A preliminary survey of antibiotic residues and viable bacteria in milk from three Caribbean Basin countries

There is widespread concern about the presence of antimicrobial drugs in milk. The presence of drug residues in milk may have public health implications. Milk samples (n = 25 to 65/country) were collected from bulk tanks and commercial vendors in Barbados, Costa Rica, and Jamaica between February 1996 and August 1997. Bulk tank samples were collected from high milk-producing regions of Jamaica and Costa Rica and from 26 dairy farms in Barbados. Milk pH, bacterial growth (total CFU/ml and the presence of Streptococcus agalactiae and Staphylococcus aureus), and the presence of antimicrobials were determined. Milk samples were tested by a microbial inhibition test (Delvotest-P, Gist-Brocades Food Ingredients, Inc.) to screen for antimicrobial drugs. All positives were retested for the presence of beta-lactam antibiotics after incubating with penicillinase and some positives were identified by high-pressure liquid chromatography-UV. Mean pH values ranged from 6.5 to 6.7. S. aureus was identified in bulk tank samples from Costa Rica (52 percent), Barbados (44 percent), and Jamaica (46 percent). S. agalactiae was identified in bulk tank samples from Barbados (8 percent) and Jamaica (10 percent) but not in samples from Costa Rica. All positives in milk from Jamaica and Barbados were determined to be beta-lactams. No residues were detected in pasteurized milk samples from Barbados or ultrahigh-temperature milk from Jamaica. The presence of beta-lactam residues in some of these samples suggests the appropriateness of testing milk prior to processing for consumption.(Au)

Effect of starvation on renal metabolism in the rat

The effects of starvation an the acid base status of the rat and on the gluconeogenic and ammoniagenic capacity of rat renal-cortical slices were examined. Starvation for 48 or 72 hrs did not affect acid-base status, and urinary ammonia production did not change. Kidney cortical slices from starved as compared to fed rats showed increased gluconeogenic capicity when incubated with the substrated pyruvate, succinate, fumarate, malate, 2-oxoglutarate, glutamine and glutamate. Renal cortical tissues from starved rats also had increased activity of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase. Renal cortical slices from starved rats did not differ from those of fed rats in the ability to produce ammonia from glutamine or glutamate, nor was there any difference in the activity of glutaminase between these groups. These results show that renal gluconeogenic capacity is increased in starved rats in the absence of systemic acidosis, and starvation does not lead to an increase in urinary ammonia excretion or renal ammoniagenic capacity. (AU)

The effect of malnutrition on the pattern of growth in the rat kidney and the renal response to acidosis

The kidneys of normal rats were analysed for water, fat, protein, RNA and DNA, at 10, 21 and 36 d after birth. The effects on growth caused by two types of malnutrition were investigated. An increase in the RNA:DNA ratio was demonstrated between 10 and 36 d, contrary to previous evidence that this ratio is fixed at birth. Energy deficiency during the first 21 d of life resulted mainly in fewer kidney cells, whereas protein-energy deficiency between 21 and 36 d reulted mainly in a smaller cellular content of RNA and protein. In response to metabolic acidosi, both groups of malnourished rats increased urinary excretion of ammonia and there was enhanced gluconeogenesis in vitro; the basal rate of gluconeogenesis was lower in the protein-energy-deficient rats than in the controls. Protein-energy-deficient rats did not exhibit the renal hypertrophy shown by the control rats in response to acidosis (AU)

Regulation of renal cortex ammoniagenesis. I. Stimulation of renal cortex ammoniagenesis in vitro by plasma isolated from acutely acidotic rats

We studied the acute renal metabolic response in rats made acidotic by a single oral dose of ammonium chloride. Cortical slices from acutely (2-h) acidotic rats utilized more glutamine and produced more ammonia and glucose from glutamine than slices from normal animals. When cortical slices from normal rats were pretreated in vitro with plasma isolated from acutely acidotic rats, they achieved similar increases in glutamine utilization, ammonia formation, and gluconeogensis from glutamine. We did not observe such stimulation in normal cortical slices pretreated in a low pH-low bicarbonate medium. Our data show that a non-dialysable factor is present plasma from acutely acidotic rats that may be responsible for the early increase in the urinary ammonia observed in such animals (AU)

The in vivo sickle phenomenon: a reappraisal

Previous studies elsewhere have cast doubt on the in vivo relationship between oxygen saturation and red cell sickling. We have reinvestigated this relationship and find the expected correlation to occur at a variety of in vivo sampling sites. The correlation is apparent within data from single individuals, but may be lost when individual susceptibility to sickle cell formation is overlooked by pooling data from different patients. Samples from the hepatic vein did not usually fit the correlation and the unusual factors at this site are discussed (AU)

Studies on acid excretion in adults with sickle-cell anaemia

The acid excretion of patients with sickle-cell anaemia has been studied. There is a mild defect in urinary acidification and a decreased H+ excretion in response to ammonium chloride loading. The acidification defect was not corrected by oral administration of a phosphate solution. Infusion of sodium sulphate solution in subjects who were avidly reabsorbing sodium produced equal degrees of urine acidification in patients and controls. Studies on bicarbonate reabsorption were inconclusive. We conclude that patients with sickle-cell anaemia have a mild form of incomplete distal renal tubular acidosis (AU)

Defect in urinary acidification in adults with sickle-cell anaemia

Eight adult patients with sickle-cell anaemia have been shown to have a significant defect in urinary acidification. After a standard dose of ammononium chloride the lowest mean urine pH obtained was 5.42 compared with 4.85 for the controls. There was no accompanying systemic acidosis (AU)