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Biomedical subjects

H Rothenbacher

Publications and source records attributed to H Rothenbacher.

36 records · Page 2Linked to original sources
PubMed1976

Eimeria juniataensis sp. n. (Protozoa: Eimeriidae) from the map turtle, Graptemys Geographica, in Pennsylvania.

Eimeria juniataensis sp. n. is described from the map turtle, Graptemys geographica, in Pennsylvania. The spherical to subspherical oocysts of E. juniataensis are 11.5 to 18.5 mu by 11.5 to 16.5 mu (mean, 13.5 by 12.9mu). The broadly fusiform sporocysts are 7.5 to 10 mu by 4 to 6.5 mu (mean, 8.3 by 5.0mu) and a Stieda body is present. Oocyst and sporocyst residua are present. This is the first report of an eimerian species from Graptemys.

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PubMed1975

Pathologie changes in endocrine glands and certain other tissues of lambs implanted with the synthetic growth promotant zeranol.

As doses of zeranol implants (0 (control), 12, 24, 48, and 96 mg) were increased, there were increased reaction and activity in target organs (such as urogenital tract and mammary, adrenal, hypophyseal, and thyroid glands) of castrated male sheep (wethers). Hyperplasia and transitional and squamous transformation in the prostate were mild (1+) in the wethers given 12- and 24-mg doses, moderate to marked (2.5+) in the wethers given 48-mg doses, and severe (4+) in the wethers given 96-mg doses. Papillary proliferation and fibrosis increased correspondingly in the seminal vesicle. Changes in the distal penile urethra increased from papillary hyperplasia in the wethers given a 24-mg dose to 100% squamous transformation in the wethers given a 96-mg dose. Mammary gland development was noticeable in the wethers given a 24-mg dose and increased thereafter to progressive alveolar growth and secretory activity in the wethers given 48- and 96-mg doses. Along with a progressive increase of adrenal gland weight and adrenal gland/thyroid gland ratios over the controls, the principals had hypertrophy and hyperplasia of the adrenal cortex. Mean adrenal cortex widths for control wethers and wethers given 24-, 48-, and 96-mg doses were 2,089, 2,140 (adjusted value, 2,194), 2,416, and 2,425 mum, respectively. Mean adrenal gland weights for control wethers and wethers given 12-, 24-, 48-, and 96-mg doses were 2.50, 2.61, 2.53, 2.70, and 2.78 g. respectively. Hyperplasia (nodule formation) plus exhaustive and pyknotic changes of the adrenal cortex increased similarly with increasing zeranol dose. After the thyroid gland weights decreased (2.19, 2.04, 2.00, and 1.72 g, respectively, for control wethers and wethers given 12-, 48-, and 96-mg doses), secretory activity of thyroid epithelial cells decreased. In the glandular portion of the hypophysis, secretory activity and proliferation of eosinophilic cells increased with the larger zeranol doses (48 and 96 mg). There was a corresponding decrease in the number of basophils. These changes are consistent with increased somatotropin and adrenocorticotropin secretion and decreased thyrotropin secretion. Muscle and ligament structures appeared looser and widened in the wethers given the 96-mg dose, and fat cell formation was increased in the muscles along ligament muscle junctions.

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PubMedDate not supplied

Infectious tenosynovitis in commercial White Leghorn chickens.

Infectious tenosynovitis was diagnosed in three separate outbreaks in a commercial White Leghorn hens, though not previously reported in adult White Leghorns (3). Clinically affected flocks had decreased production and increased daily mortality, with many hens showing signs of the so called "cage-fatigue bluecomb" syndrome. Most sick birds had lesions typical of infectious tenosynovitis, with pronounced cyanosis and dehydration. Dead birds had signs of acute septicemia. The course of the disease (about 8 weeks) was not altered by the medicinal regimens tried. Young laying-age flocks were most seriously affected. Production losses averaged 15 to 20%, and mortality reached 5% per month during the recovery phase.

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PubMedDate not supplied

An outbreak of avian urolithiasis on a large commercial egg farm.

A significant outbreak of avian urolithiasis was observed on a large commercial egg farm. From the initial outbreak site (a single laying house), the incidence of urolithiasis slowly spread in the ensuing months to numerous other laying houses. Increasing mortality associated with urolithiasis commenced during late growout to early lay and then leveled off when egg production peaked. At the height of the outbreak, mortality was typically 0.5% per week; 75% of this mortality was due to urolithiasis. The clinical and pathologic features of this condition are described. Both infectious bronchitis virus (IBV) and fowl adenoviruses were isolated from organ homogenates of sampled birds. A clone of the IBV strain was found to induce nephritis in specific-pathogen-free white leghorns.

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PubMedDate not supplied

A case of acute pulmonary edema, splenomegaly, and ascites in guinea fowl.

Acute pulmonary edema, splenomegaly, and ascites were observed in a disease outbreak in adult white and pearl guinea fowl. The clinical history and gross and microscopic lesions resembled those described for marble spleen disease of pheasants and avian adenovirus group II splenomegaly of chickens. A small number of intranuclear inclusion bodies were found in liver, spleen, and lung sections of affected guinea fowl. Attempts to isolate virus and serological tests to detect the presence of viral antigens were unsuccessful. Adult female pearl guinea fowl experimentally exposed to pheasant and turkey isolates of type II avian adenoviruses developed gross and microscopic lesions similar to those seen in the field outbreak. The pheasant isolate was the more virulent. Intranuclear inclusion bodies were observed in liver, spleen, and lung sections of pearl guinea fowl inoculated with either of the virus isolates, and direct immunofluorescent examination revealed viral antigen in the spleen and lung.

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PubMedDate not supplied

Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens.

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.

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