Effects of severe long-term food deprivation and refeeding on adipose tissue cells in the rat.

To determine whether it is possible to use diet to cause a loss of adipocytes, adipose tissue cellularity was examined in adult male rats subjected to unusually prolonged semistarvation. After 1 wk of total fast, rats were given a nutritionally inadequate glucose-electrolyte diet for up to 7 wk. This caused a 49% reduction of body weight, up to a 99% reduction in the weight of adipose tissue, and significant losses of total adipose tissue DNA content. Nevertheless, there was no evidence that fat cells had been lost. The number of fat cells in the right epididymal depots of the food-deprived rats equaled both the number seen in left depots after refeeding and the number seen in corresponding depots of nonfasted controls. Adipose tissue DNA synthesis, which declined 88% below control values during fasting, did increase as much as 2,000% above control values during refeeding. However, autoradiographs showed that the increase reflects only the replacement of lost endothelial and nonadipocyte mesenchymal cells; no labeled fat cell nuclei were found. Thus, severe, long-term food deprivation followed by refeeding causes loss and recovery of stromal-vascular cells in adipose tissue but no loss of fat cells.

Infections caused by nondiphtheria corynebacteria.

After decades of confusion about their microbiologic classification and clinical significance, the nondiphtheria corynebacteria have emerged as important pathogens. Although isolation of these organisms may represent contamination with skin flora, several species, including Corynebacterium ulcerans, Corynebacterium pseudotuberculosis (Corynebacterium ovis), Corynebacterium haemolyticum, Corynebacterium pseudodiptheriticum, Corynebacterium equi, Corynebacterium bovis, Corynebacterium xerosis, and corynebacteria of group JK, clearly cause disease in humans. Most of these organisms infect animals, which are the source of human infection with some species. Some nondiptheria species of Corynebacterium produce recognizable clinical syndromes such as granulomatous lymphadenitis, pneumonitis, pharyngitis, cutaneous infections, and, most commonly, endocarditis. Certain species infect healthy hosts, while others predominantly attack immunocompromised individuals. Several species produce toxins, including a diphtheria-like toxin, a dermonecrotic toxin, and a soluble hemolysin. A microbiologic scheme of identification of the genus Corynebacterium and its major defined species is presented.

Suppurative granulomatous lymphadenitis caused by corynebacterium ovis (pseudotuberculosis).

A 30-year-old previously healthy man developed cervical adenopathy associated with mild constitutional symptoms. Corynebacterium ovis was isolated in pure culture from lymph node tissue on two separate occasions, and small gram positive organisms were identified in both lymph nodes with tissue gram stain. Histopathologically, the nodes displayed suppurative and necrotizing granulomas. Of eight previously reported cases of C. ovis lymphadenitis in man, all but one have involved inhabitants of rural Australia, most of whom had contact with sheep, an animal reservoir of C. ovis. Necrotizing granulomas were usually observed. The patient described was an American urban dweller with a history of raw milk ingestion. We believe this to be the first reported case of C. ovis lymphadenitis from the United States. C. ovis infection should be considered n the differential diagnosis of localized lymphadenitis with necrotizing and/or suppurative granulomas. In evaluation of granulomatous lymphadenitis tissue gram stain should be performed and culture of a diphtheroid organism not readily dismissed.