cattle, is caused by a comple x interac tion of compro mised e serotyp ytica haemol ella fenses, bacteri a, viruses , and mycoplasmas. Pasteur m organis the is asmas, mycopl and/or 1, alone or in combin ation with viruses most frequen tly recove red from animals with this problem . Etiolog ic Organi sms effects The multifa ctorial pathog enesis ofbovi ne pneum onia involves the stresson asmas, mycopl and/or viruses of bacteri a, often in conjun ction with so ally potenti are that ms organis The s. defense tory compro mised respira not do and tion damagi ng are nearly ubiquit ous in the healthy cattle popula elmed by produc e pneum onia unless the pulmon ary defense s are overwh ession. osuppr immun nduced stress-i and/or multip le pathog en infections agents us infectio the on s review recent nt excelle There have been several 17 18 •41 •51 •63 • . disease tory respira bovine with ted associa um isolated Pasteurella haemolytica type lA is the most commo n bacteri 2 holds the and a Americ North in disease tory from cases of bovine respira ida multoc ella Pasteur onia. pneum cattle of enesis pathog the central role in less a with ted associa is also involve d but is less frequen tly isolated and is inhabfulmin ating pneum onia. These two organis ms are consid ered normal 63 cattle. healthy of lung, the not but , mucosa al itants of the nasoph arynge carry and Calves probab ly becom e infecte d with Pasteurella at an early age of nasal swabs them as a minor part of the nasal flora. Only a low percen tage 38 but if the heads calves, sed unstres are positiv e for P. haemolytica in healthy

PATHOLOGY

Ventral dark-red lung consolidation. Thorax may contain straw-colored effusion and fibrin, especially with P. haemolytica. Dark, dry lobules of coagulation necrosis with P. haemolytica. Lungs diffusely red-tan, enlarged, and do not collapse. All lobes are rubbery, wet, and heavy. Emphysema mainly in diaphragmatic lobes. White froth in trachea. Reddened nasal and tracheal mucosa with ulcers covered by exudate or neerotic debris. Larynx and trachea sometimes partially occluded. Occasionally, inflammation extends to bronchioles. Thick sheets of yellow fibrin over visceral and parietal pleura. Thorax contains fibrin and strawcolored fluid. Ventral lungs are pinkish-tan and firm. Lungs contain pulmonary artery aneurysms, pneumonia, and abscesses. Blood clots in airways and rumen. Liver has abscess near vena cava, which contains thrombus.

CLINICAL SIGNS

Initially, depression, an orexia and fever due to toxemia. Dyspnea absent in early cases. Later, dyspnea, cough, and mucopurulent ocular and nasal discharges. Sudden deaths. Sudden onset rapid respirations and severe expiratory dyspnea. Head extended, open-mouthed breathing. Fever.

Variable; mild rhinitis to rhinotracheitis with pneumonia. Severe cases are depressed, febrile, and cough. Mucopurulent nasal discharge and necrosis of muzzle and nasal mucosa. Sudden-onset expiratory dyspnea, high fever, and severe depression. Most cases die in 2 days or less.

Initially, signs of pneumonia. Later when aneurysm ruptures, severe respiratory distress and discharge of bright, foamy blood from nose and mouth.

Very common. Occurs 7 to 14 days after stress. Predisposing factors of long hauls, auction yards, mixing calves, crowding, surgeries and corn silage. Morbidity is 3 to 25%; mortality is 20%. Low incidence; sporadic. Equal frequency during all stages of fattening. Sometimes greater frequency in summer and fall. Mortality is high. Low incidence if cattle are vaccinated. Predisposing factors similar to shipping fever. Stress can activate latent IBR virus. Mortality is low.

Uncommon. Predisposing factors similar to shipping fever. Sometimes occurs concurrently with TEME cases. Mortality nearly 100%. Uncommon. Incidence varies with control of rumenitis-hepatic abscesses. Occurs at all stages fattening, but is more common during first 45 days. Mortality 100%.

Stress, combined with P. haemolytica, P. multocida, or H. somnus, +1- viruses or mycoplasmas, especially IBR, PI-3, BVD, or BRS viruses.

Suspected causes include bronchopneumonia sequelae, diet toxins, or hypersensitivity to antigens in feed or dust.

Stress, combined with bovine herpesvirus type I (IBR virus).

Stress, combined with H. somnus, alone, or with P. haemolytica or P. multocida.

Acid rumenitis results in liver abscess that causes caudal vena cava thrombus. Septic emboli from throm;.. bus inflame and weakened pulmonary arteries, resulting in aneurysms.

DISEASE

Shipping fever

Acute respiratory distress syndrome (atypical interstitial pneumonia)

Infectious bovine rhinotracheitis (IBR)

Fibrous pleuritis and pleuropneumonia (FPPP)

Caudal vena caval thrombosis

Pneumonias ofFeedlot Cattle

EPIDEMIOLOGY

Table 2.

ETIOLOGY

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culture d in are split at necrop sy and several areas of the nasal mucosa are that had animals from ytica haemol P. isolate to e detail, it is often possibl 46 does not ntly appare n infectio l mucosa Such swabs. nasal on e been negativ by caused n infectio lung provok e circula ting antibod ies protect ive against defense the of own breakd a causes P. haemolytica. Stress of transpo rtation g in a mechan isms that hold the nasal mucosa l infections in check, resultin 19 38 ,59 Greate r numbe rs of calves then , ytica. haemol P. of rapid prolife ration the numyield positiv e nasal mucosa l swabs and there is a large increas e in ns can infectio Viral cases. e bers of P. haemolytica on the mucosa of positiv haeP. s. defense tract tory respira on have the same effect as transpo rtation the in strated demon been has nuclei, droplet in molytica, probab ly carried 21 Some . mucosa nasal their on m organis the ing harbor calves trachea l air of normal ly of these inhaled organis ms are deposi ted deep within the lung and ary 36 pulmon ed impair of ons are cleared within hours. But under conditi is ytica haemol P. n, infectio viral sting defense s due to stress and/or pre-exi toxins, its of aid the with and lung the within able to prolife rate rapidly onia. 35 The produc e a severe, explosively spreadi ng fibrino us bronch opneum ne pneuofbovi on key positio n that Pasteurella organis ms hold in the causati where ia, Austral is on conditi this monia is suppor ted by the near absenc e of dislong calves rting transpo as such es, many stressfu l husban dry practic ted associa agents viral the of many and States United tances, are similar to the P. lly especia ms, organis ella Pasteur but read, widesp are with pneum onias 27 haemolytica, are not commo nly isolated from their cattle. onic Other bacteri a that have been less frequen tly isolated from pneum loStaphy cocci, Strepto sp. ella Salmon , lungs include Hemop hilus somnus 25 . 62 togenes monocy Listeria and sp. ia Neisser coli, coccus au reus, Escherichia melani Coryne bacteri um pyogenes is frequen tly isolated with Bacteroides been has togenes nogenicus from chronic lesions and abscesses. L. monocy sted by identif ied as the cause of a system ic feedlot cattle infectio n manife tory respira and e, digestiv , system s various combin ations of central nervou 62 lesions. Hemophilus somnus, a membe r of the nasal flora of some healthy cattle, pneum onia is being isolated with increas ing frequen cy from cases of bovine 9 24 hilus Hemop , on. conditi this of and is emergi ng as an import ant cause puventral a in g resultin tract, tory respira infectio ns usually begin in the 1 that is followe d in some cases by septice mia and a onia rulent bronch opneum le from 9 infectio n of multip le organs. The lung lesions can be indistin guishab with ted associa is those of Pasteurella sp.; howeve r, occasionally H. somnus is pleurit us fibrino termed been a very extensi ve fibrinous pleurit is that has 25 and pleurop neumo nia. pathoMycoplasmas were isolated , usually in combin ation with other . 26, 34 studies two in onias pneum cattle feedlot of cent per 50 over gens, from conly general are a The species of Mycoplasma prevale nt in North Americ ical infecsidered to be mild respira tory pathog ens, causing mainly subclin by other ns infectio and/or s stresse mental tions, unless couple d with environ 55 asmas mycopl of ce presen nt freque The . viruses or a, mycopl asmas, bacteri esosuppr immun of effects known their with ed combin lungs, in pneum onic in ism mechan rt sion in calves 3 and inhibit ion of the mucoci liary transpo

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man, 28 suggests that they may play an important contributory role in the pathogenesis of bovine pneumonia. Chlamydia} agents are occasionally isolated from pneumonic bovine lungs. These organisms are thought to only produce mild respiratory infections by themselves, but they may enhance the pathogenicity of other organisms concurrently infecting the respiratory tract. Experimental pulmonary infection of calves with a combination of chlamydia and P. haemolytica resulted in clinical disease more severe than either agent usually produced alone. 44 Many viruses have been isolated from cases of bovine pneumonia. Those present in North America include infectious bovine rhidotracheitis (IBR), malignant catarrhal fever, bovine herpesvirus type 4, adenovirus, parainfluenza-3 (PI-3), bovine respiratory syncytial virus (BRSV), bovine virus diarrhea (BVD), reovirus, rhinovirus, and enterovirus. 41 IBR virus, malignant catarrhal fever virus, bovine herpesvirus type 4, BVD virus, and BRSV are capable of causing severe primary disease. Although many of the viruses cause only mild to moderate lesions on their own (at least in experimental infections), their main significance may be impairment of the respiratory tract's resistance to the potentially more severe damage of bacterial infection. Because viruses are less stable than bacteria in cadavers and isolation of certain viruses requires special laboratory techniques, viral culture is often unsuccessful in animals with severe or fatal lung disease, so it is felt that viruses may be the initiators, but not the sole cause, of a high percentage of fatal bovine pneumonias. In experimental IBRIP. haemolytica pneumonia, calves that die early have evidence of viral tracheobronchiolitis, but calves that die later have little evidence of viral infection and IBR virus often is not isolated from their lungs. 2 Thus, even though IBR virus was isolated from only 18 per cent of the lungs in one study of feedlot pneumonias, 34 it may have been the initiator of a much higher proportion of the cases. There are several viruses that have joined the ubiquitous old standbys, IBR and PI-3 viruses, as important bovine pneumonia agents. BVD virus is frequently isolated from severe, nonresponsive pneumonia outbreaks8 and is considered to be a "respiratory virus. "51 BRSV has emerged in recent years as a cause of severe pneumonia in recently weaned beef calves. 20 Rhinoviruses are ubiquitous in the cattle population and usually associated with mild upper respiratory tract inflammation. However, some researchers feel that they are important contributors to bovine respiratory disease, because in some cases they are the only viruses demonstrable in calves with pneumonia. 51 This idea has merit, especially when consideration is made of the possible interactions between rhinoviruses, nasal mucosal defenses, and P. haemolytica. Epidemiology Shipping fever of feedlot cattle occurs during all seasons but has a much higher incidence in the fall and winter, especially following inclement weather. The disease usually strikes soon after the arrival of cattle in the feedlot, commonly betweens days 7 and 14. A Colorado study found that 72 per cent of shipping fever pneumonias occurred during days 1 to 45, with the remaining cases tapering off until fattening was completed. 34

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involves The nature of the North Ameri can beef cattle indust ry, which in a groups large in ng fatteni origin ation of calves in small groups and their aks. outbre onia pneum for ble favora ions distan t area, has resulte d in condit ine how manPredis posing factors have been studie d in an effort to determ Count y Bruce The ageme nt can be chang ed to reduce this costly proble m. ity of mortal and dity morbi Beef Projec t has identif ied factors influen cing o Ontari to a Canad n wester from d shippe recent ly weane d spring calves 39 Pneum onias were the most years. sive succes three of feedlo ts over a period of the deaths comm on cause of mortal ity, accoun ting for over 50 per cent each year. of mixing of Morbi dity and mortal ity increa sed with a greate r amoun t widely from bled assem were calves when and s source nt calves from differe r greate with filled were separa ted geogra phic locations. Feedlo t pens that 25 demr anothe and study This ity. than 142 calves suffere d higher mortal to the feedlo t onstra ted that calves shippe d directl y from the ranch of origin perfor med better than calves purcha sed from saleyards. s proces sing Bruce Count y Beef Projec t data on the effects of variou in mortal ity se increa small a ed reveal t proced ures upon arrival at the feedlo s on arrival viruse tory respira t agains ated vaccin been in calf groups that had comm on most The at the feedlo t, especi ally when such calves were fed silage. al proSurgic t. produc I-3 vaccin e used was an intram uscula r IBR or IBR/P ed elevat with ated associ were calves d cedure s perfor med on newly arrive 15 of use lactic Prophy trial. Texas a and study y Count mortal ity in the Bruce dity morbi sed increa antimi crobia ls in the drinki ng water was associated with reduce d morand mortal ity, but antimi crobia ls in starter rations may have water was the in ls crobia antimi of effect l bidity. It was felt that the harmfu , rather source water ted restric to due ption consum caused by decrea sed in a placed often are than by their presen ce in the water. Antim icrobia ls Other off. shut s source l norma single water tank in one area of the pen and cent or better resear chers have observ ed morbi dity reduct ions of 50 per 1 or parent eral feed the in tics antibio lactic prophy of use following 30-day . 37 arrival on calves admin istratio n of slow-r elease antimi crobia ls to all of calves The Bruce Count y Beef Projec t's analysis of ration manag ement during silage corn g feedin from effect ental detrim demon strated a very strong hay for dry d temme long-s fed were calves All ng. fatteni of the first month silage as a major the first 2 days after arrival. Calves that consu med corn five times the had t feedlo the in week portio n of their diet during the first amoun ts major ingest to week fourth the until waited mortal ity of calves that some reduce to of corn silage. Feedin g grain along with the silage appea red nitrootein nonpr of ion Inclus of the negati ve effects of silage consum ption. death losses. gen source s in the receiv ing diet was also associ ated with higher grass hay fed were 7 calves d arrive newly when that ed Anoth er report3 reveal accoman was there only, morbi dity and mortal ity were reduce d; howev er, chers resear Texas calves. y health panyin g decrea se in weigh t gains in the arrival on e glucos blood low with ls anima that studyi ng shippi ng fever found ing 7 to 10 days had a greate r chance of develo ping severe illness requir and mortal ity dity treatm ent. 12 They later demon strated that feedlo t morbi diet instea d trate concen cent per 55 were less in calves that had been fed a feedlot. the to ort transp to prior yard n auctio of good-q uality hay at the

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In summary, the many potentially helpful epidemiologic findings that have been recently reported should be carefully evaluated, and we should encourage our clients to minimize predisposing factors. Improved husbandry methods may be the most effective means to prevent feedlot cattle pneumonias, because the occurrence of disease is determined mainly by environmental and host factors, rather than by the presence of the infectious agents of pneumonia, which are ubiquitous in the cattle population. Vaccines, except for IBR, have had limited success. Nasal mucosal studies demonstrating that transportation of calves results in proliferation and shedding of the infectious agents of pneumonia indicate that preventative medicine measures initiated at feedlot arrival are a step or two late in the beef production cycle. Clinical Signs Shipping fever pneumonia cases usually begin 7 to 14 days after cattle arrive in the feedlot. The manager often notices initially that fewer cattle come up to be fed, the pen's feed consumption declines, and some animals appear gaunt. The onset of an outbreak is occasionally signaled by the sudden deaths of one or two animals that had not been noticed to be ill. The earliest clinical sign is depression, characterized by separation from the group, lowered head and ears, droopy eyelids, and a reluctance to move. A human observer is often viewed out of the "corner" of the eye, as if it were painful to move the head for direct viewing. 25 Rectal temperatures of affected cattle are elevated from slightly above normal to 108° F. In these early stages, there is no dyspnea; however, respirations sometimes are shallow and rapid, especially in animals with high fevers, and auscultation will reveal an increase in vesicular sounds and bronchial tones over ventral areas of the lungs. 4 There is a serous nasal discharge at this time. Animals with fully developed clinical signs exhibit a mucopurulent conjunctivitis and nasal discharge. Depression is profound and expiratory dyspnea, sometimes with a grunt, is accompaned by head-extended, openmouthed breathing. Auscultation of ventral lung fields at this time reveals decreased vesicular sounds, loud bronchial tones indicating lung consolidation, and coarse rales. 49 Cases with pleuritis may exhibit "sandpapery" pleural friction rubs or an absence of ventral lung sounds due to effusions. Some animals develop mucoid diarrhea, purulent otitis, or tonic-clonic convulsions. 29 The duration of illness in treated individual animals is usually short, with recovery occurring in 3 to 7 days. 29 However, cases that are not treated early may have a prolonged course, tend to relapse after antibiotics are stopped, and never do well. The duration of a pneumonia outbreak with its resultant morbidity and mortality is dependent on the condition of the cattle and whether or not they are mass-medicated. 25 Well-nourished, vigorous cattle originating from one ranch and maintained as a single group in the feedlot may experience a pneumonia outbreak of very low morbidity and only several days in duration. At the other extreme, groups of very young, unthrifty cattle assembled from a variety of sources, moved through a saleyard, hauled a long distance, and co-mingled in the feedlot may undergo what is known as a "wreck," which is a prolonged pneumonia outbreak that

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cent morb idity and high lasts a mont h or longe r and has great er than 50 per yearli ngs is abou t 3 to 4 per mortality. The avera ge popul ation morb idity for lation morb idity for calves popu the cent, with a case morta lity of 20 per cent; 29 cent. per 20 of lity is abou t 25%, with a case morta

Patho logy

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logically as a fibrinous Shipp ing fever pneu moni a is chara cteriz ed patho s in the bronc hiole s begin it ; enous aerog is ion bronc hopen umon ia. The infect g paren chym a. The varand exten ds throu gh their walls into the surro undin pneum onia, begin s in lobar or iation of this pneum onia, terme d fibrinous or more virule nt host nt esista less-r a the same mann er, but becau se of short -lasti ng and is phase is hiolit bronc the a), bacte ria (usually P. haemolytic on of entire lung lidati conso the swift sprea d of inflam matio n result s in rapid lobes . 35 ed lungs are swollen, The ventr al areas of the usually bilate rally affect a often have a great er red, firm, and heavy. Cases cause d by P. haemolytic amou nts of yellow Large area of conso lidati on than those due toP. multocida. a straw -colo red by d panie accom be fibrin may overl y affect ed areas and may howe ver, only ly, usual lA); (Fig. a olytic haem effusion in cases cause d by P. (Fig. 2). 53 cida by P. multo a light film of fibrin is prese nt in cases cause d ble amou nt of emph ysem a The cauda l lung lobes some times conta in a varia hiole s conta in small to bronc and hi secon dary to force d respir ation s. Bronc h nodes are wet, dark lymp hial Bronc te. exuda large quant ities of purul ent tissue is usually invol ved red, and swollen. Some 60 to 80 per cent of the lung Howe ver, when other onia. in fatal cases of uncom plica ted bacte rial pneum nitis, or traum atic rume tic myco is, disea ses such as IBR, BVD , salmonellos the lung may be of cent per 50 to 30 only y, phary ngitis occur concu rrentl affected. 25 by carefu l gross exInfor matio n conce rning etiolo gy can be obtai ned lack dry areas of Red-b . lungs c moni pneu amin ation of sectio ned portio ns of cteris tic of P. haemolytica coagu lation necro sis resem bling infarcts are chara virus can be ident ified by infections. 50 The necro tizing bronc hiolit is of IBR 58 hial tree on cut sectio n. bronc pale to white foci that repre sent the termi nal 25 Cut by Hjerp e. Aging of lesions has been descr ibed in excel lent detail due to a mixtu re rance appea bled" "mar a have often sectio ns of affect ed lungs progr essin g Cases n. izatio of lobul es in vario us stage s of red or grey hepat 3 days, than less is e cours al clinic rapid ly to a lobar pneum onia, in which the es becom a chym paren The 18). (Fig. e surfac ar have a reddi sh black cut lobul yellow sh reddi and red to reddi sh black to red at 3 to 5 days of illness days of illness, the lobul ar 14 to 7 After s. illnes of days 7 and 5 betw een than 7 to 10 days usually r longe for surface is yellow. Cattl e that survi ve seen in cattle that die of be may s lesion ced recov er; howe ver, more advan clinical signs, most affected other causes. By 14 to 30 days after the onset of sation or abscessation. By lobul es are necro tic and may be devel oping inspis the lung may be adhe rent and nt prese be 30 to 60 days, matu re absce sses may a inclu de septic emia, moni pneu ous fibrin of ons to the chest wall. Comp licati infarcts. 25 renal and empy ema of the thorax, peric arditi s, perito nitis, clinical cours e is less In fatal cases of bronc hopn eumo nia, in which the Betw een 7 and 14 n. brow sh reddi is es than 7 days, the cut surface of lobul

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Figure 1. A, Fibrinous pleuritis and lobar pneumonia caused by P. haemolytica. Fulminating case, with consolidation of almost entire lung, abundant fibrin overlying apical lobe, and copious effusion. Right lateral view. B, Cut section of diaphragmatic lobe of lung in part A. Affected lobules are diffusely reddish-black.

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toP. multocida. Ventra l consolidation with Figure 2. Fibrin ous bronc hopne umon ia due view. lateral a few small fibrin tags on the pleura . Right

mato ry cells give the lung days, small whit e foci of perib ronch iolar inflam of illness, the white foci days 21 to 14 surface a speck led appe aranc e. After eter) and are pack ed closely reach maxi mum numb ers and size (2 mm in diam color. Thick ribbo ns of yello w toget her, givin g the lobul es a yello w to white hiole s (Fig. 3). Betw een bronc exud ate may be expre ssed from cut ends of in inspi ssate d exud ate conta es lobul 21 and 30 days, the yello w to white

Figure 3. Cut sectio n of a chroni c bronon. chopn eumon ia case of 2 to 3 weeks durati Thick exuda te exude s from the cut ends of bronchioles.

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within areas of necrosis and early abscess formation. After 30 to 60 days of illness, mature abscesses and thick-walled, dilated bronchioles may be present. At this stage, there may be fibrous adhesions between lung lobes or between the pleura and the chest wall. A knobby appearance of the apical and cardiac lobes due to bronchiectasis may be a sequel to bronchopneumonia in a small percentage of cases. 31 Other possible complications include empyema of the thorax secondary to rupture of a lung abscess, metastatic abscessation to other organs, 35 and renal infarcts. 25 Healing is usually complete in either type of pneumonia by 90 days after the onset of illness, except when there is extensive abscessation or chronic bronchiolitis. Residual lung damage occurs in most cases, because in-situ organization of exudate with production of much fibroblastic tissue results in shrunken, fibrotic tissue in severely affected areas. 35 ACUTE RESPIRATORY DISTRESS SYNDROME Acute respiratory distress syndrome (ARDS), also called atypical interstitial pneumonia, of feedlot cattle is a sporadic condition characterized by sudden onset of severe expiratory dyspnea, refractoriness to treatment, and a short, often fatal, course. 29 The main pathologic features are noncollapsible, firm lungs containing edema and emphysema. The term acute respiratory distress syndrome has been suggested by Breeze and colleagues7 to describe any sudden onset of dyspnea that is the result of any combination of pulmonary congestion and edema, hyaline membrane formation, alveolar epithelial hyperplasia, and interstitial edema--other specific causes of respiratory distress, such as parasitic bronchitis, having been excluded. This definition accurately describes the main clinicopathologic features shared by a group of respiratory syndromes of multiple etiologies and has been utilized by others in a clinically useful classification of bovine pneumonias. 48 Etiology The cause(s) of ARDS of feedlot cattle is not known. There are several known causes of ARDS in pastured cattle, such as tryptophan-rich forages, 6 rape, kale, or turnip tops, 4 and fields infested with the weed Perilla frutescens (purple mint). 61 ARDS of feedlot cattle has several features that do not fit the tryptophan-3-methyl indole pathogenesis of acute bovine pulmonary emphysema (ABPE), a well-defined ARDS of adult cattle moved to lush pasture. There are major epidemiologic differences between the two conditions: ABPE occurs in outbreaks and affects multiple animals shortly after dietary change, but ARDS of feedlot cattle is sporadic and unrelated to diet. 25 Although monesin supplementation has been reported to reduce the occurrence of ABPE, 6 it has no effect on the morbidity and mortality of ARDS of feedlot cattle. 25 Another inconsistency is that although the Hereford breed of cattle has been observed to be the most commonly affected breed in field ABPE outbreaks6 and has been shown to be the most susceptible of several breeds to experimental administration of tryptophan, 42 there is no breed predilection in feedlot ARDS. 25•29 BRSV infection is another known cause of respiratory distress and em-

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logic patter ns differ physe ma. 20 Howe ver, its know n epidem iologi c and patho cattle. t feedlo of from those of ARDS of cattle either Fungi growi ng in feeds have been shown to cause ARDS a, such as edem nary pulmo e induc direct ly by elabo ration of chemi cals that 47 initiat ion the by ps perha or es, potato sweet of Fusar ium solani infest ation ora polysp Micro ed with of a hyper sensit ivity reacti on, as in hay conta minat a as e diseas lung oping faeni. 60 Howe ver, the vast major ity of cattle devel l typica show they ; ARDS an op devel result of expos ure toM. faeni do not ent differ quite is which e, diseas lung r's farme of s clinica l signs and lung lesion Adult Cattle "). Group from ARDS (see the article "Resp irator y Disea se in occur red in these have , ARDS outbre aks, rather than sporad ic cases of nism may be a mecha ivity sensit hyper a funga l-relat ed instan ces. Howe ver, the Color ado in cases of ity major the se becau , signif icant cause of ARDS on hisbased ry, catego study fit a hyper sensit ivity, rather than a dietar y, ver howe view, 30 this to ribe subsc e topath ologic classification; not all peopl "). Cattle Adult in se Disea (see the article "Resp irator y hopne umon ia in ARDS has been found to occur as a seque l to bronc 25 and dairy calves in Canad a. 14 Califo rnia feedlo t cattle

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Epide miolo gy d in incide nce ARDS of feedlo t cattle is a major cause of death , secon ing fever, shipp to st contra only to shipp ing fever pneum onia (see Table I). In ution distrib even fairly a with time, a at l ARDS usuall y affects only one anima 30 are ages and sexes, s, breed All . period g feedin of cases at all stages of the of years 3 to 1 cattle equal ly susce ptible , but the incide nce is greate st in nce incide an with ation, age. A Color ado surve y revea led a season al fluctu ly owing to the highe r that nearly doubl ed in the summ er and fall, possib s. 30 In anoth er study , season those g durin dust re amou nts of soil and manu r, a season al incide nce in which the incide nce of ARDS was slight ly greate minim al pen dust. 25 with floors was not noted in cattle maint ained on slatte d had chron ic inacti ve In that situat ion, over 99 per cent of affect ed cattle additi on to diffuse in lobes lung l crania in ia umon lesion s of bronc hopne . It was also noted lesion s of edem a and emph ysema associ ated with ARDS frequ ent in fatal more icantly signif that lesion s of bacter ial pneum onia were ng cattle dying yearli Also, psied. necro cattle ARDS cases than in all other usly treate d previo been have to likely more icantly signif from ARDS were feedlo t. the in cattle ng for bacter ial pneum onia than the remai ning yearli Clinical Signs dyspn ea accom There is a sudde n onset of tachy pnea and expira tory with heads stand ls anima ted panie d by a grunt and abdom inal lift. Affec If there ding. protru es tongu and open, s exten ded, nostri ls dilate d, mouth and an mouth the at ng frothi be may There it. is a breez e, they may face . ysema emph us occasi onal cough . Some cases have dorsal subcu taneo g from 101.8° Affec ted cattle have a variab le rectal tempe rature rangin time of initial the at cases 53 in rature tempe to 107.3° F; howev er, the mean dull areas and s 25 sound ed referr s reveal ltation Auscu F. treatm ent was 104. 8° throu ghout all lobes. days with a mean The clinica l cours e in fatal cases range s from 1 to 42

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Figure 4. Acute respiratory distress syndrome. Swollen, emphysematous diaphragmatic lobe and heavy, edematous tan anterior lobes. Right lateral view.

survival time of 5.2 days. Around 15 per cent of the cases are found dead in the fattening pen. 25 Pathology The lungs are reddish-tan, enlarged, and do not collapse (Fig. 4). This is especially noticeable in the diaphragmatic lobes, which have rounded borders and sometimes bear the indentations of overlying ribs. A mosaic pattern of multiple small air bubbles may be seen through the transparent pleura of the diaphragmatic lobes due to emphysema of the subpleural and interlobular lymphatics. Large gas bullae are sometimes present. The cranial lung lobes are firm or rubbery and contain mainly fluid and little emphysema. The lungs are very heavy, weighing up to two or three times normal values. The trachea and bronchi are often filled with white froth. Upon sectioning, the wet, glistening, firm lung lobules have a glass-like appearance and are separated by widened interlobular lymphatics filled with edema and gas bubbles (Fig. 5). Edema and emphysema are not apparent on gross examination in approximately 20 to 25 per cent of cases. 25 The main lesion in these cases is diffuse alveolar epithelial hyperplasia.

INFECTIOUS BOVINE RHINOTRACHEITIS Infectious bovine rhinotracheitis (IBR) is a contagious upper respiratory tract disease caused by the effects of stress plus a herpesvirus and is characterized by depression, rapid respirations, coughing, and mucopurulent nasal discharge.

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Figure 5. Glistening , wet surface of cross section of diaphragm atic lobe of lung in Figure 4. Interlobu lar lymphatic s distended with edema and gas bubbles.

•, I 'I I•

Etiologi c Organis m IBR is caused by stress combin ed with bovine herpesv irus type 1 (IBR 41 virus), which is capable of causing several other disease syndrom es of cattle. In feedlot cattle, this virus causes IBR, follicular conjunc29tivitis, and participates in the pathoge nesis of shippin g fever pneumo nia. Epidem iology IBR occcurs in all breeds of cattle of any sex and age but has its highest n inciden ce in animals 6 months to 3 years of age. In feedlots, the conditio and spring during than winter and fall during occurs with greater frequen cy summer . Occurre nce of IBR in feedlot cattle is greatly reduced by intramuscula r adminis tration of modifie d live IBR vaccine within 24 hours after per arrival. In this situatio n a mortalit y rate from IBR no greater than 0.02 . effective 25 cent per 100 not is tion vaccina course, cent can be anticipa ted. Of cent per 5 0. about in develop IBR of cases sporadic that One source states 29 of vaccina ted cattle on feed 70 to 80 days. In another report, IBR virus e, was isolated from nasal swabs of feedlot cattle with a mild rhinitis syndrom modia with sly previou days 21 over ted vaccina even though they had been fied live IBR virus. 10 Acute outbrea ks of IBR develop when cattle are crowde d togethe r, especial ly after shipping . IBR virus is capable of existing in clinically normal al cattle in a latent form. It is thought to reside quiesce ntly in the trigemin 54 Stressor s such as transpo rt, ganglia. sensory cral lumbosa the or ganglia are adverse weather , crowdin g, or exogeno us corticos teroid adminis tration 43 subthese from spread is disease The g. capable of initiatin g viral sheddin clinical shedder s or clinically affected cattle by coughin g of virus-la den nasal

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secretions onto susceptible animals or by dropping nasal, oral, and ocular discharges containing virus into the feed and water of susceptible penmates. Clinical Signs There is a great variation in the severity of clinical signs of IBR; signs may range from mild rhinitis to severe fatal rhinotracheitis with secondary bronchopneumonia. Variation is mainly dependent on host susceptibility and environmental factors. The severe form can be devastating to feedlot cattle. Affected animals become very depressed, inappetent, and rapidly lose weight. They develop a nasal discharge that is at first clear but later becomes mucopurulent or sanguineous. Some cases develop muzzle and nasal mucosal lesions of hyperemia and ulceration covered by mucopurulent exudate or necrotic debris. Drooling of frothy or ropy saliva is often seen. The respiratory rate is elevated, and there is a frequent cough that varies from moist to sharp and explosive. 63 Auscultation reveals increased vesicular sounds and loud referred tracheal sounds or, in cases with secondary bacterial infection, rales due to pneumonia. Some cases develop profuse epiphora due to a follicular conjunctivitis, which is usually not accompanied by corneal ulceration. The clinical course in affected animals is usually 7 to 14 days, although some cases succumb within 24 hours. The most severely affected animals are usually the first ones to become ill. There are two patterns ofiBR in a feedlot. 40 In an outbreak, the number of new cases will peak at 12 to 15 days and then gradually decline, with no new cases after 3 to 4 weeks. The average outbreak morbidity is 30 per cent, with a case mortality of about 3 per cent. 29 In the sporadic pattern of IBR, occasional individual cases occur over a period of many weeks. Pathology There is a spectrum of severity of lesions that corresponds to the clinical picture. The mucous membranes of the nasal passages contain lesions varying from hyperemia and edema to necrosis, which begins in small focal areas and appears as white foci against a hyperemic background. These lesions may enlarge and become confluent, forming large ulcerated areas covered by mucopurulent exudate or diphtheritic membranes. 57 The larynx and trachea may be similarly involved and, in severe cases, are partially blocked by copious amounts of mucopurulent exudate and necrotic debris. In some cases, there is severe pharyngitis, which may be related to the excessive salivation exhibited by some affected animals. 63 Usually the inflammatory process does not extend to the airways within the lung. In some cases, however, severe necrotizing bronchitis and bronchiolitis results in ventral lung consolidation resembling bronchopneumonia. 35 White foci of bronchiolitis can be seen in cut sections of the consolidated areas. 58

FIBRINOUS PLEURITIS AND PLEUROPNEUMO NIA Fibrinous pleuritis and pleuropneumonia ( FPPP) is an acute, sporadic, highly fatal respiratory disease of feedlot cattle that is caused by stress and

Hemophilus somnus.

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Etiolo gic Organ isms

Pasteurella, 25 FPPP is caused by H. somnus, alone or somet imes with t fattening. Sercouple d with predis posing stresse s of shippi ng and feedlo on, but the incomm is sm organi the to re ologic data indica te that exposu 16 of the norma l part be may s somnu H. low. is e diseas cidenc e of clinical ted that viral56 sugges bovine nasal mucos al flora, and experi menta l work has of viruse s those to r simila are a Hemophilus interac tions in the nasal mucos 13 and Pasteurella at this site. damag e in H. somnus readily invade s the blood stream to produ ce separa te of cause the as multip le organ system s. It has been incrim inated chroniC itis, laryng acute onia, pneum respira tory condit ions charac terized by 9 45 •52 • is. trache itis, or fibrino us pleurit Epidem iology

respira tory FPPP has recent ly been descri bed as a specific feedlo t cattle onia pneum and/or is 25 pleurit of s report other been diseas e entity. There have 9 45 •52 The condit ion is usually charac terized • s. somnu H. by of cattle caused mortal ity but has by a very low popula tion morbi dity and very high case tion mortal ity popula a for sible been observ ed in one outbre ak to be respon 25 Animals are . month single a during ed receiv of 0.38 per cent of cattle FPPP and of usually affecte d during the first 30 days of fatteni ng. Cases er in togeth occur imes throm boemb olic menin goenc ephali tis (TEM E) somet a group of feedlo t cattle. Clinic al Signs

tory dyspn ea Cattle affecte d with FPPP have a sudde n onset of expira d animals affecte Most sion. depres accom panied by high fever and marke d 25 less. or days die after a short illness of 2 Pathol ogy

occasionally Fibrin ous pleuro pneum onia is usually presen t, althou gh covere d by is pleura The d. affecte are ) only the pleura and pleura l space(s l spaces pleura both or one and 6), (Fig. fibrin of a thick 2- to 3-inch sheet and fibrin yellow of are compl etely oblite rated by massive accum ulation s hpinkis and firm are lungs d straw- colore d fluid. Depen dent parts of affecte septa. bular interlo white ed, enlarg by ted tan in color, and lobule s are separa monia are also In some cases, lesions of acute or subacu te bronch opneu presen t. 25 CAUD AL VENA CAVAL THRO MBOS IS

onia, pulCauda l vena caval thromb osis (also called metast atic pneum of feedlo t lism) oembo thromb nary pulmo and monar y embol ic aneury sm, secoccurs cattle is a sporad ic, fatal condit ion of low incide nce that usually is and cava vena caudal ondary to septic embol i from a throm bus of the , cough by ed follow tion, respira lt difficu charac terized initially by rapid and hemop tysis, and anemi a.

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Figure 6. Fibrinous pleuritis and pleuropneumonia caused by H. somnus. Thick layer of fibrin overlying consolidated lung. Cross section of diaphragmatic lobe. (Courtesy of Dr. C.A. Hjerpe.)

Etiology This condition is usually the result of a four-step sequence of events that ends with the rupture of a pulmonary artery aneurysm into a bronchus. 29 It begins with the development of rumenitis secondary to lactic acidosis caused by high-concentrate diets. Bacteria such as Fusobacterium necrophorum and Corynebacterium pyoge,nes, which normally inhabit the rumen, are then able to penetrate into the devitalized mucosa, enter vessels of the hepatic portal vein, and shower the liver. Hepatic abscesses then develop and, when located adjacent to the caudal vena cava, the inflammation can spread into its wall and initiate clotting and thrombosis (Fig. 7). Septic emboli detach from the thrombus and are transported by the blood to the lungs, where they lodge in small arteries and arterioles. Suppurative metastatic pneumonia, arteritis, and aneurysms develop at these sites, and eventually the wall of an aneurysmal sac becomes so thin that it ruptures, sending blood into adjacent alveoli (Fig. 8) or into the lumen of a parallel bronchus that has also been eroded by the purulent inflammatory reaction. Another type of metastatic pneumonia, occurring even less often than the one just described, is pulmonary thromboembolism and suppurative pneumonia secondary to infectious processes in other areas of the body, such as phlebitis of the jugular veins, endocarditis, hepatic abscesses, mastitis, or metritis. 5 These cases do not develop pulmonary arterial aneurysms and hemoptysis.

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Figure Thrombus (T)the in the intrathoracic of caudal the caudal midway between Figure 7. 7.Thrombus (T) in intrathoracic partpart of the venavena cava,cava, midway between right atrium Openings of the hepatic veins are marked. thethe right atrium (RA)(RA) andand the the liverliver (L). (L). Openings of the hepatic veins (HV)(HV) are marked.

Figure A ruptured pulmonary arterial aneurysm has caused a massive hematoma to Figure 8. A8. ruptured pulmonary arterial aneurysm has caused a massive hematoma. to form form in theinlung parenchyma. the lung parenchyma.

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Epidemiology

This condition has been reported to be responsible for from 0. 2 per cent25 to 1.3 per cent33 of the diagnosed fatalities in feedlot cattle disease surveys. Its incidence may be expected to vary with the degree of success of control of the rumenitis-hepatic abscess complex. 5 In a Canadian survey, caudal vena caval thrombosis was present in 19.3 per cent of cattle with . hepatic abscesses. 23 Caudal vena caval thrombosis does not have a seasonal incidence. It occurs during all stages of fattening but has its greatest incidence (40 per cent) during the first 45 days. 33 Clinical Signs

Some animals are noticed to have rapid, shallow breathing and elevated temperatures that correspond to initial showering of the lungs with septic emboli. 48 Cattle in later stages of the disease are inactive and may have a painful cough, anemia, and melena. Auscultation of these cases reveals scattered rales. Occasionally, ascites, edema of posterior limbs, and hepatomegaly are present. Some of the affected animals develop a chronic ill thrift. Discharge of bright, foamy blood from the nose and mouth, respiratory distress with head and neck extended, groaning on expiration, pale membranes, generalized weakness, and widespread pulmonary rales indicate a ruptured pulmonary aneurysm. 48 Some animals not previously noticed to be ill are found dead with evidence of profuse hemoptysis. The clinical course ranges from 0. 5 to 90 days, with an average of 7 days. 29 The mortality rate is 100 per cent. Pathology

Lungs of animals that have died from caudal vena caval thrombosis contain pulmonary artery aneurysms and areas of pneumonia and multiple abscesses. 33 Lungs that contain ruptured aneurysms are large, uncollapsed, and firm. The pulmonary artery is distended and distorted. Careful dissection is needed to reveal the sacculated ruptured aneurysm, which usually is 3 to 10 em in diameter and surrounded by hemorrhage (see Fig. 8). 29 Cases that had hemoptysis have blood clots in airways, aspirated blood in alveoli, blood in the mouth and on the face, and swallowed clots in the rumen. Mucous membranes are pale. The liver usually contains at least one abscess located near the vena cava or one of the large hepatic veins. Thrombi within the vena cava are pale, soft, and friable, and measure 1 to 3 em in diameter (see Fig. 7). 33 They are best found by removing the larynx, trachea, lungs, liver, and diaphragm together, then opening the vascular system. 5 The thrombus may be located near the liver abscess or may have moved to other segments of the vena cava, the right side of the heart, or the pulmonary artery. ACKNOWLEDGEMENTS I would like to thank Ms. Cynthia Dowers, Washington Animal Disease Diagnostic Laboratory, and Mr. Fritz Rathjens, Biochemical Communications Unit, Washington State University College of Veterinary Medicine, for their kind assistance in photography.

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