Pathology of experimentally induced quail bronchitis

Bobwhite quails (Colinus virginianus) were inoculated with 10(6) mean tissue-culture infective dose of quail bronchitis virus at 1, 3, 6, or 9 weeks of age by intratracheal, intraperitoneal, or subcutaneous routes. Quails developed necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia; multifocal necrotizing hepatitis; necrotizing splenitis, with or without hyperplasia of splenic mononuclear phagocytes; bursal lymphoid necrosis; and bursal atrophy. Lesions were more extensive and severe in quails inoculated at 1 or 3 weeks of age than in older quails. Large intranuclear inclusions, characteristic of adenovirus infection, were identified in trachea, lung, liver, and bursa of Fabricius. This is the first report of the histopathology of experimentally induced quail bronchitis.     

Adult Coturnix quail bronchitis

Quail bronchitis was confirmed by recovery of fowl adenovirus serotype 1 from 2 flocks of adult birds (Coturnix coturnix japonica) that were reared commercially for their eggs in the Republic of Singapore. Both flocks were reported to have a fall in egg numbers of 10-15%. The main clinical signs were respiratory distress and soft-shelled and white eggs lacking shell pigmentation.     

Observations on erythrocytic acetylcholinesterase activity in experimentally induced anaplasmosis in calves

Erythrocytic acetylcholinesterase (AChE) activity was assessed in splenectomized bovine calves inoculated with Anaplasma marginale. Other parameters, i.e., haematological values (haemoglobin, packed-cell volume, and total erythrocytic count), percentage parasitaemia and the ensuing host reactions during Anaplasma infection were also studied in relation to AChE activity. There was significant inhibition of red blood cell-AChE activity commencing soon after inoculation of infected blood; this preceded a substantial decrease in haematological values along with high parasitaemia. The changes in AChE activity may possibly be associated with increased cell membrane permeability, thus triggering the entry of A. marginale organisms into red blood cells.     

Isolation of avian infectious bronchitis virus from experimentally infected chickens.

Virus was recovered from the faeces of chickens infected at three or four weeks of age for more than 20 weeks after infection with commercial vaccines or with the T strain of avian infectious bronchitis virus (IBV). Virus was not recovered from the trachea, liver, spleen, bursa or kidneys of T strain infected birds longer than 29 days after infection at which point IBV was recovered from the bursa of a single infected bird. In a subsequent experiment IBV was recovered from the caecal lymph nodes and faeces of one of five birds 14 weeks after infection with a commercial vaccine but no virus was isolated from the trachea, kidneys, duodenum, bursa, ovaries or testes of any of the five birds at this time.     

Nephropathogenesis of chickens experimentally infected with various strains of infectious bronchitis virus

Four-day-old specific-pathogen-free chickens were inoculated by eyedrop with four different strains (Gray, JMK, CV56b, and Wolgemuth) of infectious bronchitis virus (IBV). Birds were monitored clinically and euthanatized at 1, 4, 7, and 14 days postinfection and tissues were collected for virus isolation, histopathologic examination, in situ hybridization (ISH), and immunohistochemistry (IHC). Clinical disease was severe in chickens infected with Wolgemuth, but no overt disease was observed with the other strains. Virus was isolated from the kidneys of chickens infected with the Gray-, CV56b-, and Wolgemuth-strains of IBV. Histologically, interstitial nephritis was evident in chickens infected with these same 3 strains. However, viral nucleic acid and antigen were detected only with Wolgemuth-infected kidneys by ISH and IHC. These results indicate that the pathological changes in kidneys from chickens infected with Gray and CV56b may not have resulted from the cytolytic action of the virus.     

Ultrastructural and cytochemical studies in normal Japanese quail (Coturnix coturnix japonica) eosinophils and in those from birds with experimentally induced eosinophilia

Normal eosinophil development in the Japanese quail (Coturnix coturnix japonica) was similar to that described in the fowl and the duck, with granulogenesis occurring in the Golgi apparatus. The characteristic lipid droplets were small in the immature eosinophils, and after staining specifically for lipid, small moieties were also traced to the Golgi apparatus. In mature eosinophils the lipid droplets measured between 1.0 and 1.5 micron in diameter and they were surrounded by profiles of smooth endoplasmic reticulum. Eosinophilia was difficult to induce in quails; injections of either horse serum or bovine serum albumin (BSA)/aluminium hydroxide produced a poor response. In some quails in which eosinophilia was produced, however, eosinophil granules showed many crescentic and vacuolated forms. The lipid droplets in the activated eosinophils were fused in many cells to form large intracellular aggregates of lipid. Quail eosinophils, which hitherto have been regarded as peroxidase-negative, had strong activity in the lipid droplets of cells from stimulated birds. It is postulated that this peroxidase-positive reaction may represent a form of ceroid or lipofuscin pigment resulting from lipid peroxidation. Acid phosphatase and trimetaphosphatase reactions were reduced in many activated cells, with a large proportion of granules being non-reactive. The results of dietary manipulations in quails appear to suggest that in stressful situations the eosinophil metabolism is altered and there is a reduction in the number of lipid droplets in the cell.     

鸡传染性支气管炎人工感染模型的中药保护作用

传染性支气管炎(IB)是由传染性支气管炎病毒(IBV)引起的急性、高度接触性呼吸道传染病,其特征是咳嗽、打喷嚏和气管哕音、呼吸困难.该病可引起鸡的增重、饲料报酬以及生产性能降低,当继发或并发感染支原体或大肠杆菌等时可使鸡群死亡率增加,是严重危害世界养禽业的重大传染病之一.由于IBV毒株具有高度易变异和多血清型的特点,给该病的免疫和防治带来了很大困难,因此,研制有效的防治药物具有重要意义.     

Immunopathogenesis of experimentally induced proliferative enteropathy in pigs

To characterize the immune response associated with Lawsonia intracellularis infection, twenty-eight, 7-week-old pigs were dosed orally with a pure culture of L. intracellularis. Animals were killed 3, 7, 14, 21, 28, 35, and 42 days postinfection. Light microscopic studies were undertaken to immunophenotype the immunologic response using specific antibodies to T-cell subsets (CD3, CD4, and CD8), B cells, major histocompatibility complex class II, cadherin, and macrophages over the course of time. The results indicate that there is a direct association between the presence of L. intracellularis and reduced T-cell and B-cell numbers. For the first time, this provides evidence of the presence of an immunosuppressive mechanism operating in this disease. Furthermore, macrophage marker studies indicated that macrophages may play a more complex and significant role in the disease process than has been previously reported, with activated macrophages accumulating in infected hyperplastic crypts.     

Ultrasonographic imaging of experimentally induced pancreatitis in cattle

This study was conducted to determine the ultrasonographic patterns of pancreatitis evoked in cattle, with reference to laboratory and pathological findings. Using ultrasonographic guidance, acute necrotizing pancreatitis was induced in six cows by injecting chloroform into the pancreatic tissue. Ultrasonographic examination was then performed once daily for nine days. Pancreatic lesions were visible 24h after induction of pancreatitis, as represented by a uniform increase in echogenicity and by intralobular and subcapsular fluid accumulation. As the experiment progressed, patchy hypoechogenic foci appeared within the gland parenchyma. Amylase and lipase activities showed rapid increases. Post mortem examination revealed gross and microscopic necrotic and haemorrhagic lesions in the body and right lobe of the pancreas, accompanied by oedema and fibrosis. Ultrasonography was found to be extremely useful for the detection and characterization of experimentally induced pancreatitis and to monitor its progression in the cow. These findings are of potential value as a reference for the diagnostic workup of bovine pancreatitis, and ultrasonography is seen as a promising non-invasive technique for the diagnosis of suspected pancreatitis in cattle.     

Healing of experimentally induced corneal ulcers in horses

Corneal ulcers to the depth of the anterior third of the stroma were created surgically in both eyes of 10 ponies. One eye in each pony was treated topically with chloramphenicol and 1% atropine ophthalmic ointments 3 times per day; the contralateral eye was not treated topically. All ponies were given phenylbutazone orally for relief of ocular pain. Fluorescein-stained ulcers were measured once a day. The median healing time of the treated eyes (11 days) and the median healing time of the nontreated eyes (13.5 days) were found not to be significantly different. Clinically, however, more severe complications arose in the nontreated eyes.     

Neutrophil apoptosis during experimentally induced Staphylococcus aureus mastitis

The objective of this study was to determine whether neutrophil apoptosis and their consequent elimination by macrophages from the mammary gland is modulated by an infection caused by Staphylococcus aureus (S. aureus). The study was performed on twenty mammary glands of 5 virgin heifers. A buffered physiological solution (PBS) was administered as a means of control into the mammary glands of the heifers and after 168 h, the glands were inoculated with S. aureus. The samples of cell populations were obtained by lavages of the mammary glands in 4 intervals (24, 48, 72 and 168 h) after the experimental infection. Flow cytometry was used for determination of Annexin-V positivity and propidium iodide (PI) negativity of neutrophils. Light microscopy was used for determination of neutrophil karyopyknosis. Cytochemistry was used for the detection of myeloperoxidase-positive (MPO+) macrophages. Instillation of S. aureus resulted in an intramammary infection which persisted during the following experimental period. The total number of both Annexin-V-positive and PI negative neutrophils and karyopyknotic neutrophils peaked at 24 h after both of PBS and S. aureus administration. The highest percentages of Annexin-V-positive and PI negative neutrophils and karyopyknotic neutrophils were detected 48 and 168 h after PBS and S. aureus administration, respectively. The total number of MPO+ macrophages was the highest 24 h and 48 h after PBS and S. aureus administration, respectively; the percentage of MPO+ macrophages was the highest at 72 h in both cases. The dynamics of resolution of mastitis caused by S. aureus was very similar to the resolution of inflammatory response of the mammary gland after PBS administration. Mechanisms of cell pathogen elimination as well as inflammation resolution were very intensively involved; nevertheless, the mammary gland infection persisted. An early inclusion of the mechanisms of an acute inflammatory resolution thus paradoxically led to chronic infection.     

Acute experimentally induced aflatoxicosis in the weanling pony

Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.     

Streptokinase treatment of cats with experimentally induced aortic thrombosis

An investigation was initiated to determine the dosage of streptokinase (given IV) that would consistently produce systemic fibrinolysis, as determined by laboratory evaluation, and to determine the relative safety of this drug in the cat. Results indicated that a loading dose of 90,000 IU of streptokinase (given by continuous infusion over 20 to 30 minutes) and a maintenance dosage (IV) of 45,000 IU of streptokinase/hr predictably produced systemic fibrinolysis in the cat. There were no detectable adverse affects seen on physical examination, necropsy, or histopathologic examination. Using the foregoing dosage regimen, investigation was begun to evaluate the use of streptokinase for treatment of feline thromboembolism. Aortic thrombosis was created experimentally in 15 cats. There was no clearly predictable improvement in nonspecific venous angiograms or thermal circulatory indices for the cats given streptokinase, compared with the values for the control cats. After a total of 180 minutes of treatment, the mean weight of remaining clot removed at necropsy from the aortic trifurcation was 7.3 mg in the streptokinase-treated cats, compared with 13.4 mg in the control cats.