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Biomedical subjects

B M McCraw

Publications and source records attributed to B M McCraw.

33 records · Page 2Linked to original sources
PubMed1975

Experimentally induced Fasciola hepatica infection in white-tailed deer. II. Pathological features.

Six white-tailed deer (Odocoileus virginianus) and six sheep were inoculated with metacercariae of Fasciola hepatica. Two animals of each species were given 100, 500 or 2500 metacercariae. One animal in each inocluated group was killed and examined at six weeks postinoculation and the remainder at 15 weeks postinoculation. At six weeks postinoculation the parietal surface of the livers from inoculated deer was covered with gray fibrous plaques and rust colored patches. Fibroplasia with mononuclear cell infiltration characterized Glisson's capsule on the parietal surface. Granulomas were found in the hepatic parenchyma and on the dorsal surface of the lung. Fresh and healing tracks were occasionally found in the liver. In the sheep fibrinous exudate and numerous subcapsular tracks were found on both surfaces of the liver. Inflammatory changes in portal areas and numerous fresh and healing tracks in the hepatic parenchyma were prominent features. At 15 weeks postinoculation inflammatory changes in Glisson's capsule of inoculated deer were less marked than at six weeks but portal fibrosis and hyperplasia of bile duct epithelium were more advanced. A zone of hemorrhage surrounded ducts that contained mature F. hepatica in one deer. The livers from the sheep were rough, pitted and covered with fibrous tags and adhesions to the diaphragm and greater omentum were common. Hemorrhagic tracks were common in the sheep given 500 and 2500 metacercariae. Portal fibrosis and hyperplasia of bile duct epithelium were seen in the sheep (100 metacercariae) that harbored mature F. hepatica.

Animals↗
PubMed1975

Suppression of the pathogenic effects of Strongylus edentatus larvae with thiabendazole.

Four pony foals were inoculated with Strongylus edentatus infective larvae and on days 3 and 4 postinfection two of the ponies were treated with thiabendazole, each at the rate of 440 mg/kg of body weight. Total circulating eosinophil counts in untreated ponies increased to over 1700 per cu mm after the second week postinfection. In the treated ponies as well as in an uninfected untreated pony eosinophil counts did not increase beyond 100 per cu mm. At necropsy on day 35 postinfection the cecum, colon and omentum of treated ponies were normal and few tracks were present on the surface of the liver. In untreated ponies nodules were observed on the serosal surface of the cecum and right ventral colon and white foci and tracks were numerous on the surface of the liver. A total of 53 fourth stage larvac was recovered from the livers of the thiabendazole treated ponies and 1194 from the untreated ones.

Animals↗
PubMed1975

The development of Ascaris suum in calves.

To determine the development of Ascaris suum after a primary and a secondary infection, 18 calves were inoculated with 2,000,000 infective eggs and examined from 18 hours to 13 days postinfection. At 18 hours larvae were recovered from the wall of the abomasum, duodenum and jejunum. They were found in small intestine lymph nodes on the third day, in the liver at five days and were most abundant in the lungs on days 7 and 9. The pattern of recovery of larvae from the lung between days 5 and 13 postinfection was similar after a primary or a secondary infection. Slower growth of larvae following a secondary infection was the only evidence of resistance to A. suum. There were no pathological changes observed in the alimentary canal. White foci were found on the surface of the liver as early as the third day. The rapid decline in the number of A. suum in the lungs after the ninth day was considered to be related to immobilization or death of larvae soon after the reaction to them commences.

Abomasum↗
PubMed1974

Early development of and pathology associated with Strongylus edentatus.

Pony foals inoculated with infective Strongylus edentatus larvae were monitored for clinical signs and selected blood changes and were examined at necropsy from two to 56 days postinfection. Larvae penetrated the intestine and reached the liver intravenously before 40 hours postinfection. Occasional thrombi and larval tracks associated with the intima of cecal and colic veins suggested aberrant paths. Larvae in the liver doubled in width between seven and 15 days postinfection and a sudden increment in circulating eosinophils occurred between 11 and 15 days. These changes were probably associated with the third molt. At 30 days fourth stage larvae were migrating in the liver; at 42 days they were present in the hepatorenal ligament. White foci were observed in the liver from two to 56 days. They contained mononuclear cells and eosinophils and later necrotic cores of eosinophils. By one month foci were overshadowed by tortuous tracks of migrating larvae. Aberrant larvae in the lungs were confined in granulomas. Massive granulomas in the wall of the cecum and colon contained small larvae which were probably inhibited by antibody associated with the third molt. Severe disruption of omental architecture and adhesions involving the intestine occurred several weeks after infection.

Animals↗
PubMed1974

Early pathological changes associated with Fasciola hepatica infections in white-tailed deer.

Three white-tailed deer (Odocoileus virginianus) were inoculated with 1000 metacercariae of Fasciola hepatica and examined on days 7, 14, and 28 postinoculation to determine the early response of a resistant host to this infection. It was concluded that only small numbers of the metacercariae penetrated the intestinal wall into the peritoneal cavity. Flukes that migrated to the liver penetrated through Glisson's capsule, primarily on the parietal surface. Marked fibroplasia and cellular infiltration of the capsule were induced and flukes were killed and destroyed in granulomas immediately beneath the capsule. Migration in hepatic parenchyma was minimal and immature flukes or migratory tracks were not found. There were infiltrations of eosinophils and mononuclear cells, bile duct hyperplasia and fibroplasia in portal areas. A few flukes penetrated through the diaphragm within 14 days postinoculation and on day 28 granulomas were observed on the dorsal surface of the lung where F. hepatica had penetrated this organ. The early reaction of Glisson's capsule to F. hepatica infection in white-tailed deer has not been described in cattle, sheep or swine infected with this fluke.

Animals↗
PubMed1973

Reinfection of yearling calves with Ascaris suum.

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.

Animals↗
PubMed1970

Ascaris suum infection in calves. 3. 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.

Age Factors↗
PubMed1970

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.

Age Factors↗
PubMed1970

Ascaris suum infection in calves. II. Circulating and marrow eosinophil responses.

An increment in the number of circulating eosinophils occurred between the 11th and 14th days after infection with Ascaris suum and this increase was generally greater after a challenge infection. Continual infection with small numbers of A. suum eggs over prolonged periods resulted in circulating eosinophil levels which fluctuated and were dose-dependent. The per cent marrow eosinophils always increased after a primary infection and a greater increase usually followed a challenge infection. The maximum increment of marrow eosinophils occurred between the tenth and 12th days and preceded the rise in circulating eosinophils by 36 hours. Antihistamine therapy did not alter eosinophil responses to A. suum. Circulating eosinophilia was not usually reflected by drastic changes in differential white cell counts. However, an increase in total white cell count often followed infection with A. suum and frequently parallelled changes in eosinophil counts. Hemoglobin and P.C.V. values remained within normal limits in A. summ infected calves.

Age Factors↗