Infectious porcine atrophic rhinitis: a review

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Transcript of Infectious porcine atrophic rhinitis: a review


    November 1966


    H. G. Pearce* and C. K. Roe*

    ATROPHIC RHINITIS (AR) was initially de-scribed by Franque in 1829 (109). Sincethat time, the disease has been reportedthroughout the world (1, 9, 16, 17, 22, 27,61, 62, 115, 116). In Canada, the inci-dence in infected herds has been foundto vary from 21 to 45% (66, 92); similarfigures have been reported in Europe (7).In Ontario, up to 88% of herds may beaffected (76) and within a herd, the inci-dence may be as high as 45% (98). Allbreeds and both sexes appear to be equallysusceptible to infection (9, 28, 37, 62).Experimentally, young pigs were morereadily infected than older pigs (41).Several workers have reported that ARmay be contracted during intrauterine life(9, 41). Dietary deficiencies, helminthiasis,and poor ventilation were considered topredispose pigs to the disease (48). Pig-lets that have a light birthweight appearto be more susceptible than their heavierlitter mates (48). It has been reportedthat AR was more common in spring littersand that litters from gilts were moresusceptible than those from older sows(53, 54).Gendreau (36) and Goldstein (38)

    stressed the economic importance of thedisease and claimed that the mortality ofthis disease may be as high as 30%. Doubthas been expressed that AR alone is ofeconomic importance, but the disease maypredispose to other infections (e.g., peri-carditis and pleurisy have been reportedto be more common in the presence ofsevere AR lesions (6)). Malocclusion of

    'Ontario Veterinary College, University ofGuelph, Guelph, Ontario.

    the jaws and faulty mastication may impairdigestion (48).

    Pigs with AR have been reported toweigh significantly less at various agesthan their normal litter mates (66).Studies at the Ontario Veterinary Collegehave shown no significant difference inthe maturity time of normal and AR-affected litter mates from herds free ofvirus pneumonia (VPP) or from herds inwhich VPP was present and pigs werereared under R.O.P. conditions (86).Feeding trials with a university swineherd have shown an improvement of feedefficiency and rate of gain when comparingthe old herd, which had a high level ofAR and VPP, and the present herd whichis certified free of both diseases (82).

    Early investigators considered that ARwas an hereditary abnormality (defectivedevelopment of turbinates occurred first,infection was secondary) because inflam-mation was not always coincident withturbinate atrophy and the disease couldexist in clinically normal pigs (12, 28, 57,63, 64, 112). By selective breeding, thedisease was eliminated in East Prussia(64). The high incidence of AR in thebetter herds in that area was attributed totheir breeding methods. Krage later modi-fied his view that AR was an hereditarydisease but still denied that the conditionwas due to infection or to avitaminosis Abecause pigs, from both affected and pre-viously non-affected herds, had AR follow-ing breeding trials (65). Duthie wasunable to transmit the disease to pigs 40to 90 days of age and concluded that ARwas hereditary or there was an hereditarysusceptibility (28).

    Scandinavian workers demonstrated that


    CAN. VET. JOUR., vol. 7, no. 11, November, 1966

    Volume 7 Number 1 1


    the disease was not hereditary by raisingpigs of the same breeding from two con-secutive litters. The first litters were bornnaturally and reared by the sows. AR waspresent when the pigs were examined atmarket weight. The second litters wereremoved at birth and reared artificially; inthese litters, there was no turbinateatrophy (13, 34).AR has been ascribed to faulty nutrition

    with infection playing a secondary role.Bendixen (6, 8) noted that the diseasewas more common in spring-born littersthan in other litters. Since the incidenceof AR tended to parallel the incidence ofanopthalmia, he considered that vitamin Aplayed an important role. Later, he con-cluded that AR was of complex nutritionalorigin. Bjorklund (9) considered thedisease to be of metabolic origin relatedto rapid growth, and that infection wassecondary to faulty bone development. Hewas unable to support the contention thatvitamin A deficiency was significant, sinceexamination of livers from affected pigsindicated a normal level of vitamin A, norwas he able to produce evidence of dis-turbed calcium or phosphorus metabolism.

    Other workers noted that the diseaseoccurred on farms on which breedingstock was reared and when boars wereintroduced from these breeding farms toother farms, the disease appeared. Forthis reason, they considered the disease tobe infectious (113). Clinical and experi-mental investigation has tended to sup-port this view (22, 59, 84). Bacilluspyocyaneus was the first organism to beinvestigated as a possible cause of thedisease. Broth cultures of this organismwere instilled intranasally into two pigs;the two experimental pigs died and thecontrol pig survived. From this experi-ment, it was concluded that AR wascaused by B. pyocyaneus (63). Jensen wasunable to confirm this work (51, 63).Pigs were injected with cultures of Pseudo-monas aeruginosa and filtrates of Ps.aeruginosa broth cultures obtained frompigs with AR. The pigs thus injected diedand it was considered that the toxin ofthis organism was the etiologic agent.These workers also prepared an auto-genous Ps. aeruginosa vaccine which theyclaimed was effective in preventing thedisease (31). Radtke stated that AR wasa manifestation of "Ferkelgrippe" (suck-

    ling pig influenza) since he observed nasallesions only where this condition occurred;he was the first person to transmit thedisease (91). Crude nasal material, nasalexudate, or washings, have been used toreproduce AR in young pigs (41, 42, 59,60, 89).

    Bacteriological surveys of the nasalpassages of affected pigs have consistentlydemonstrated that P. multocida is present(52, 76). The incidence of this organismin specific pathogen free (S.P.F.) andknown infected herds has been found tobe 1% and 2%, respectively (85). Trans-mission experiments using cultures of P.multocida have been inconsistent (44, 45,76, 97). P. multocida bacterin or anti-serum had no protective value when ad-ministered prior to intranasal instillationof crude infectious material (46, 60). Byusing a rabbit passage technique, it hasbeen possible to produce AR in pigs byinstilling intranasally, mixed cultures ofP. multocida and Actinomyces necrophorusof swine nasal origin. McKay inoculatedyoung pigs with rabbit passage materialand reproduced the disease in 82% of theexperimental animals (76). Other workershave been unable to reproduce these re-sults (42). Schofield and Robertson wereable to reproduce AR in piglets givenmultiple instillations of pure cultures ofPseudomonas aeruginosa and P. multocida(97). AR in young pigs was reproducedfollowing intranasal instillation of culturescontaining P. multocida and Haemophilussuis and streptococci (34). Van der Schaafwas unable to reproduce AR in month oldpiglets using intranasal instillation of cul-tures of H. suis (115). On the basis ofclinical observation it has been suggestedthat Erysipelas and AR may be related(79, 80), but Borgman was unable todemonstrate Erysipelothrix rhusiopathiae inground up nasal material from affectedpigs (11).

    Moynihan was unable to reproduce ARwith mixed cultures of Alcaligenes bronchi-septica, Staphylococcus albus and S. aureus(81). McKay observed an incidence of16% of Bordetella bronchiseptica in thenasal passages of 31 normal pigs (76).More recently, workers were able to pro-duce turbinate atrophy experimentally inyoung pigs (24). Initially, they reproducedthe disease in eight out of nine specificpathogen free (SPF) piglets using a



    turbinate homogenate in saline. From thepigs thus infected, they were able to isolateB. bronchiseptica. Using 48-hour nutrientbroth cultures of B. bronchiseptica, turbin-ate atrophy was produced in four out ofsix pigs. It was found that nine out of tenpigs, all from different herds, harbouredB. bronchiseptica in their nasal passages.

    Ross et al. reported an incidence of B.bronchiseptica of 54% on a herd basis,when they examined the nasal passages offour pigs, from each of 87 swine herds(93). Using egg-passaged B. bronchisep-tica cultures turbinate atrophy was pro-duced in 66% of four-week-old pigs, and in95% of pigs aged one to three days (94).In Canada, it was demonstrated that B.bronchiseptica was present in the nasalpassages of pigs from herds free of thedisease and AR affected herds (85). Cul-tures of this organism were not capableof producing turbinate atrophy in naturallyborn SPF piglets but did so when instilledintranasally into caesarean derived, colos-trum-deprived pigs (86).

    It has been reported that 80% of affectedswine harbored trichomonads in theirnasal passages, whereas the figure for nor-mal pigs was 2.8% (104). The incidenceof nasal trichomonads in pigs has beenreported by other workers as 35.2%, 39.6%,56.3%, and 75-90%, respectively (16, 49,50, 72). The successful transmission of ARto piglets with trichomonads has been re-ported (103) but this has not been con-firmed (50, 69). Trichomonads werefound, in the absence of bacteria, in thenasal passages of pigs on farms where ARoccurred but not on AR-free farms (91).Lyubimoya (72) was able to establishnasal Trichomonas suis in the nasal pas-sages of swine but not trichomonads iso-lated from feces. He noted that while acatarrhal rhinitis occurred, this was notfollowed by turbinate atrophy.From observations of the clinical disease

    and initial experiments, Phillips considereda filterable agent to be important becausehe was able to reproduce sneezing in pigswith the supematant of centrifuged nasalmaterial obtained from pigs with AR(8