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1.
Two experiments were conducted. In the first, 16 crossbred Hereford calves were divided into two equal groups. The first group was vaccinated intranasally with a commercial vaccine against bovid herpesvirus 1 and the second group was unvaccinated. The calves were later exposed to an aerosol of bovid herpesvirus 1 (strain 108) for five minutes. Four calves from each group were subjected to transportation and four calves from each group were kept in an environmental chamber for four days. Four days after viral aerosol all calves were exposed to an aerosol of Pasteurella haemolytica and the same subgroups were again transported or held in the chamber for a further four days.

The calves that did not die from pneumonia were necropsied ten days after the final day of transport. Pulmonary lesions were present in both vaccinated and control animals but were less extensive in the vaccinated calves. Six of eight vaccinated but none of the eight control calves survived.

In the second experiment, eight crossbred Hereford calves were divided into two equal groups. One group was vaccinated with bovid herpesvirus 1 (strain 108) and the other acted as controls. Four weeks later all calves were sequentially exposed to aerosols of bovid herpesvirus 1 (strain 108) and P. haemolytica four days apart. Three of the four controls but none of the vaccinates died from pneumonia. Every lobe of the lungs in all the controls was affected by pneumonia while no pulmonary lesions were found in the vaccinated calves. The differences in efficacy of the modes of vaccination and the possible role of transport stress are discussed.

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2.
Four month-old foals were infected orally with 75 mL of a suspension of 5.0 × 108 Corynebacterium equi per mL. Two foals were killed after ten days and had scanty number of C. equi in the caeco-colic lymph nodes. No C. equi were recovered from the other two foals, killed 20 days after infection. No gross pathological change was detected in these four foals, although mild microscopic lesions were seen in the ileum of one foal. Results of lymphocyte blastogenesis using peripheral blood lymphocytes and C. equi antigens showed, however, that lymphocytes became sensitized to C. equi following this challenge.

In a second experiment four month-old foals were given orally the same dose of organisms but on five consecutive days. Two foals were killed ten days after infection and showed mild histological changes in the large bowel mucosa and C. equi could be recovered from all intestinal lymph nodes cultured. In one of these foals moderate numbers of C. equi were present in the bronchial lymph node. Of the other two foals, one died after 22 days with severe ulcerative enterocolitis and intestinal lymphadenitis. Only one small pulmonary abscess was detected despite large numbers of C. equi in the lungs. The other foal developed similar intestinal changes and was euthanized 25 days after infection. No C. equi were detected in the lungs or bronchial lymph node. Lymphocyte blastogenesis in these animals showed a rapid rise in response to C. equi antigens.

These studies suggest that C. equi pneumonia in foals does not always arise from an intestinal infection, that minor intestinal infection causes a cellular immune response and that massive exposure of the bowel over a sustained period is necessary to induce intestinal lesions.

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3.
The influence of pulmonary edema, hydrocortisone, immunization against Pasteurella hemolytica and concurrent infection with parainfluenza-3 virus upon pulmonary clearance of aerosolized P. hemolytica was studied in 31 calves. Following the various treatments calves were challenged with an aerosol of P. hemolytica. One control calf was killed immediately after the aerosol and the numbers of bacteria in the lung taken as 100%. Two calves were killed four hours after challenge and the numbers of bacteria in the lungs were compared to the 100% of the control calf. The result was the percentage clearance of bacteria at four hours.

Pulmonary edema was induced by three different methods: by an aerosol of histamine, by intravenous injection of endotoxin and by intravenous injection of croton oil emulsion. The edema impaired the clearance of P. hemolytica, which was reflected in high numbers of P. hemolytica present in the lungs at four hours after challenge: 260% after histamine, 300% and 400% after endotoxin and 92% after croton oil.

Six days of treatment of four calves with high doses of hydrocortisone acetate produced inconsistent results: two calves treated with a higher daily dose (36 mg/kg) had normal clearance whereas two calves treated with a lower dose had pulmonary edema and displayed lowered clearance with 111% and 31% respectively of P. hemolytica retained in the lungs four hours after challenge.

Immunization of calves by three different methods, a subcutaneously injected bacterin of P. hemolytica (2 calves), single aerosol (2 calves) and four aerosols (4 calves) of live P. hemolytica was reflected in an accelerated pulmonary clearance of P. hemolytica (with a mean of 1.55% of bacteria retained at four hours).

Concurrent infection with parainfluenza-3 virus did not lower the clearance of P. hemolytica in the lungs of 12 calves over 15 days except on the first day following the exposure to parainfluenza-3 virus. These calves had hemagglutinating antibodies against P. hemolytica before exposure.

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4.
Gross changes in the lungs of Ascaris suum- infected calves consisted of atelectasis and hemorrhagic foci, edema and emphysema, frequently with bullae. Prominent microscopic lung lesions were edema and emphysema of the interlobular septa with large numbers of eosinophils within and around lymphatics, peribronchiolar lymphoid nodules and parasitic granulomas. Many of the microscopic features were consistent with those found in atypical interstitial pneumonia. Changes in the alveoli were atelectasis, the exudation of plasma proteins, mononuclear cells and eosinophils, and alveolar wall thickening. Lesions found later included fibrosis and fetalization of the alveolar walls. Plasma cells and neutrophils were not common. Challenge with Toxocara canis after sensitization with A. suum resulted in the lungs developing a few areas of atelectasis. Migration of T. canis to lungs of calves is slower than A. suum. A. suum larvae were always found in bronchi, bronchioles and alveoli of calves that died. Lesions were observed in the liver but not the kidney of A. suum infected calves; both lung and liver lesions tended to resolve with time.  相似文献   

5.
In four outbreaks of indoor calf pneumonia, dyspnoea was a prominent clinical finding. At necropsy it was associated with pneumonia involving the cranial lobes of the lung and severe pulmonary emphysema. Histological examination of lung tissue revealed bronchiolitis and alveolitis with alveolar epithelial cell hyperplasia and multinucleate syncytium formation. Intraalveolar haemorrhage, intra-alveolar oedema and hyaline membrane formation were also noted. In all cases parainfluenza type 3 (PI3) virus was isolated from the lungs. In each of the four outbreaks there was evidence of PI3 virus and respiratory syncitial virus (RSV) infection.  相似文献   

6.
Thirteen of 100 fallow deer, aged between 6 months and 10 years, died over a 5 week period. The deaths occurred in 2 outbreaks 3 weeks apart. Both outbreaks were preceded by at least 3 days of cold wet and windy weather, and were associated with water-logged pastures. Affected animals were usually found dead, with a frothy blood-stained nasal discharge. In the 8 deer necropsied, gross lesions included widespread subserosal petechial haemorrhages, severe pulmonary congestion and oedema with froth-filled airways, and fibrinous pneumonia and pleurisy in 4 deer. Two deer, also, had extensive subcutaneous petechial and ecchymotic haemorrhages and oedema of skeletal musculature. Histologically, the most significant lesions were present in the lungs. Moderate to severe pulmonary congestion and oedema, with fibrinous exudation into alveoli and septal oedema, were present in all deer. In some deer these changes were accompanied by a diffuse infiltration with polymorphonuclear leucocytes. Pasteurella multocida was isolated from a range of tissues from 7 of 8 deer examined. The remaining animal had been treated with antibiotics 8 hours before death. The isolates had identical polyacrylamide gel electrophoresis patterns and were of the same antigenic type-Carter group A, Heddleston type 3,4.  相似文献   

7.
Ascaris suum Infection in Calves I. Clinical Signs   总被引:2,自引:2,他引:0       下载免费PDF全文
Clinical signs consistent with those of atypical interstitial pneumonia (AIP) were induced in calves sensitized with infective Ascaris suum eggs at seven to 20 weeks of age and challenged at three-week intervals one or more times. These signs usually appeared on the sixth or seventh day postinfection and reached maximum severity between the tenth and 13th days following infection. Prominent signs were: dyspnea, often with expiratory grunt, coughing, mouth breathing and emphysema as well as increased respiration and heart rates. In general, the intensity of signs was dependent upon dose size, although a single small dose resulted in acute signs and death in one calf. Intermittent coughing and vesicular sounds were induced in calves given A. suum eggs continually over prolonged periods. No respiratory abnormalities resulted from challenge with Toxocara canis after sensitization with A. suum. Antihistamine therapy did not alter the clinical signs in A. suum infected calves.  相似文献   

8.
9.
Naturally occuring outbreaks of Ascaris suum infection in calves have usually beeen found in animals nine to 12 months of age. The circumstances surrounding these outbreaks suggest that yearling calves are either particularly susceptible to a primary exposure to A. suum or react strongly to A. summ after sensitization early in life to this or some related ascarid. To determine the effect of reinfection with A. suum nine to 12 months after varying levels of exposure to this nematode, six calves were inoculated with 200,000 to 9,000,000 eggs. Neither death nor, in general, severe clinical signs resulted from reinfection. All calves were examined 15 days after reinfection with pathological changes noted only in the lungs and consisting of emphysema, alveolar wall thickening as well as accumulations of fibrin, eosinophils and hemorrhage in the lumina of alveoli. The findings suggested that exposure to A. suum early in life is not a factor in the development of disease in calves infected at one year of age. It was also found that the eosinophilia that develops following a primary infection with A. suum evidently persists for at least one year.  相似文献   

10.
An outbreak of fibrinous pleuropneumonia was observed in October 1971 in Saskatchewan on a farm of 900 feeder pigs. Morbidity and mortality were low. Pathologic-anatomic findings included fibrinous pleuritis, pulmonary vascular thrombosis and necrotizing fibrinous pneumonia. Hemophilus parahemolyticus was isolated from the lungs of affected animals. In addition pulmonary lesions were found which suggested an adenovirus infection. It was speculated that the viral infection possibly predisposed the pigs to the Hemophilus infection. The H. parahemolyticus isolate was sensitive to common antibiotics.  相似文献   

11.
A 1.5‐year‐old, 23 kg intact male Dalmatian dog was evaluated for acute respiratory insufficiency without a previous history of trauma or toxic exposition. Imaging revealed pneumomediastinum, pneumothorax, diffuse unstructured interstitial pulmonary pattern, pulmonary interstitial emphysema, and pneumoretroperitoneum. Histopathological evaluation of the lungs revealed perivascular and peribronchial emphysema, mild lymphocytic interstitial pneumonia with atypical proliferation of type II pneumocytes in bronchioles and alveoli. A lung disease resembling fibrosing interstitial pneumonia in man and cats has been previously reported in Dalmatians and should be included as a differential diagnosis for Dalmatians with this combination of clinical and imaging characteristics.  相似文献   

12.
Guinea pigs and swine were exposed to sulphur dioxide concentrations varying from 5-40 P.P.M.

The average daily weight gains of young guinea pigs were impaired by gas concentrations of 10 P.P.M. and 18 P.P.M. for periods of 96 hours or more. A single experiment failed to indicate any synergism between sulphur dioxide and hydrogen sulphide. Studies on the effect of exposure to 5 P.P.M. for an extended period were inconclusive.

Young swine under seven days of age were exposed to sulphur dioxide concentrations of 5, 10, 20, and 40 P.P.M. for a single eight-hour period for each group. All concentrations caused the animals to display some evidence of irritation from the gas, ranging from eye irritation, nasal secretion, salivation and altered respirations at levels of 10 P.P.M. and higher to slight eye irritation and salivation at levels of 5 P.P.M. Haemorrhage and emphysema were present in the lungs of swine exposed to 40 P.P.M., and sacrificed at twenty-four hours and seven days post-exposure. At 158 days post-exposure, two of two swine exposed to 40 P.P.M., and one of two swine exposed to 20 P.P.M. showed a pulmonary fibrosis that was attributed to the gas.

Impaired weight gains of exposed animals raised to market weight (158 days) could not be attributed to the gas.

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13.
Immunofluorescent staining has been used to identify Mycoplasma hyopneumoniae in smears of broth cultures, in infected pig testicle cell cultures, and in frozen cut sections of pneumonic lungs from field and experimentally produced cases of enzootic pneumonia. In the pneumonic pig lung, fluorescent staining was limited to the surface of the bronchial and bronchiolar epithelium and to the contained exudate. In a series of trials using experimentally infected pigs fluorescence was not detected until 25 days post-infection and was regularly seen in pigs killed thereafter. Porcine immune globulin precipitated from the serum of experimentally infected pigs and conjugated with fluorescein isothiocyanate was reactive and specific for the detection of M. hyopneumoniae. Immune globulin conjugates prepared from the serum of hyperimmunized rabbits were reactive but in some cases produced a faint non-specific staining of frozen tissue sections. No such non-specific reactions were noted on stained culture smears or cell cultures.

Fluorescence was not seen in known positive preparations stained with non-immune pig globulin conjugates or in preparations from uninoculated cell cultures or pigs, stained with non-immune or immune globulin conjugates.

Mycoplasma hyorhinis was detected by immunofluorescent staining with homologous conjugates, in smears of broth cultures and in tissue sections from pigs with polyserositis.

Immunofluorescent staining was found to be species specific and useful for the early species identification of mycoplasma isolated from pigs.

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14.
This study was carried out with the aim of identifying types of gross and histopathological lesions in lungs of camels slaughtered between October 2009 and April 2010 at Addis Ababa abattoir enterprise, Ethiopia. All camels were originated from Borana and Kereyu areas. A total of 387 slaughtered camel lungs were inspected during the study period. Of which, one or more gross lesions were encountered on 300 lungs. Lesions were further subjected for detail gross and histopathological examinations. The occurrence of pulmonary lesions was 77.5%. The gross and histopathological examination of these lesions had revealed 60.2% emphysema, 21.2% hydatidosis, 18.6% pneumonia, 10.6% atelectasis, 4.9% aspiration of blood, 3.9% pneumoconiosis, 2.6% pulmonary edema and congestion, 1.6% abscess, 1% pleurisy, and 0.8% granulomatous pneumonia. Most camels had one or more pulmonary lesions on postmortem examination, but they were apparently healthy during antemortem inspection. Therefore, the prevailing stressful environmental condition coupled with the existing poor level of veterinary service in camel-rearing areas of the country might reverse these hidden inactive lesions and thereby contributed for the higher occurrence of respiratory diseases in camels.  相似文献   

15.
The antibody response in serum and nasal secretions of groups of ponies vaccinated or infected with Myxovirus influenzae A-equi 2 was examined. Following infection by aerosol with live virus, a weak antibody response was recorded in both serum and secretions. Antibody levels were undetectable in secretions at 31 days after infection.

After primary intramuscular vaccination with killed virus, using sodium alginate as an adjuvant, antibody was detected only in the serum. However, following revaccination, a pronounced antibody response was demonstrated in both serum and secretions. Antibody was still detectable in all four ponies when tested 135 days later.

Only a serum antibody response was detected in ponies after primary intramuscular vaccination with a commercial vaccine. Upon revaccination nasal antibody occurred in all ponies but this only persisted for about 30 days.

Neither serum nor nasal antibody response occurred following intranasal vaccination and revaccination with a killed virus vaccine.

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16.
Summary

Thirty‐five 6‐week‐old guinea fowl keets, seronegative for maternal antibodies to Newcastle disease virus, were infected with Hens strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (IM) or intranasally (IN).

Clinical signs were first noticed four days post infection (PI) in the group infected al but five days PI in the group infected IN with Hens strain of Newcastle disease virus. These clinical signs were similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Hens strain.

The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets.

The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets.

Neither gross or microscopic lesions were observed in keels that had received the Kumarov strain.  相似文献   

17.
An outbreak of acute bovine atypical interstitial pneumonia is reported in association with feeding mouldy hay. Results of serological investigation and of provocation challenge indicated a hypersensitivity pneumonitis due to allergens of Micropolyspora faeni. Macroscopic and microscopic pulmonary changes were predominantly those of oedema and emphysema. These lesions were contrasted with more chronic changes reported in allergic pneumonitis of housed cattle.  相似文献   

18.
Experimental Atrophic Rhinitis in Gnotobiotic Pigs   总被引:5,自引:0,他引:5       下载免费PDF全文
Twenty-nine caesarian derived colostrum deprived germfree pigs were reared in isolators in groups of three to four per isolator. At seven days of age each group was inoculated intranasally with one of four strains of Bordetella bronchiseptica (designated B, J, L and 55B), or Pseudomonas aeruginosa or a mucoid strain of Escherichia coli, all previously isolated from nasal mucus of pigs affected with clinical atrophic rhinitis. Another group was inoculated simultaneously with B. bronchiseptica B and Pasteurella multocida. The animals were observed for clinical signs of atrophic rhinitis and monitored bacteriologically at weekly intervals for seven weeks. Then they were bled for serology and killed and their respiratory organs examined for gross and histopathological lesions.

All of the pigs inoculated with the Bordetellae had inflammation of the nasal mucosa and developed positive serum antibody titers against all four of the Bordetella strains used in this study. Strain J caused sneezing and turbinate atrophy in three of four pigs. One of the three pigs inoculated with strain L died in ten days from bronchopneumonia and pericarditis and had turbinate atrophy. Strains B and B55 caused no turbinate atrophy, but two out of three pigs inoculated with both B. bronchiseptica B and P. multocida had turbinate atrophy. No nasal lesions were observed in the pigs inoculated with E. coli or P. aeruginosa or in the noninoculated germfree controls.

The results indicate a variation in the ability of different strains of B. bronchiseptica to cause turbinate atrophy in pigs and demonstrate that nasal infections by these organisms stimulate serum antibody response. Presence of P. multocida appears to increase the severity of the lesions. As the E. coli and Pseudomonas failed to produce atrophic rhinitis, they are probably of no significance as primary etiological agents in the atrophic rhinitis syndrome in swine.

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19.
Anomalities of the coronary arteries may include one or more of the following variations: abnormal number, abnormal course, or abnormal origin. Many of these anomalies have been described in man.(28) Anomalous origin of the left coronary artery from the pulmonary artery (A.O.L.C.A.) has been estimated (19) to occur in one of 300,000 children and to represent approximately 0.5% of all types of congenital heart disease. In a recent review(28) of these conditions in man, anomalous origin of the right coronary artery from the pulmonary artery (A.O.R.C.A.) had been reported 16 times, A.O.L.C.A. 39 times, and anomalous origin of both coronary arteries from the pulmonary artery (A.O.B.C.A.) 5 times.  相似文献   

20.
Two hundred and three isolates of Pasteurella haemolytica from cattle were studied. They originated from the nasal cavity of cattle in housed herds; the nasal cavity and pneumonic lungs of experimental feedlot calves and from pneumonic bovine lungs submitted for bacteriological diagnosis.

To determine whether a single characteristic or combination of characteristics might be a feature of isolates collected from animals with pneumonic pasteurellosis (Shipping Fever), the following tests were made. Cultures were serotyped by indirect haemagglutination; the ability to produce beta-galactosidase was examined in the ortho-nitrophenyl-beta-D-galactopyranoside (ONPG) test and antibacterial sensitivity tests were done. None of these factors could be directly related to the role of P. haemolytica in “Shipping Fever”.

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