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Biomedical subjects

D J Steffen

Publications and source records attributed to D J Steffen.

11 recordsLinked to original sources
PubMed1995

Detection and characterization of Salmonella typhimurium from a dairy herd in North Dakota.

Nasal secretions, faecal samples and buffy coats were obtained from 102 cattle from a North Dakota dairy herd with a history of calf scours. Treated buffy coats, faecal samples and nasal secretions were inoculated into tetrathionate broth (TB), incubated at 37 degrees C overnight, and plated onto brilliant green agar medium with novobiocin (BGAN). The TB was left at room temperature for 5 days and then used to inoculate fresh TB. The fresh TB was incubated at 37 degrees C over night and plated onto BGAN medium. All the plates were incubated at 37 degrees C over night and observed for Salmonella-like growth. Suspect colonies were further tested and Salmonella isolates were serotyped by the National Veterinary Services laboratory. Twenty-two of the 36 calves sampled harboured S. typhimurium in their faeces, but no samples from cows were positive. No Salmonella were isolated from the buffy coats, but 4 calves were shown to have Salmonella in their nasal secretions. Extended enrichment of the faecal cultures in TB resulted in a significant increase in Salmonella isolations, although 2 samples were positive following the initial enrichment period and not after secondary enrichment. The typical Salmonella isolate detected from this herd contained a transmissible R-plasmid encoding resistance to tetracycline, kanamycin, sulphisoxazole and ampicillin. This study confirmed that delayed secondary enrichment in TB is superior to primary enrichment for detection of Salmonella from cattle.

Animals↗
PubMed1994

Multifocal subacute necrotizing encephalomyelopathy in Simmental calves.

In 24 cases of multifocal necrotizing encephalopathy (MNE) in Simmental and Simmental-cross cattle, clinical features varied, consisting of mild rear limb ataxia, caudal paresis, and, less often, sudden death. Bilateral and symmetric malacic lesions were present in the brain stem (olivary nucleus) of all affected calves. Foci of malacia affecting thoracic spinal cord and additional brain stem sites were common. Neuronal cell bodies and hypertrophied capillaries were present within malacic foci. Rarefaction of neuropil, progressing to complete parenchymal loss, characterized advanced lesions. Pathologic features were similar to those of Leigh syndrome in humans, and a similar defect in aerobic metabolism is hypothesized. Occurrence of the syndrome within 1 breed over a wide geographic area suggests that hereditary factors contribute to development of MNE.

Animals↗
PubMed1993

Congenital skin abnormalities.

It must be remembered that viral infections and maternal nutritional deficiencies can and do cause congenital skin diseases and must be included in a complete differential diagnosis list. These disorders are covered adequately in most current texts on infectious and nutritional diseases and therefore are not described here. When an hereditary, congenital skin disease is suspected, biopsy specimens should be submitted for diagnosis. Many breed associations have control programs for these types of diseases and only with veterinary and producer cooperation will these programs be successful.

Animals↗
PubMed1992

Hind limb paralysis from electrical shock in three gilts.

Three crossbred gilts developed hind limb paralysis attributable to multiple vertebral body fractures after nonfatal electrical shock. Fractures have been reported in swine and other animals that died from electrocution, but in this case, the pigs were not killed, and lesions that suggested electrical shock were not observed. Electrical shock should be considered as a cause of unexplained spinal cord injury in swine in intensive production units, and electrical service to the pens should be carefully checked.

Animals↗
PubMed1992

Ultrastructural findings in congenital anemia, dyskeratosis, and progressive alopecia in Polled Hereford calves.

Ultrastructural evidence of dyserythropoiesis was found in ten calves (ages 1 to 16 months) previously diagnosed as having congenital anemia, dyskeratosis, and progressive alopecia. Morphologic abnormalities found in erythroid precursors of all calves were associated with the nucleus. Rubriblast nuclei were irregular with numerous blebs, indentations, and deep clefts. Elongated blebs appeared as satellite nuclei in some sections. Nuclear membranes had numerous defects or gaps, which were frequently present in, but not limited to, recently divided cells. Cytoplasmic material could be found within these gaps and extending into the nucleus. Rubricytes had chromatin that was abnormally condensed and hyperosmiophilic, with numerous translucent vacuoles present. Binucleate rubricytes occurred frequently in affected calves. These changes resemble those of type I congenital dyserythropoiesis in human beings, and we suggest congenital anemia, dyskeratosis, and progressive alopecia of Polled Hereford calves as the appropriate diagnostic terms to describe this disease.

Alopecia↗
PubMed1992

Congenital dyserythropoiesis and progressive alopecia in Polled Hereford calves: hematologic, biochemical, bone marrow cytologic, electrophoretic, and flow cytometric findings.

Congenital dyserythropoiesis with dyskeratosis is a slow, progressive, and often fatal disease in Polled Hereford calves. Affected calves have a macrocytic normochromic anemia with a mild reticulocytosis. Studies indicate that calves are hyperferremic with increased saturation of serum total iron binding capacity, which rules out iron deficiency as a cause. Other secondary causes of dyserythropoiesis, including cobalamin and folate deficiencies, are unlikely because serum cobalamin and folate levels of affected calves were normal. Virus isolation was negative, and failure to identify bovine retroviral antigens or antibodies from several calves suggested that viral agents were not involved. Bone marrow cytologic findings were similar to those in congenital hereditary dyserythropoiesis in humans and included occasional multinucleate cells, internuclear chromatin bridging between nuclei of partially divided cells, and, more frequently, irregular nuclear shapes and chromatin patterns. DNA content and cell cycle distribution of erythroid cells appeared normal, and no electrophoretic abnormalities were detected in erythrocyte membrane proteins. The Polled Hereford syndrome is similar in many ways to type I congenital dyserythropoiesis in humans and may be an appropriate biomedical model for studying erythroid proliferation during dyserythropoiesis.

Alkaline Phosphatase↗
PubMed1991

Congenital anemia, dyskeratosis, and progressive alopecia in Polled Hereford calves.

A new syndrome of anemia, alopecia, and dyskeratosis was identified in Polled Hereford calves in this study. Cutaneous changes included hyperkeratosis and hair loss around the muzzle and ear margins, which progressed to a generalized alopecia and hyperkeratotic dermatitis. Histologically, orthokeratotic hyperkeratosis with dyskeratosis of epidermal and follicular keratinocytes was present. Alopecia was correlated with dyskeratosis of Huxley's layer and an increasing proportion of follicles in the telogen phase of the hair cycle. Dermatitis was characterized by a mild dermal mononuclear cell infiltrate and mild lymphocytic perivascular dermatitis. The anemia present at birth was nonprogressive and was classified as normochromic and normocytic to macrocytic. Reticulocytosis was absent, but bone marrow was markedly hyperplastic. Nuclear cytoplasmic asynchrony of the rubricyte and metarubricyte stages occurred in the bone marrow. Abnormal rubricyte nuclei and maturation arrest at the late rubricyte stage were common. Cytologic features of the erythroid series are similar to those of type I congenital dyserythropoietic anemia of human beings. Genealogic features suggest that this is a primary hereditary defect. The mode of inheritance, however, remains to be determined.

Alopecia↗
PubMedDate not supplied

Epidemiologic findings in congenital anemia, dyserythropoiesis, and dyskeratosis in polled Hereford calves.

Congenital dyserythropoiesis and dyskeratosis occur within certain lines of Polled Hereford cattle. Eighty-nine of 90 alleles in 45 affected calves had a mechanism in which they could be identical by descent from an identified common ancestor. The line allele may have been a recurrence of the mutation, or the mutation may have occurred earlier in the breed's history and been distributed throughout the breed by the extensive use of several ancestors. No evidence of disease has been identified in sire and dams of affected calves, suggesting that the allele is not acting in a dominant or incompletely dominant manner. Even distribution of cases between sexes suggests that the disease is not sex linked or sex influenced. A higher degree of inbreeding in the affected calves and temporal and spatial features that separated individual cases also suggest a genetic cause. Segregation ratios were not significantly different from those of the hypothesized simple autosomal recessive inheritance.

Anemia, Dyserythropoietic, Congenital↗