scholarly journals Contributory and Exacerbating Roles of Gaseous Ammonia and Organic Dust in the Etiology of Atrophic Rhinitis

1999 ◽  
Vol 6 (2) ◽  
pp. 199-203 ◽  
Author(s):  
T. D. C. Hamilton ◽  
J. M. Roe ◽  
C. M. Hayes ◽  
P. Jones ◽  
G. R. Pearson ◽  
...  

ABSTRACT Pigs reared commercially indoors are exposed to air heavily contaminated with particulate and gaseous pollutants. Epidemiological surveys have shown an association between the levels of these pollutants and the severity of lesions associated with the upper respiratory tract disease of swine atrophic rhinitis. This study investigated the role of aerial pollutants in the etiology of atrophic rhinitis induced by Pasteurella multocida. Forty, 1-week-old Large White piglets were weaned and divided into eight groups designated A to H. The groups were housed in Rochester exposure chambers and continuously exposed to the following pollutants: ovalbumin (groups A and B), ammonia (groups C and D), ovalbumin plus ammonia (groups E and F), and unpolluted air (groups G and H). The concentrations of pollutants used were 20 mg m−3 total mass and 5 mg m−3 respirable mass for ovalbumin dust and 50 ppm for ammonia. One week after exposure commenced, the pigs in groups A, C, E, and G were infected with P. multocida type D by intranasal inoculation. After 4 weeks of exposure to pollutants, the pigs were killed and the extent of turbinate atrophy was assessed with a morphometric index (MI). Control pigs kept in clean air and not inoculated with P. multocida (group H) had normal turbinate morphology with a mean MI of 41.12% (standard deviation [SD], ± 1.59%). In contrast, exposure to pollutants in the absence of P. multocida (groups B, D, and F) induced mild turbinate atrophy with mean MIs of 49.65% (SD, ±1.96%), 51.04% (SD, ±2.06%), and 49.88% (SD, ±3.51%), respectively. A similar level of atrophy was also evoked by inoculation with P. multocida in the absence of pollutants (group G), giving a mean MI of 50.77% (SD, ±2.07%). However, when P. multocida inoculation was combined with pollutant exposure (groups A, C, and E) moderate to severe turbinate atrophy occurred with mean MIs of 64.93% (SD, ±4.64%), 59.18% (SD, ±2.79%), and 73.30% (SD, ±3.19%), respectively. The severity of atrophy was greatest in pigs exposed simultaneously to dust and ammonia. At the end of the exposure period, higher numbers of P. multocida bacteria were isolated from the tonsils than from the nasal membrane, per gram of tissue. The severity of turbinate atrophy in inoculated pigs was proportional to the number of P. multocida bacteria isolated from tonsils (r 2 = 0.909, P < 0.05) and nasal membrane (r 2 = 0.628, P< 0.05). These findings indicate that aerial pollutants contribute to the severity of lesions associated with atrophic rhinitis by facilitating colonization of the pig’s upper respiratory tract byP. multocida and also by directly evoking mild atrophy.

1998 ◽  
Vol 36 (5) ◽  
pp. 1260-1265 ◽  
Author(s):  
T. D. C. Hamilton ◽  
J. M. Roe ◽  
C. M. Hayes ◽  
A. J. F. Webster

Pigs reared in intensive production systems are continuously exposed to ammonia released by the microbial degradation of their excrement. Exposure to this gas has been shown to increase the severity of the disease progressive atrophic rhinitis by facilitating colonization of the pig’s upper respiratory tract by Pasteurella multocida. The etiological mechanism responsible for this synergy was investigated by studying the colonization kinetics of P. multocida enhanced by ammonia and comparing them with those evoked by an established disease model. Three-week-old Large White piglets were weaned and allocated to five experimental groups (groups A to E). Pigs in groups A and B were exposed continuously to ammonia at 20 ppm for the first 2 weeks of the study. Pigs in group C were pretreated with 0.5 ml of 1% acetic acid per nostril on days −2 and −1 of the study. On day 0 all the pigs in groups A, C, and D were inoculated with 1.4 × 108 toxigenic P. multocida organisms given by the intranasal route. The kinetics of P. multocida colonization were established by testing samples obtained at weekly intervals throughout the study. The study was terminated on day 37, and the extent of turbinate atrophy was determined by using a morphometric index. The results of the study showed that exposure to aerial ammonia for a limited period had a marked effect on the colonization of toxigenic P. multocidain the nasal cavities of pigs, which resulted in the almost total exclusion of commensal flora. In contrast, ammonia had only a limited effect on P. multocida colonization at the tonsil. The exacerbation of P. multocida colonization by ammonia was restricted to the period of ammonia exposure, and the number ofP. multocida organisms colonizing the upper respiratory tract declined rapidly upon the cessation of exposure to ammonia. During the exposure period, the ammonia levels in mucus recovered from the nasal cavity and tonsil were found to be 7- and 3.5-fold higher, respectively, than the levels in samples taken from unexposed controls. Acetic acid pretreatment also induced marked colonization of the nasal cavity which, in contrast to that induced by ammonia, persisted throughout the time course of the study. Furthermore, acetic acid pretreatment induced marked but transient colonization of the tonsil. These findings suggest that the synergistic effect of ammonia acts through an etiological mechanism different from that evoked by acetic acid pretreatment. A strong correlation was found between the numbers of P. multocida organisms isolated from the nasal cavity and the severity of clinical lesions, as determined by using a morphometric index. The data presented in the paper highlight the potential importance of ammonia as an exacerbating factor in respiratory disease of intensively reared livestock.


1990 ◽  
Vol 50 (1) ◽  
pp. 173-182 ◽  
Author(s):  
J. F. Robertson ◽  
D. Wilson ◽  
W. J. Smith

ABSTRACTInfectious atrophic rhinitis is a disease of the upper respiratory tract of pigs, characterized in the live animal by deformation of the snout and conchal atrophy. However, the severity of the disease in pigs on commercial units is highly variable and air quality may be implicated as a significant factor in addition to the recognized pathogens. In this study the aerial environment was monitored in 49 pig buildings on 12 commercial farrowing-finishing units. A total of 1117 pigs from the 12 farms were examined individually at commercial slaughter weight to quantify the severity of conchal atrophy, using snout scoring and morphometric techniques.A number of significant relationships were shown between environmental variables in the farrowing house and the severity of conchal atrophy. Mean snout score (MSS) and the percentage of snouts from each herd sample with a score of three or more (SS3) were correlated with total bacterial counts (r = 0·78 (P < 0·01) and 0-83 (P < 0·01) respectively), counts of 10 [mi to >15 urn particles (r = 0·67 (P <0·05), 0·73 (P <0·05)) and concentrations of gravimetric dust (r = 0·65 (P <0·05), 0·64 (P <0·05)). Concentrations of ammonia were correlated with SS3 (r = 0·68 (P <0·05)).Dust in the first-stage weaner houses was again a significant component of the aerial environment associated with the severity of the disease. MSS and SS3 were correlated with counts of 10 urn to >15 μm particles (r = 0·66 (P <0·05), 0·68 (P <0·05)), concentrations of respirable dust (r = 0·67 (P <0·05), 0·63 (P <0·05)), total dust (r = 0·75 (P <0·05), 0·87 (P <0·001)), and gravimetric dust (r = 0·83 (P <0·01), 0·88 (P <0·001)). The results support the theory that the mass or number of particles present as inspirable aerosols, and the presence of large numbers of viable bacteria may compromise the local defence mechanism of the upper respiratory tract in the pig and facilitate colonization by Bordetella bronchiseptica and Pasteurella multocida. Saturation deficit in the second-stage weaner houses was correlated with both mean morphometric index and SS3 (r = 0·860 (P <0·01) and 0·683 (P <0·05) respectively), and volumetric stocking density in the finishing houses was correlated with both MSS and SS3 (r = -0·84 (P <0·01), -0·64 (P <0·05)). It is hypothesized that the severity of the disease may be lessened by reducing the concentrations of dust, microbes and ammonia which may play a significant role in the development of the disease.


2002 ◽  
Vol 70 (2) ◽  
pp. 481-490 ◽  
Author(s):  
Susan L. Brockmeier ◽  
Karen B. Register ◽  
Tibor Magyar ◽  
Alistair J. Lax ◽  
Gillian D. Pullinger ◽  
...  

ABSTRACT Bordetella bronchiseptica is one of the etiologic agents causing atrophic rhinitis and pneumonia in swine. It produces several purported virulence factors, including the dermonecrotic toxin (DNT), which has been implicated in the turbinate atrophy seen in cases of atrophic rhinitis. The purpose of these experiments was to clarify the role of this toxin in respiratory disease by comparing the pathogenicity in swine of two isogenic dnt mutants to their virulent DNT+ parent strains. Two separate experiments were performed, one with each of the mutant-parent pairs. One-week-old cesarean-derived, colostrum-deprived pigs were inoculated intranasally with the parent strain, the dnt mutant strain, or phosphate-buffered saline. Weekly nasal washes were performed to monitor colonization of the nasal cavity, and the pigs were euthanized 4 weeks after inoculation to determine colonization of tissues and to examine the respiratory tract for pathology. There was evidence that colonization of the upper respiratory tract, but not the lower respiratory tract, was slightly greater for the parent strains than for the dnt mutants. Moderate turbinate atrophy and bronchopneumonia were found in most pigs given the parent strains, while there was no turbinate atrophy or pneumonia in pigs challenged with the dnt mutant strains. Therefore, production of DNT by B. bronchiseptica is necessary to produce the lesions of turbinate atrophy and bronchopneumonia in pigs infected with this organism.


2018 ◽  
Vol 97 (1) ◽  
pp. 65-69
Author(s):  
Elena M. Vlasova ◽  
N. K. Voznesenskiy ◽  
V. B. Alekseev ◽  
A. A. Vorobeva

The working conditions, occupational and non-occupational risk factors, prevalence rate and peculiarities of the course of respiratory diseases in smelters of titanium alloys were studied. Working conditions of smelters are estimated as harmful (class of working conditions: 3.3-3.4.) due to factors: heating microclimate, chemicals (chlorine and hydrochloride, sulfur dioxide, nitrogen oxide), industrial dust. A feature of the respirable dust fraction is the high content of titanium oxide particles of the PM10 dimension. There was made an analysis of the health status of workers exposed to industrial dust, depending on the length of service. Diseases of the upper respiratory tract in smelters of titanium alloys were shown to be prevalent, simple catarrhal nasopharyngitis prevails with the subsequent formation of atrophic rhinitis, its prevalence rate among smelters of titanium alloys increases with the experience. The peculiarity of the development of diseases of the upper respiratory tract in smelters of titanium alloys are: deterioration of nasal breathing in workers with experience of from 1 year to 5 years already, in patients with experience from 10 to 15 years the prevalence of catarrhal nasopharyngitis and atrophic rhinitis as its outcome in cases with experience from 15 to 20 years. The bronchial damage in the smelters of titanium alloys develops under the experience more than 5 years. The clinical forms are dominated by the phenomena of catarrhal bronchitis followed by obstruction of the bronchi progressing with the experience, with the formation of irreversible ventilation disorders. With the depletion of antioxidant protection, as a rule, with long duration of the exposure of up to 10 years, aseptic inflammation is formed, which is pronounced clinically as catarrhal endobronchitis. This is a partially reversible pathological process. The described features of the development and course of respiratory diseases in smelters of titanium alloys should be taken into account during periodic medical examinations in order to timely prevent them


2011 ◽  
Vol 35 (1) ◽  
pp. 42-53
Author(s):  
Al-Najjar S. Sarhad

In order to study the pathogenesis of the Pasteurella multocida in its natural rout of infection, this study was done to investigate and compare its pathogenesis after intranasal and intraocular infection.Thirty (30) rabbits were divided into three groups, the 1st group (n=12) infected with 240 CFU of Pasteurella multocida intra-nasal, the 2nd (n=12) infected with 240 CFU of P. multocida intra-ocular (eye drop), and the 3rd group (n=6) served as control negative. The animals were sacrificed if they did not die naturally at 24-48hr, 3, 6, 9, 30 day post-infection (p.i.). The results showed dullness of the animals with nasal and ocular discharge and some animals dead at 48hr and 72 hr p.i. (two animals from the 1st group and four animals from the 2nd group). The gross examination of the dead and sacrificed animals showed hemorrhage in the upper respiratory tract with fibrinous pleuropericaditis and emphysematous lung in the 1st group, while the 2nd group showed eye opacity and in some animal’s eye swelling in addition to the feature noticed in the 1st group. Pasteurella multocida was isolated from the organs of all the infected animals.The histopathological changes in the 1st group were more intense than the 2nd group and concenterated at the upper and lower respiratory tract as acute hemorrhagic treacheatis with fibrinous pneumonia , while the kidney showed hypercellularity of the glomeruli with cellular degeneration of renal tubule and lymphocytic hepatitis, also there is focal gliosis. Conclusion, intranasal infection was the effective route and the main pathological changes observed in the respiratory system characterized by fibrinous pleuropneumonia.


PEDIATRICS ◽  
1992 ◽  
Vol 89 (6) ◽  
pp. 1262-1265
Author(s):  
JEFFREY L. WINTERS ◽  
WILLIAM N. O'CONNOR ◽  
ROBERT A. BROUGHTON ◽  
JACQUELINE A. NOONAN

Bordetella bronchiseptica is primarily an animal pathogen, responsible for canine tracheobronchitis (kennel cough) and bronchopneumonia, as well as porcine atrophic rhinitis and otitis media. It readily colonizes the upper respiratory tract and oropharynx of these species.1 This organism rarely has been recognized as a human pathogen, causing mild upper respiratory tract infections in animal caretakers,1 subacute bacterial endocarditis,2 and a pertussis-like illness in children.3 Although asymptomatic nosocomial colonization of humans occurs,4 it also has been reported in immunocompromised Patients as a cause of sepsis,5 peritonitis,6 bronchitis,4,7 and pneumonia.4,8-13 To date, seven cases of human B bronchiseptica pneumonia have been reported in the literature with five of these occurring in immunocompromised patients.


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