Alpha-2-adrenoceptor-mediated effects of pergolide.

The alpha-adrenoceptor-mediated effects of pergolide were investigated in a number of biochemical and pharmacological test systems. In radioligand binding studies, pergolide more effectively competed for alpha 2-adrenoceptors than for alpha 1-adrenoceptors in membranes prepared from rat cerebral cortex. Consistent with this finding was the observation that pergolide was several orders of magnitude more effective in activating presynaptic alpha 2-adrenoceptors in rat vas deferens to inhibit stimulation-evoked [3H]-norepinephrine release than in activating postsynaptic alpha 1-adrenoceptors in the same tissue to produce a contractile response. Pergolide elicited a potent vasopressor response in pithed rats that was highly sensitive to antagonism by the selective alpha 2-adrenoceptor antagonist, yohimbine, and resistant to blockade by the selective alpha 1-adrenoceptor antagonist, prazosin, suggesting that pergolide selectively activates postsynaptic vascular alpha 2-adrenoceptors. The results of the present study indicate that the alpha-adrenoceptor-mediated effects commonly associated with pergolide result from selective stimulation of alpha 2-adrenoceptors.

Staphylococcus aureus: biology, mechanisms of virulence, epidemiology.

The prominence of Staphylococcus aureus as a cause of serious human infection has prompted extensive studies of the microbiology, pathogenesis, and epidemiology of staphylococci and staphylococcal infections. Staphylococci are of the family Micrococcaceae, although there are diverse genetic and phenotypic differences between them and other members of this family. Of the more than 20 species of staphylococci, only three are clinically significant: S. aureus, S. epidermidis, and S. saprophyticus. These species can be distinguished by coagulase production and novobiocin resistance. Staphylococci produce a variety of structural, enzymatic, and toxic products, which are associated with adherence, invasion, toxicity, and avoidance of host defense mechanisms. In addition, a variety of host characteristics increase susceptibility to staphylococcal infection. Staphylococci are an important cause of infection in hospitals and the community. Following the introduction of antimicrobials, staphylococci rapidly developed resistance. A penicillin-resistant specific phage type, designated 80/81, caused severe outbreaks of nosocomial disease in the 1950s and 1960s. Staphylococci recently acquired resistance to methicillin and other antimicrobials, and persist as important nosocomial pathogens. Although S. aureus is one of the earliest recognized and most studied human pathogens, it is a perplexing, ever-changing, recurring public health problem.

Traveler's diarrhea at sea: two multi-pathogen outbreaks caused by food eaten on shore visits.

In 1976 and 1981, two outbreaks of gastrointestinal illness aboard cruise ships occurred within 24 hours following onshore visits to Haiti and Mexico, respectively. Three hundred eighty-six of 600 (64 per cent) and 98 of 260 (38 per cent) passengers became ill following luncheons in Port-au-Prince, Haiti, and Cozumel, Mexico. No increase in illness was observed among those passengers who did not attend the onshore luncheons. In both outbreaks, unrefrigerated seafood dishes served at outdoor buffets were epidemiologically incriminated as the vehicles of transmission. Several species of Vibrion, Salmonella, and toxigenic Escherichia coli were recovered from stool specimens of ill passengers in both outbreaks. In addition, invasive Escherichia coli and Shigella were isolated from stool specimens of ill passengers who ate at the Haitian buffet. Previous investigations of outbreaks of gastrointestinal illness aboard cruise ships have implicated exposures on board as the source and have involved only a single pathogen.