Development of turbinate lesions and nasal colonization by Bordetella bronchiseptica and Pasteurella multocida during long-term exposure of healthy pigs to pigs affected by atrophic rhinitis.

Natural transmission of atrophic rhinitis from pigs from a herd with an endemic atrophic rhinitis problem to pigs from a herd free of atrophic rhinitis was demonstrated. Six replicates each with five pigs from the endemic atrophic rhinitis herd (Group A) and five pigs from the atrophic rhinitis-free herd (Group B) were housed together from 5 wk of age, with each replicate kept in isolation rooms maintained at optimal and controlled environmental conditions. Three replicates each with six pigs/room from the atrophic rhinitis-free herd (Group C), served as nonexposed controls. Group C pigs remained healthy and had no turbinate atrophy at either 10 or 17 wk of study (atrophic rhinitis score = 0 on a 0 to 3 scale). Group A pigs had a mean atrophic rhinitis score of 1.85 +/- 0.84, and group B pigs developed atrophic rhinitis to a mean score of 1.57 +/- 0.70. The isolation rate and quantity of Pasteurella multocida found on nasal swabs was directly related to lesions while those for Bordetella bronchiseptica were inversely related to turbinate atrophy. Of the various types of P. multocida evaluated, nontoxigenic type A and toxigenic type D were both directly related to atrophic rhinitis while nontoxigenic type D strains were not. No toxigenic type A P. multocida strains were isolated.

[Epidemiological problems of ozena and the means for controlling this infection]. / Voprosy épidemiologii ozeny i puti bor'by s étoi infektsiei.

Clinical, bacteriological, serological and epidemiological studies of ozena morbidity among the population of Minsk were carried out in 1970-1980. On January 1, 1981, the ozena morbidity rate among the inhabitants of Minsk was 26.72%. Ozena was found to affect mainly children and women. A wide spread of the family foci of this disease (31.68%) was revealed. The results of this study indicate that the source of K. ozaenae is a sick person who begins to excrete the bacteria in the prodromal period of the disease and may continue to excrete them for many years. The transfer of K. ozaenae occurs probably by droplet or contact infection. The droplet infection is less active in the absence of symptoms (coughing, sneezing) facilitating excretion of the infective agent into the air and in cases of the low susceptibility of persons to ozena. The main measures for controlling ozena are the timely detection and sanitation of the sources of ozena, as well as the current disinfection of the infection foci in apartments.

[Contamination and age as factors in the pathogenesis of atrophic rhinitis (author's transl)]. / De invloed van besmetting en leeftijd op het ontstaan van atrofische rhinitis.

The relationship between contamination with Bordetella bronchiseptica or Pasteurella multocida and the age of the piglets on the one hand and the pathogenesis of atrophic rhinitis on the other, is discussed. Minimal disease-free piglets born and reared on farms on which pigs affected with clinical atrophic rhinitis were present, developed clinical atrophic rhinitis at the age of six weeks. Piglets born in the Central Veterinary Institute (CVI) of sows from herds including pigs affected with atrophic rhinitis and reared under normal CVI conditions, did not develop clinical atrophic rhinitis. These sows are believed to be factors of minor importance in the pathogenesis of clinical atrophic rhinitis in piglets. When minimal disease-free piglets were contaminated during the third or fourth week of life, a slight degree of foreshortening of the upper jaw was observed in three out of nine pigs, the carcase weights of these animals not differing markedly from those of normal swine. When they were contaminated at the age of eight weeks, clinical atrophic rhinitis did not appear. It is essential that young piglets should be protected against atrophic rhinitis during the first few weeks of life.

Atrophic rhinitis in swine fattener herds. A field study of the spread of the disease with infected pigs bought at market.

In three different fattener herds pigs primarily AR infected as baby piglets were mixed in the fattening units with healthy pigs at an age of 11--13 weeks. Snout alterations were registered on cut snouts at a slaughter weight of about 70 kg. Severe AR was registered in the groups of primarily infected pigs (Tables I--III). The incidence of snout alterations was lower in the groups of pigs infected at an age of 11--13 weeks, but was much higher than in the groups of healthy control pigs or in the normal pig population in the region (Table IV). The results indicate that pigs infected at a rather late age in the fattening units can develop severe atrophic rhinitis.