Roles of cortisol and carbonic anhydrase in acid-base compensation in rainbow trout, Oncorhynchus mykiss.

Fish compensate for acid-base disturbances primarily by modulating the branchial excretion of acid-base equivalents, with a supporting role played by adjustment of urinary acid excretion. The present study used metabolic acid-base disturbances in rainbow trout, Oncorhynchus mykiss, to evaluate the role played by cortisol in stimulating compensatory responses. Trout infused with acid (an iso-osmotic solution of 70 mmol L(-1) HCl), base (140 mmol L(-1) NaHCO(3)) or saline (140 mmol L(-1) NaCl) for 24 h exhibited significant elevation of circulating cortisol concentrations. Acid infusion significantly increased both branchial (by 328 µmol kg(-1) h(-1)) and urinary (by 5.9 µmol kg(-1) h(-1)) net acid excretion, compensatory responses that were eliminated by pre-treatment of trout with the cortisol synthesis inhibitor metyrapone (2-methyl-1,2-di-3-pyridyl-1-propanone). The significant decrease in net acid excretion (equivalent to enhanced base excretion) of 203 µmol kg(-1) h(-1) detected in base-infused trout was unaffected by metyrapone treatment. Acid- and base-infusions also were associated with significant changes in the relative mRNA expression of branchial and renal cytosolic carbonic anhydrase (tCAc) and renal membrane-linked CA IV (tCA IV). Cortisol treatment caused changes in CA gene expression that tended to parallel those observed with acid but not base infusion. For example, significant increases in renal relative tCA IV mRNA expression were detected in both acid-infused (~2x) and cortisol-treated (~10x) trout, whereas tCA IV mRNA expression was significantly reduced (~5x) in base-infused fish. Despite changes in CA gene expression in acid- or base-infused fish, neither acid nor base infusion affected CAc protein levels in the gill, but both caused significant increases in branchial CA activity. Cortisol treatment similarly increased branchial CA activity in the absence of an effect on branchial CAc protein expression. Taken together, these findings provide support for the hypothesis that in rainbow trout, cortisol is involved in mediating acid-base compensatory responses to a metabolic acidosis, and that cortisol exerts its effects at least in part through modulation of CA.

Outbreak of early onset group B streptococcal sepsis.

During January and August, 1990, 23 cases of early onset Group B Streptococcus (GBS) disease occurred in a Kansas City, MO, hospital with an attack rate of 14/1000 live births, compared with an annual rate of 1.2 cases/1000 live births for 1988 through 1989. Case infants were compared with controls matched by birth weight, race, maternal age and day of delivery and to a second group of infants of mothers colonized with GBS to identify risk factors and consider intervention strategies during the outbreak. The presence of multiple serotypes among the invasive strains suggested that the outbreak was not caused by a common source. Case mothers were more likely than control mothers to have chorioamnionitis, intrapartum fever or rupture of membranes > 12 hours, and premature case infants were more likely to have a history of rupture of membranes before onset of labor. Multiparous mothers of case infants were more likely to have a history of spontaneous abortion (odds ratio, 6.7; 95% confidence interval, 1.0 to 45.9). No single factor could explain the increase in GBS disease. If intrapartum antibiotic prophylaxis had been used for selected GBS carriers based on presence of either rupture of membranes > 12 hours, intrapartum maternal fever or preterm labor, 7.4% of all deliveries would have received antibiotics and 73% of cases could potentially have been prevented. We conclude that identification of colonized mothers with perinatal risk factors and use of intrapartum antibiotics could be expected to prevent substantial disease during an outbreak of early onset GBS disease.