Fatal rectal perforation following boar-to-boar mounting.

Although abnormal sexual behavior, including boar-to-boar mounting with anal penetration, is recognized in pubescent pigs, reports of the pathologic consequences are scarce. A 7-month-old male minipig, housed with age-matched males, died within 1 day of the onset of lethargy and reluctance to rise. At necropsy, 2 rectal tears were identified as the cause for fibrinous peritonitis, and spermatozoa were identified in the pelvic and peritoneal cavity by light and transmission electron microscopy. According to DNA typing results, using 11 porcine microsatellites, the intraperitoneal semen was from at least 2 pen mates. The prohibition of castration of fattening pigs, implemented or planned in multiple European countries, could increase the risk of rectal perforation in co-housed pigs.

[Osteopenia as a result of copper deficiency in a dwarf Thuringian Forest goat]. / Osteopenie infolge eines Kupfermangels bei einer zwergwüchsigen Thüringerwald Ziege.

In a female Thuringian forest goat osteoporosis, dwarfism and anaemia were found. The animal was kept on a hobby farm with 30 further goats that did not show clinical signs. Radiological examination, computed tomographic imaging and pathological examination revealed reduced bone density and numerous fractures associated with limited or completely absent callus formation. Incineration of selected bones did not show any differences concerning the contents of calcium and phosphorus when compared to two control goats. Therefore, a regular mineralisation of the bone matrix was indicated. The dysfunction associated with the osteogenesis was assumed to be a copper deficiency.

Guillain-Barré syndrome in children: evidence of axonal degeneration and long-term follow-up.

A retrospective study was done of 12 children who met the NINCDS clinical criteria for the diagnosis of Guillain-Barré syndrome and who were hospitalized with this diagnosis. Electrodiagnostic testing was sufficiently complete for interpretation of the neuropathophysiology in six children. Long-term outcome was determined through examination by a physician one to eight years after onset in all six children, and was supplemented by telephone follow-up with the children or their parents by the authors five to eight years after onset. Long-term clinical outcome was analyzed for any correlation between poor outcome and axonal degeneration. The electrodiagnostic tests were consistent with primarily axonal neuropathophysiology in three of the six children. Poor clinical outcome appeared to correlate with electrodiagnostic evidence of primarily axonal pathophysiology, or absence of an evoked M-response, or both.