Porcine Haemophilus Pleuropneumonia Epizootic inSouthwestern Ontario: Clinical, Microbiological,Pathological and Some Epidemiological Findings

S.E. Sanford and G.K.A. Josephson*

ABSTRACT

A fibrinous necrotizing pleu-ropneumonia with a predominantmononuclear cell infiltrate com-menced January 1978. Thepneumonia, caused by Haemo-philus pleuropneumoniaeassumed epizootic proportionsand affected mainly feeder pigs inthe intensive pig rearing area ofsouthwestern Ontario. A fewabortions occurred. Winterstorms, recent transportation andother potentially stressful situa-tions were associated with herdoutbreaks. Broad spectrum anti-biotics were usually effective instopping deaths.

RISUMP

Une pleuro-pneumonie fibrino-necrotique qui s'accompagnaitd'une infiltration marquee demononuclEaires, commenca As6vir en 1978. Cette maladie,imputable A Haemophilus pleu-ropneumoniae, prit bient6t desproportions 6pizootiques dans lesporcheries d'engraissement, dansla r6gion de l'Mlevage porcinintensif du sud-ouest de l'Ontario.Quelques avortements se produis-irent aussi. Les temp6tes del'hiver, un transport recent ou

d'autres conditions stressantescontribuaient A l'Mclosion de lamaladie. L'emploi d'antibiotiquesA large spectre permit d'enrayerles mortalitks.

INTRODUCTION

Porcine haemophilus pleurop-neumonia (PHP) was described in1963 by Olander in the U.S.A. (24)and in 1964 by Shope from Argen-tina (28). There is strong circum-stantial evidence however that thedisease was observed in Englandin 1957 (25). Throughout the 1970'sinterest in Haemophilus pleurop-neumoniae increased and numer-ous reports of this agent associatedwith outbreaks of pleuropneumo-nia were reported from severalEuropean countries (6, 8, 15, 18,20), Australia (17), Taiwan (13)and Japan (4). In North America,the disease is now present in Mex-ico (Lopez, A. personal communi-cation), several American States(5, 12, 24) and Canada (27).The aetiological agent was orig-

inally classified as Haemophilusparahaemolyticus (24) based on itsV-factor growth requirements andhaemolysis which corresponded tothe existing human species, H.parahaemolyticus, Pittman 1953(24). Since the demonstration ofseparate genetic identities for theporcine and human haemophilusstrains (14), the name H. pleurop-neumoniae originally suggested byShope (28) for the porcine haemo-philus organism has been proposedto replace H. parahaemolyticus(14) and has gained wider accep-tance (8, 9).This paper describes the clini-

cal, microbiological, pathologicaland some epidemiological findingsof an epizoOtic of PHP in south-western Ontario.

MATERIALSANDMETHODS

This is a retrospective studybased on laboratory findings fromexamination of over 600 porcinecarcasses or lungs with PHP sub-mitted to the Veterinary ServicesLaboratory, Ontario Ministry ofAgriculture and Food at HuronPark from approximately 200farms between January 1978 andDecember 1979. During this sameperiod PHP was diagnosed fromapproximately 100 more farms bythe Guelph and Ridgetown labora-tories (Van Dreumel, A.A. per-sonal communication).

EPIDEMIOLOGICAL ANDCLINICAL INFORMATION

Histories and clinical signs wereobtained by interviewing produc-ers and/or their veterinarianswhen carcasses or lungs weresubmitted.

PATHOLOGY

Necropsies were performed onall carcasses. Samples for histopa-thological examination werefixed in 10% neutral buffered for-malin, sectioned at 6 ,Mm andstained with haematoxylin andeosin (H & E).

MICROBIOLOGY

Portions of lung, liver, spleen,kidney, intestine and occasionallybrain, tonsil and joint fluid werestreaked on 5% bovine blood agarplates containing nicotinamideadenine dinucleotide (NAD)1 andincubated for 24 hours at 37C.

Can. J. comp. Med. 45:2-7 (January 1981)

*Veterinary Services Laboratory, Ontario Ministry of Agriculture and Food, Huron Park, Ontario NOM 1YOSubmitted March 24, 1980.'NAD, Sigma Chemical Co., St. Louis, Missouri.

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C.untfrw oiibe .....................M........,..

Figure obtAnd fro ;O ?fla1PoPoducrs Marketing Bord. . -

Fig. 1. County map of Southern Ontario.

Approximately 5% of isolates weretested for antibiotic sensitivityusing the disc diffusion technique.Ground tissue from two frozenlungs were inoculated on porcineprimary kidney cell cultures andexamined for viral cytopathiceffect.

RESULTS

EPIDEMIOLOGICAL ANDCLINICAL INFORMATION

Outbreaks first occurred inearly 1978 and soon developed intoan epizootic in the dense pig farm-ing counties of southwestern Onta-rio (Fig. 1). Two outbreaks withvery low morbidities and mortali-ties were reported from easternOntario late in 1979 (Binnington,

B. personal communication). Nocases were reported from northernOntario. Feeder/finisher farmscomprised approximately 80% ofaffected farms in this epizootic.The remainder was nearly equallydivided between farrow-to-finishand breeder/weaner operations.Pigs submitted from the feeder/finisher and farrow-to-finish oper-ations were primarily in the 30 kgto 50 kg weight ranges. Introduc-tion of new stock or moving ofexisting stock prior to an outbreakwas a common history. At the onsetof an outbreak, pigs were oftenfound dead. On closer examina-tion, respiratory distress and ano-rexia could be noted in 40 to 50% offeeder pigs. Rectal temperaturesof up to 41°C were observed. Mor-tality varied greatly but initially itoften approached 20% before ther-

apy could be instituted. Epistaxisas a terminal or near terminalevent was frequently observed. Sixbreeder herds experienced abor-tions and these and a few otherherds had sudden deaths in neo-nates, sucklings and weaners.Deaths after periods of respiratorydistress occasionally occurred inboars and in pregnant and opengilts and sows.There was usually a dramatic

clinical response to mass medica-tion with broad spectrum antibio-tics administered via the drinkingwater combined with intramuscu-lar injections of the same antibioticto animals which were obviouslyill. Deaths generally ceased withintwo to four days after commencingtherapy, but in a few cases deathsdue to PHP recurred within daysor weeks after withdrawal of med-

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ication. Occasionally, one antibio-tic would seem ineffective in a herdand in these cases a switch toanother broad spectrum antibioticwas usually successful in stoppingfurther deaths.As the epizootic entered its

second year it became evident thatexacerbations frequently followedabrupt climatic changes, espe-cially cold snaps or storms in thewinter months. Submissions to thelaboratory and field reports ofPHP fell off precipitously duringthe summer months only to pick upagain in the fall and peak in thewinter and spring.

GROSS PATHOLOGICAL FINDINGSLesions were usually confined to

the thoracic cavity. In acute andperacute cases there was a lobarpleuropneumonia characterizedby extensive congestion and hae-morrhage of the lung and up toseveral hundred mL of serosan-guinous fluid and a yellowish fib-rinous exudate in the pleural andpericardial cavities. Adhesionswere present on parietal and vis-ceral pleurae and sometimes onpericardia (Fig. 2). All lobes werefrequently affected (Figs. 2 and 3)but a highly characteristic featurewas involvement of the caudallobe, especially the craniodorsalaspect where firm, raised, cir-cumscribed, haemorrhagic areasup to 6 cm in diameter were com-monly observed. In approximately10% of all cases, lung lesions werepredominantly unilateral and in90% of these, the right lung wasaffected (Fig. 3). When unilateral,the entire lung on that side wasoften involved. On cut surface,firm haemorrhagic, irregularlyshaped areas, often with centrallylocated necrotic foci, were seen.Interlobular oedema was promi-nent. Bronchial and mediastinallymph nodes were enlarged andoedematous. Tracheae containedblood-tinged froth. In more chroniccases, extensive fibrous pleuraladhesions were present especiallyover well demarcated, irregularareas of necrosis. Numeroussequestra of various sizes wereobserved in lungs, both superfi-cially and on cut surface.

Fig. 2. Acute PHP with fibrinous pleuri-tis and haemorrhagic pneumonia of alllobes of lung.

Fig. 3. Unilateral acute PHP. Haemor-rhagic pneumonia of all lobes of rightlung. Note fibrin tags on dorsal aspect ofthe caudal lobe.

An extrathoracic lesion consist-ing of increased amounts of perito-neal fluid containing fibrinstrands was occasionally observed.The sporadic abortions occurredduring the third trimester of ges-tation. There were diffuse renalcortical haemorrhages and con-gested livers in aborted foeti.HISTOPATHOLOGICAL FINDINGS

Lesions were most prominent inthe lung and the pleura. In theperacute cases there was markedcongestion of the alveolar capillar-ies and larger blood vessels withhaemorrhages into the alveoli.Alveoli were flooded by copiousamounts of eosinophilic, oedemafluid. Lymphatics were distendedby similar fluid with interstitiallymphatics markedly so. Fibrinthrombi were present in many ves-sels throughout the lungs (Fig. 5).Mononuclear cells (macrophagesand lymphocytes) present in smallnumbers, and coccobacillary bac-teria, diffusely scattered and occa-sionally in small clumps, wereusually seen in this fluid.

In most cases, however, the moststriking lesion was seen by viewingthe slide with the naked eye orunder a very low power magnifica-tion of the microscope. Areas ofnecrosis of varying sizes andshapes were outlined by darklystained bands (Fig. 4). These deli-

Fig. 4. Subgross photomicrograph show-ing irregular, sometimes coalescingzones of necrosis delineated by darkbasophilic bands in lung parenchyma. H& E. X7.5.

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Fig. 5. Irregular coalesced area of coa- Fig. 7. Higher magnification of swirlinggulative necrosis surrounding hyper- mononuclear cells. H & E. X175.plastic, partially collapsed bronchiole(centre) and thrombosed blood vessel(bottom). Necrotic zone is delineated bydark basophilic band. H & E. Xll.

neated, necrotic zones usually sur-rounded scattered bronchioles andlymphatics and sometimes encom-passed entire lobules (Figs. 4 and5). On higher magnification thedarkly stained bands were made

AZ w v A

4 0

Fig. 6. Closer view showing delineatingband consisting of large numbers ofprimarily mononuclear cells in a char-acteristic streaming, swirling orienta-tion. H & E. X44.

up of densely packed alveolar mac-rophages and lymphocytes thatoccluded alveoli (Figs. 6 and 7) andwere themselves surrounded byfibroblastic proliferations andconnective tissue in older lesions.Alveoli and bronchioles were filledwith macrophages, lymphocytes,desquamated alveolar cells andfibrin. Bronchioles were usuallyintact but sometimes had a moder-ately hyperplastic, occasionallyfragmented epithelium and con-tained similar cellular exudate(Fig. 5). Macrophagic cells wereroutinely oriented in a characteris-tic swirling pattern (Figs. 6 and 7).Neutrophils were seldom seen.Subpleural lymphatics and peri-cardium were also delineated byswirling mononuclear cells.Clumps of bacteria were occasion-ally seen in necrotic parenchyma.Focal congestion and disruption ofalveolar capillaries with alveolaroedema and accumulations ofsmall numbers of mononuclearcells were occasionally observed ingrossly unaffected lung.

In a few cases thrombi were seenin medium sized vessels in the kid-ney near the corticomedullaryjunction and in the liver in sinu-soids, portal and central veins.Lesions were not found in thebrains and joints examined. Dif-

fuse haemorrhages in kidneys andsinusoidal congestion and haemor-rhage in livers were the main find-ings in aborted foeti. In addition,meconium was present in alveoli oflungs from foeti of one near termabortion.

MICROBIOLOGICAL FINDINGS

A few lung cultures yielded oneor more of several bacterial speciesincluding Pasteurella multocida,Pasteurella haemolytica, Escheri-chia coli, Streptococcus sp. andStaphylococcus sp. However, inover 90% of lungs, the predominantand usually the only isolates wereluxuriant growths of small, trans-lucent, mucoid, usually haemolyticcolonies. Stained smears revealedsmall, gram negative coccobacilli.The bacterium was nonmotilewhen viewed in a hanging dropunder the light microscope. Iso-lates were susceptible in vitro tomost commercially available anti-biotics, but were frequently resist-ant to cloxacillin, lincomycin andstreptomycin.

Occasionally this organism wascultured from spleen, liver, kid-ney, tonsil and joint fluid. Theorganism was not recovered frombrain, but this organ was culturedin only a few cases. No viruses wereisolated.

DISCUSSION

The explosive nature, gross, his-topathological and microbiologicalfindings in these outbreaks wereessentially identical to numerousprevious reports of PHP (4, 6, 10,13, 17, 18,20,21,24,27,28). In thisepizootic, septicaemia and abor-tion but not meningitis were alsoobserved. The gross and histopa-thological findings associated withabortion were deemed nonspecific.

Recognition of the intensifica-tion of the Ontario swine industryin the last decade seems necessarysince, although this epizooticcommenced in January 1978, theH. pleuropneumoniae organism,despite differing nomenclature,had probably been in Ontario fornearly 20 years (26, 29) having

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been implicated in meningitis (26),septicaemia (29) and abortion (30)in pigs. While in 1970 there were25,142 hog producers who mar-keted 1,847,419 hogs, by 1978 therewere 16,442 who marketed2,626,476 hogs.2 It is also pertinentthat most of this intensificationoccurred in the counties of Huron,Perth and Waterloo and the coun-ties that bordered them in southw-estern Ontario (Fig. 1). Thesetrends resulted in (i) pig herdsbecoming large and in a few casesmassive and (ii) finishing opera-tors being frequently forced topurchase stock from multiplesources, thus mixing pigs of differ-ent ages and of heterogeneousimmunological backgrounds. Theclinically inapparent carrier stateof PHP is well recognized (21, 23)and Nicolet has suggested that thismodern swine production systemhas created a new epidemiologicalsituation in which a "sleepingendemic disease comes to fullexpression" (19).The sequestra and fibrosed

necrotic lesions of chronic casesharbour H. pleuropneumoniaeorganisms which would be pro-tected from antibiotics and wouldserve as constant sources of orga-nisms for new outbreaks andwould support the need for prompttherapy. Unlike reports from otherworkers (17, 23) slaughter housecondemnations due to chronicPHP have not been presented as aproblem in this epizootic to date.With few exceptions (11, 24, 27,

28) very little has been writtenabout the possible pathogenesis ofPHP. Even less has been doneexperimentally to investigatethese mechanisms (11, 24). Furth-ermore, the presence of such largenumbers of pulmonary alveolarmacrophages (PAM) in lungs withPHP and other fibrinous pneumo-nias of animals, e.g. pneumonicpasteurellosis, need further inves-tigation into their involvement inor contributions to the pathogene-sis of these pneumonias. Other bac-teria (13, 17) and viruses (27) havebeen associated with PHP. Otherbacteria were infrequently cul-

tured and, although virus isolationwas seldom and mycoplasma isola-tion was not attempted, none ofthese agents seemed to signifi-cantly influence the cases in thisepizootic. However, various poten-tially stressful situations such astransportation, extremely coldwinter conditions, storms and sud-den changes of weather were fre-quently associated with herd out-breaks of PHP. Stress in general(6, 17, 21), especially climate (6)and recent transportation (17)have been implicated in the precip-itation of PHP outbreaks.Experimentally, H. pleuro-

pneumoniae has been shown toproduce necrotizing pleuropneu-monia identical to the peracuteform seen in natural outbreakswithin six hours (10, 15) of intrat-racheal inoculations. Although H.pleuropneumoniae has been reco-vered from tonsils of pigs withchronic PHP (22, 23), it is not con-sidered a normal resident of theupper respiratory tract (2, 24).However, once it has been intro-duced into a herd, stress may besignificant in allowing it to escapethe natural defenses of the upperrespiratory tract and invade thelung. After the bacteria gainaccess to the smaller bronchiolesand alveoli a rapid multiplicationin this favourable environment fol-lowed by their death either spon-taneously or after interaction withPAM may be anticipated to releaseendotoxin. The endotoxin soreleased could be involved in pro-ducing the marked oedema and thevascular thrombosis of the pera-cute cases (11, 27, 28) and the char-acteristic necrotizing pleurop-neumonia (11, 27) of PHP.Endotoxin is both cytotoxic to andactivates PAM (3). The combina-tion of endotoxin and the release ofproteolytic, lysosomal enzymes byspent macrophages could contrib-ute significantly to the observedgross and histopathological lunglesions. Markham and Wilkie (16)and Benson et al (1) have recentlydemonstrated cytotoxicity andimpaired phagocytosis of bovinePAM by an as yet unindentified

fraction of P. haemolytica, theagent responsible for bovinepneumonic pasteurellosis. Pneu-monic pasteurellosis resemblesPHP in many respects (7). Mark-ham and Wilkie have further pos-tulated an enhanced severity of thedisease process by increased deathof PAM after phagocytosis ofopsonized P. haemolytica (16). Theunidentified fraction may well beendotoxin, or if not, H. pleuro-pneumoniae may have a similarcytotoxic fraction.

In the second and third years ofthis epizootic, more intensive andsophisticated prevention and con-trol measures were instituted.Purchasing weaners from knowndisease-free herds on an all in, allout basis is perhaps the bestmethod of prevention, but becauseof the inapparent carrier state, thelack of a serological test in Ontarioand the scarcity of availableweaner pigs, this method has beengenerally deferred in favour ofvaccinating dams and weaners onbreeding farms with autogeneousbacterins prepared from formalindeactivated H. pleuropneumoniaeisolates. A few breeding unitshave, however, opted for depopula-tion and restocking with SPF pigs.Although not subjected to con-trolled experimental conditions,vaccinations to date seem to havehad some success in controlling theviolent outbreaks, though severalcases of vaccine breaks and even afew exacerbations after vaccina-tion have occurred. This is consist-ent with experience from bothfield and experimental vaccina-tion regimens in other countries(22). The postulated exacerbationsafter opsonization (16), if also truefor H. pleuropneumoniae, mayaccount for some of these vaccinefailures. Others are learning to livewith the disease and trying to keeplosses to a minimum by reducingstressful conditions.

ACKNOWLEDGMENTS

We thank Drs. J. Prescott andM.R. Wilson of the Ontario Veteri-

2Figures provided by the Ontario Pork Producers' Marketing Board.

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iary College for assistance withnicrobiological techniques.

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