Virus pneumonia of pigs (VPP) is an inflammation of the lungs usually confined to the anterior-ventral portion and lower borders of the apical and cardiac lobes. It is usually a chronic disease that may develop into acute and subacute forms, particularly if  secondary break down  occurs due to secondary bacterial invasion. The disease is characterized by a chronic cough, consolidation of the anterior ventral portions of the lung, and secondary bacterial invasion. It is a distinct disease and is in no way related to the common swine influenza described by Shope in 1931

Kennedy, Gerald

English

Virus pneumonia of pigs (VPP) is an inflammation of the lungs usually confined to the anterior-ventral portion and lower borders of the apical and cardiac lobes. It is usually a chronic disease that may develop into acute and subacute forms, particularly if "secondary break down" occurs due to secondary bacterial invasion. The disease is characterized by a chronic cough, consolidation of the anterior ventral portions of the lung, and secondary bacterial invasion. It is a distinct disease and is in no way related to the common swine influenza described by Shope in 1931.</p

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Virus Pnewnoniaof PigsGerald KennedyVIRUS PNEUMONIA OF PIGS (VPP) isan inflamnlation of the lungs usuallyconfined to the anterior-ventral portioll andlower borders of the apical and cardiaclobes. It is usually a chronic disease thatmay develop into acute and subacuteforms, particularly if "secondary breakdown" occurs due to secondary bacterialinvasion. The disease is characterized bya chrollic cough, consolidation of the an-terior ventral portions of the lung, andsecondary bacterial invasion. It is a dis-tinct disease and is in no way related tothe common swine influenza described byShope in 1931.Incidence of VPPVPP is widespread throughout thenlajor swine producing areas of the world.It is of particular importance in Englandand extensive research work has beendone on the disease there. It is also veryprevalent in the United States.Although this disease is described as arelatively new disease in swine, just namedas VPP by Betts in 1952, there is strongfeeling that it has been present in swinefor quite sometime. There is a report ofa disease with similar characteristics in1948 and Young reports on observing lunglesions similar to VPP in Eastern Nebraskain 1930. Just how long the disease hasbeen present can be, at best, only purespeculation.The lungs of over half of the pigsslaughtered in Britain are pneumonic andmost of these belong to one distinct clini-cal and pathological entity, VPP. A viruscan be isolated which is very differentGerald Kennedy is a senior student in theCollege of Veterinary Medicine at Iowa StateUniversity.Issue 2, 1960from the virus of swine influenza as des-cribed by Shope. Forty to seventy five per-cent of the pigs slaughtered in the UnitedStates show evidence of virus pneu-monia. The lesions are microscopically in-distinguishable from those of VPP as des-cribed in England. Studies have shownthat occurrence of significant antibodytiters against swine influenza is less than15 per cent. It is worth pointing out thatthe incidence of lesions at slaughter doesnot give a true indication of the actual in-cidence of virus pneumonia, since experi-ments show that many pigs that havebeen injected will have recovered com-pletely by the time marketable weight isreached.Economic ImportanceVPP does not have a high mortalityrate. Rarely does a pig die from the diseaseunless complicated by secondary infec-tion. The concern for VPP comes fronl itshigh incidence, conservatively estimatedto effect 50 percent of the swine in theU.S. and its costliness because of slowgrowth and poor feed conversion. It hasbeen shown that pigs infected with VPPrequire 17 per cent longer to get to marketweight and require 22 per cent more feedto produce each 100 Ibs. of pork. Theanimal loss in the United States due toslow growth and poor feed conversion hasbeen conservatively estimated at $120,-000,000.EtiologyThe etiologic agent is a virus which iscapable of causing an extensive pneu-monia by itself, but rarely does. In mostnatural infections both the secondary or-81ganisms, P.P.L.O. and bacteria are found.The Pasturella sp. are possibly the mostimportant bacteria involved, but otherbacteria may also be involved such asCorynebacterium pyogenes and the strep-tococci. The virus is unusual in several re-spects; one of its most unusual featuresis its failure to produce any demonstrableimmunity, thus precluding the possibilityof using a vaccine as a control measure.Demonstration of antibodies against thevirus in infected pigs has not been accom-plished. Successful propagation of thevirus in chick embryos has not beel1 ac-complished. Cytopathogenic effect has notbeen observed in tissue cultures. The onlyisolations made 11ave been by passagethrough the natural host and this becomesdifficult if the number of passages exceedsthree or four.Experimentally, the infection can beprevented by large doses of the tetracyclinegroup of antibiotics. These antibioticshave no curative effect upon estabilshedlesions and thus are of no practical valuein the treatment of the virus. The virus isnot affected by chlormycetin, streptomy-cin, penicillin and sulfa drugs. All thesedrugs nlay cause a temporary clinicalimprovement by their action on secondaryinvading microrganisms.The virus dies within a day outside theanimal's body under farm conditions. Inthe lungs of the affected pigs it can persistfor long periods of time and has been re-covered from the lungs sixty-six weeksafter infection.The main differences between theviruses causing swine influenza and theVPP virus are the failure of any demon-stratable immunity being produced by in-fection; failure of chick embryo propa-gation of the virus; and no cytopathogeniceffect observed with VPP virus..symptomsPigs of all ages are susceptible to thedisease, but it is most obvious in youngpigs. Transmission is purely airborne andfomites play little or no part in the spreadof infection. Pigs thus become infectedfrom their dams or when diseased andhealthy pigs are mixed together.82About the only obvious sign of the dis-ease is a non-productive cough, whichusually develops two or three weeks aftercontact. This cough may continue for therenlainder of the pig's life or it may dis-appear after a few weeks.The important thing about V.P.P. is thatan affected pig does not thrive as well asa normal animal. Once a pig becomes in-fected there seems to be set up a delicatebalance between the virus and secondaryorganisms on the one side, and the hoston the other. Under conditions of poorhusbandry and management the balancemoves against the host, and the pig be-comes more severly affected. If, however,the environment is good, the effect of thedisease is minimized but is certainly noteliminated.An interesting feature of the disease isthat a number of pigs, which have con-tracted infection earlier in life, quite sud-denly develop acute pneumonia at 19 to26 weeks of age. This phenomenon hasbeen termed "secondary breakdown" andis associated witll the extension of a pre-existing virus lesion and rapid multipli-cation of secondary organisms. At suchtimes, pigs lose their appetites, becomefebrile and sometimes prostrate. Greatdifficulty in breathing is observed, and thepigs will "thump". The difficulty in breath-ing is a manifestation of the lesions pres-ent in the lungs. The pigs seem to eat wellunless they are hopelessly sick. Althougha few pigs die, the majority recover withina week or two. The malady is reflected ina sudden temporary reduction in growthrate or even an actual loss of weight. Ac-tual weight loss and complete stunting ofgrowth is more likely to occur 'underCOllditions of poor husbandry. Someanimals are turned into hopeless runts dueto permanent damage to the lungs. It ishighly probable that Dlany cases of so-called "pasteurellosis of swine" or "ship-plng fever of hogs" are, in fact, "second-ary breakdown".Quite apart from the spectacular effectson growth-rate caused by secondary break-downs, the overall effect of VPP is a vari-able, but general depression of growtllrate and efficiency of food utilization.Iowa State University VeterinarianLesionsThe appearance of the lung in uncom-plicated cases is quite typical. The apical,cardiac, a11d adjacent borders of the dia-phragmatic lobes are the areas most com-monly affected. The ventral portions ofthese lobes are usually consolidated, firmto the touch, and red or brownish in color.The affected lobe may have a mottled anduneven appearance due to the presenceof alternate diseased and healthy lobules.A narrow streak of collapse and fibrosismay be observed along the course of thebronchial tree. The adjacent healthy lob-ules are usually en1physen1atous. If "sec-ondary breakdown=" has occurred, areas ofsuppuration will be found. The bronchialand mediastinal lymph nodes are enlargedand edematous and sometimes pleurisyand pericarditis accompany the pneu-monia.The characteristic microscopic changesare, lymphocytic infiltration and prolifer-ative changes around the bronchioles withfoci of interstitial pneumonia scatteredthroughout the lobule, often becomingconfluent and more evident at the peri-phery. The alveoli may contain few ormany cells. The alveolar lining cells usu-ally predominate with many lymphocytes,plasma cells, a few histocytes, neutro-phils, and occasionally giant cells arepresent. Marked hyperplasia of the lymphnodules with scattered foci of lymphocyticinfiltration are constant features. Perivas-cular cuffing is frequently seen. Prolifer-ative vascular lesions are also frequentlyseen. Varying degrees of fibrosis are pres-ent. The hyperplasia of the lymphoid tissueis, in many cases, remarkable, occurringin circumscribed masses which may causepressure collapse of both bronchioles andalveoli.Pattison has pointed out that histo-pathology seems to offer the more specificmethod of diagnosis of VPP. Lesions selec-ted with the naked eye, as being typicalof VPP, showed such variation, that whenexamined microscopically, add i t ion a 1causes of the lesions seemed probable. Theprincipal histopathological finding ofnaturally and artifically infected animalswas extensive lymphoid hyperplasia of theIssue 2, 1960peribronchial, peribronchiolar, and peri-vascular tissues.Pigs dying from "secondary break-downs=" frequently have in their lungs,necrotic areas which teem with bipolarorganisms. Pleurisy is almost always pre-sented and often pericarditis. The com-mon occurrence of atelectatic lungs inswine may be due to VPP.Differential DiagnosisVirus pneumonia must be differentiatedfrom other pneumonia in swine. In mak-ing a diagnosis of virus pig pneumonia,the primary disease that it must be dis-tinguished from is swine influenza.Chronic and recurrent respiratory illnesseswith "secondary breakdowns=" should bediagnosed as virus pneumonia. Swine in-fluenza may be differentiated by its acutenature, sudden 011set, high temperature,anorexia and seasonal incidence. Animalssuffering from "secondary breakdown" willexhibit an acute pneumonia, but theherd incidence of this acute pneumoniawill be relatively low, whereas in swine in-fluenza, which is also acute, the morbidityrate is high.Transmission and ControlIn view of the economic importance ofvirus p11eumonia of pigs, a method of con-trol is highly desirable. The fact thatswine do not develop an appreciable im-munity precludes the use of a vaccine.The antibiotics that are currently availableare non-effective against the virus, al-though their use may give temporary im-provement of clinical symptoms due totheir action on secondary bacteria. Thelack of a vaccine or an effective chemo-therapeutic agent to control the diseaseplaces the veterinarian in a unique posi-tion as far as service to the client is con-cerned. Service will be rendered notthrough medication or vaccination, butthrough council and advice on how tomaintain a herd of swine free of VPP andother diseases of similar nature. Such aventure will require much thoughtfulnessand patience of both the veterinarian andthe client.83Only control based on epidemiologicalconsideration is possible. The followil~gbasic facts must be taken into consider-.ation:1. Virus pneumonia is a specific contag-ious disease and the only natural hostis the pig.2. The virus is not a common inhabitantof the respiratory tract of "normalpigs" with no pneumonia. If the virusis present, lesions of VPP will be pres-ent.3. Almost indefinite persistence of thevirus in the lungs, up to at least 66weeks, presents a carrier problem bywhich the disease is passed from damto offspring in succeeding generations.4. The virus does not survive outside thenatural host for more than a day underfarnl conditiol~s.5. The disease spreads solely by the air-borne route; mechanical or internled-iate vectors play no part in its trans-mission.A control method based 011 epidemiolog-ical consideration has been developed andsuccessfully applied under field condi-tions. It consists, essentially, of breakingthe cycle of infection and is comprised ofthe followil~g stages:1. Farrowing sows in isolation to insurethat any infection of the litter comesfrom the dam.2. Determination of whether or not thethe litter is infected by means of clin-ical examination supplemented by post-mortem examination of one or morepigs per litter at weaning time. Thismethod also determines the carriersows.3. Litters judged to be free from the dis-ease may be grouped but retained inisolation.4. Examination of lungs at slaughterfronl a considerable portiol~ of the pigswhen they reach market weight.5. Replacement of original breeding stockwith healthy progeny as soon as pos-sible.A more drastic method of control, butone whicll should be very effective is thatdescribed by Young and Underhal where-84by "disease-free" pigs are obtained byhysterectomy.Pasturella bacterin has b~en used onfarms where VPP is a problem. Autogen-ous bacteril~ is believed to give the bestresults.Brood spectrum antibotics are some-what effective in preventing "secondarybreakdown." Expectorants have been usedto relieve chronic coughing but relief isusually only temporary.Good management along with adequatenutrition will benefit pigs that are clini-cally sick. The elimination of dust ac-companied by ascarid control is impor-tal~t. Dust may act as an irrital~t ag-gravating the condition. The migration ofascarid larvae through the lungs increasesthe severity of tIle lesions.REFERENCESBetts, A. O. Pneumonic Diseases of the PigCaused by Viruses. A review of the Literature.(1953) British Vet. Journal. 109, 99-106.Betts, A. O. Virus Pneumonia of Pigs, PigBreeders Gazette. 72 January 1953 27-33.Betts, A. 0., Whittlestone, P., and Beveridge, W.I. B., Investigations on the Control of VirusPneumonia of Pigs in the Field..The Veteri-nary Record 67, 685. September 10, 1955.Betts, A. 0., Whittlestone, P., Beveridge, W. I. B.,Taylor, J. H., and Campbell, R. C. VirusPneumonia of Pigs. Further InvestigationsUpon Growth Rate and Efficiency of FoodUtilization. (1955) Vet. Rec. 67, 661-665.Betts, A. O. Virus Pneumonia Found in Swine.Journal of A.V.M.A. 128:301. March 15, 1956.MacPherson, R., and Shanks, P. L. The Com-parative Incidence of Pneumonia in Sows andin Bacon Pigs with Suggestions on the Estab-lishment of a Pneumonia-free Herd. TheJournal of the British Veterinary Association.Vol. 67, No. 28. Issue No. 4032 525-542.Pattison, I. H. A Histological Study of Trans-missable Pneumonia of Pigs Characterized byExtensive Lymphoid Hyperplasia. Vet. Rec.68:490-4. July 28, 1956.Young, George A. Virus Pneumonia of Pigs(VPP). Diseases of Swine, textbook. HowardW. Dunne, Editor. 1958 99-104.Young, George A. and Underdahl, Norman R.An Evaluation of Influenza in MidwesternSwine. The American Journal of VeterinaryResearch Vol. 16, No. 61, Oct., 1955, pp. 545-552.Underdahl, Norman R. and Kelley, George W.The Enhancement of Virus Pneumonia ofPigs by the Migration of Ascaris Suum Larvae.The Journal of the American Veterinary Med-ical Association. Vol. 130, No.4, Feb. 15, 1957,pp. 173-176.Whittlestone, P. and Betts, A. O. The Eradicationof Virus Pneumonia of Pigs from a Commer-cial Herd. The Veterinary Record 67, 692.September 10, 1955.Iowa State University Veterinarian

Virus Pneumonia of Pigs

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Virus Pneumonia of Pigs

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