scholarly journals Ultrastructural pathology of the upper respiratory tract of rabbits experimentally infected with Pasteurella multocida A:3

1999 ◽  
Vol 67 (2) ◽  
pp. 163-170 ◽  
Author(s):  
M.H. AL-HADDAWI ◽  
S. JASNI ◽  
M. ZAMRI-SAAD ◽  
A.R. MUTALIB ◽  
A.R. SHEIKH-OMAR
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.


1981 ◽  
Vol 90 (3_suppl) ◽  
pp. 1-12 ◽  
Author(s):  
Fred S. Herzon

Nasal and sinus ciliary ultrastructure was evaluated in 16 patients with various pathologies of the upper respiratory tract including sinusitis, nasal polyposis, purulent rhinitis, and rhinitis medicosa. Ultrastructural findings include absent dynein arms, central tubule disorientation, radial spoke defects, atypical microtubule patterns and ciliary membrane abnormalities. Examples of each condition are presented and the implications of these findings are discussed.


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.


Author(s):  
T. I. Stetsko

In the article a literature review of Bovine respiratory diseases (BRD) is presented. Respiratory diseases are considered to be one of the most harmful diseases of cattle, which cause great economic damage for the operators of the cattle industry. The BRD complex is a multifactorial and multi-etiological disease. The BRD complex is a multifactorial and multi-etiological disease. The main factors providing the BRD development are the management status of rearing cattle, the impact of the environment and pathogens. Without neglecting the importance of the first two factors, pathogenic microorganisms remain the major etiological factor of BRD. Respiratory tract infections in cattle are caused by viruses and bacteria, moreover the diseases often develop in an associated form. However, the bacterial factor in the etiology of respiratory diseases plays a main role. Mannheimia haemolytica serotype 1 is the main pathogen of BRD, which can cause disease as a single etiologic agent and as in association with other pathogens (Histophilus somni, Mycoplasma bovis). In most cases, fibrinous pneumonia or fatal acute pneumonia is often associated with Mannheimia haemolytica. Pasteurella multocida is considered to be a less virulent bacteria than Mannheimia haemolytica, and for a higher level of infection need to initiate the inflammatory process in the respiratory tract of animals. Pathogenic strains of Pasteurella multocida serogroup A are a significant etiologic factor of severe enzootic pneumonia in dairy calves. Respiratory diseases caused by mycoplasma remain one of the serious infectious diseases of cattle. Mycoplasma bovis is the most invasive and dangerous mycoplasma for young cattle. This type of mycoplasma is usually present in the upper respiratory tract of clinically healthy calves who are bacterial carriers. When the zootechnical conditions of brieding and feeding the calves are disturbed and for other stress factors there is an active proliferation of mycoplasmas and they successfully colonize the lower respiratory tract of the animals, causing an inflammatory process in the lungs. Other commensal bacteria of the upper respiratory tract, Histophilus somni, can cause pneumonia that usually occurs in subacute or chronic form. The pathogenic forms of this bacteria are often isolated together with Mannheimia hemolytica. Other opportunistic bacteria (Arcanobacterium pyogenes, Streptococcus pneumoniae, Staphylococcus aureus, Chlamydiales spp., Fusobacterium necrophorum, Corynebacterium bovis) may be etiological factors for the development of BRD. Depending on the etiologic agent, the clinical symptoms of calf bronchopneumonia have some specificity, herewith the degree of lung damage depends on the duration of the disease and the virulence of the pathogen.


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