Strongylus equinus: development and pathological effects in the equine host.

The development and pathological effects of Strongylus equinus were studied in 17 pony foals and one horse foal raised in isolation and examined at necropsy from seven days to 40 wk postinfection (PI). Following inoculation of 15000 +/- 6% or 16000 +/- 6% infective larvae by stomach tube foals were monitored for clinical signs and selected blood changes. Larvae penetrated the wall of the ileum, cecum and colon. The molt to the fourth stage occurred mostly in the wall of the ventral colon before 2 wk PI and larvae attained the liver mainly via the peritoneal cavity as early as eight days PI and persisted in the liver until 17 wk PI. Following active migration within the liver, invasion of the pancreas was accomplished at least by 7 wk PI with maximum numbers at 17 wk. The fourth molt occurred about 15 wk PI and preadults were present in the wall of the ventral colon at 30 wk PI and in the lumen of the colon at 40 wk. Strongylus equinus tends to wander retroperitoneally to the flanks, perirenal fat, diaphragm, omentum and occasionally to the lungs. Between 1 and 4 wk PI small raised hemorrhagic areas were present on the serosa of the ileum and colon. Small white foci on the surface of the liver at 1 wk PI were followed by tortuous tracks 3 wk later. Pathological changes in the pancreas were evident at three months PI and more severe by four months. Granulomas containing larvae were common in the flanks, diaphragm, omentum and occasionally beneath the pleura of the lungs. Clinical signs were correlated with invasion of the pancreas, the fourth molt, maximum globulin values and high eosinophil counts.     

Experimental studies on the pathogenicity of Mycoplasma ovipneumoniae and Mycoplasma arginini for the respiratory tract of goats.

Mycoplasma ovipneumoniae and Mycoplasma arginini were the species of Mollicutes most commonly isolated from 175 goats with respiratory disease in Ontario. The pathogenicity of M. ovipneumoniae, strain B321B and M. arginini, strain D53e, was assessed in goats following endobronchial inoculation. One out of three two year old goats developed fever after inoculation with a pure culture of strain B321B, and it had extensive subacute fibrinous pleuritis when necropsied three weeks later. Neither of the remaining goats had lesions in the respiratory tract. Mycoplasma ovipneumoniae was recovered from one of the animals four days after inoculation, but not at necropsy from any of the goats, at which time a marked humoral immune response with growth inhibiting antibodies was detected. In a second experiment three four to five week old goats were inoculated with the same strain and three other goats were given placebo treatment. One experimental goat developed fever and coughing, and it had extensive subacute fibrinous pleuritis in the right side and pneumonia. Another goat had focal pneumonia in the left diaphragmatic lobe. Microscopically there was subacute hyperplastic suppurative bronchiolitis, atelectasis and nonsuppurative alveolitis. The infected animals did not clear the mycoplasma and not all of them produced antibodies. Mycoplasma arginini, strain D53e, did not induce lesions in any of four goat kids within 14 days after inoculation but did cause transient elevations in rectal temperature, circulating monocytes, circulating neutrophils and blood fibrinogen. Mycoplasma arginini was infective and immunogenic for all inoculated animals and showed a particular affinity for the tonsil. Thus, this study provides the first evidence that M. ovipneumoniae is pathogenic for goats causing pneumonia and pleuritis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ascaris suum Infection in Calves III. Pathology

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.     

Ascaris suum Infection in Calves I. Clinical Signs

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.     

Detection of Aphanomyces invadans and epizootic ulcerative syndrome in the Murray‐Darling drainage

Epizootic ulcerative syndrome was diagnosed, and the presence of Aphanomyces invadans confirmed, from an outbreak of clinical disease in wild‐caught bony bream (Nematalosa erebi) from the Darling River near Bourke, in New South Wales, Australia, during 2008. This confirms a significant extension of the agent beyond its historical range.     

Involvement of ATP‐sensitive K+ channels in the peripheral antinociceptive effect induced by ketamine

ObjectiveTo investigate the contribution of K⁺ channels on peripheral antinociception induced by ketamine.Study designProspective experimental study.Animals110 male Wistar rats weighing 160–200 g.MethodsThe paw pressure required to elicit limb flexion was designated as the nociceptive threshold. Hyperalgesia was induced by intraplantar injection of prostaglandin E₂. All drugs were administered locally into the right hind paw of rats. Ketamine was administered into the right hind paw 2 hours and 55 minutes after local injection of PGE₂. Tetraethylammonium was administered 30 minutes prior to ketamine and the other K⁺ channel blockers, glibenclamide, dequalinium and paxilline, were administered 5 minutes prior to ketamine.ResultsProstaglandin E₂ (2 μg per paw) induced hyperalgesia. Ketamine (10, 20, 40 and 80 μg per paw) elicited a local peripheral antinociceptive effect that was antagonized by a specific blocker of ATP‐sensitive K⁺ channels, glibenclamide (20, 40 and 80 μg per paw). In another experiment, the non‐selective voltage‐dependent K⁺ channel blocker tetraethylammonium (30 μg per paw) and small and large conductance blockers of Ca²⁺‐activated K⁺ channels, dequalinium (50 μg per paw) and paxilline (20 μg per paw), were ineffective at blocking the effect of a local ketamine injection.Conclusions and clinical relevanceAnalysis of these results provides evidence that ketamine, may in part, induce peripheral antinociceptive effects by ATP‐sensitive K⁺ channel pathway activation.