In 1926,1 one of us (Dr. Killian) and his associate reported that spinal fluid from cases of meningitis showed unusually high values for lactic acid and low ones for sugar. The source of the increased lactic acid appeared to lie in the metabolic activity of the leukocytes. These studies were continued, and in 1928 2 we came to the conclusion that the changes in lactic acid concentration were a better index of the progress of the infection than the changes in the sugar content. In meningitis the lactic acid of the spinal fluid was greater than that of the blood, but the sugar of the spinal fluid was less than that of the blood. Furthermore, the lactic acid of the spinal fluid may fluctuate within a wide range, although the amount of sugar remains normal. Since our first observations, similar studies have been reported by others.3 In the recent paper by Wright, Herr and Paul 4 on the spinal fluid in suppurative meningitis, an excellent review on this subject is found, and it is therefore unnecessary to repeat such a summary here.In the present report we wish to add further evidence to support the original conclusions and to enlarge on their significance. An intensive study of the sugar, lactic acid and cell count of the spinal fluid in various types of meningitis was made in order to determine whether the lactic acid varies with the cell count and whether it may be utilized as an index of the progress of the infection or of the From the
CASE DESCRIPTION 4 alpacas and 2 llamas (11 months to 11 years old) from 2 properties were examined for lethargy (6/6), salivation and regurgitation (4/6), and recumbency (3/6). Signs developed approximately 48 to 72 hours after accidental access to black oil sunflower seeds. CLINICAL FINDINGS 3 alpacas died suddenly prior to treatment and were necropsied. One llama survived, and 1 alpaca and 1 llama died after days of medical treatment. All 3 treated animals had systemic inflammatory signs including tachycardia, fever, and hematologic changes. Biochemical anomalies included azotemia, hyperglycemia, hyponatremia, hypochloremia, and hypoalbuminemia. Necropsy identified numerous sunflower seeds in the gastrointestinal tract of all 5 animals that died, with pulmonary congestion (5/5 animals), mild centrilobular vacuolar hepatic degeneration (4/5), and erosions of the esophagus (3/5) and first (3/5) and third (1/5) compartments of the forestomach. Renal tubular necrosis was found in the 2 animals that died on day 4 of treatment. TREATMENT AND OUTCOME One llama responded successfully to intensive medical management including supplemented IV fluid therapy, oral and partial parenteral nutrition, and administration of antimicrobials, furosemide, and insulin and was clinically normal with plasma biochemical analysis values within reference range 12 weeks later. Vitamin D, oxalates, heavy metals, and mycotoxins were excluded as the cause of clinical signs on the basis of screening of uneaten seeds and tissue samples and gastric content from the treated llama that died. CLINICAL RELEVANCE Inadvertent large volume black oil sunflower seed ingestion resulted in a high mortality rate in camelids. A specific toxic principle was not identified. Feeding this product to camelids is not recommended to avoid the risk of accidental overingestion and subsequent disease. (J Am Vet Med Assoc 2021;259:406–414)
A review of the literature on glycolysis warrants the conclusion that the sugar of shed blood tliminishes on standing, independent of bacterial contamination. \\'ith respect to the fate of the lost sugar, several papers have heen reported in the literature, ctetfucing somewhat similar conclusions, that a portion of the lost sugar is converted into lactic acict. 1 I onw-er. there remained the uncertainty as to the quantitative relation of the sugar lost to the amount of lactic acid produced.In order to clear up this point, we careiully studied the blood glycolysis iiz 7 i f r o from the point of view of the simultaneous changes taking place in the glucose and lactic acid contents o i the blood.The blood was drawn in all instances iron1 the veins under aseptic conditions and maintained at 38" C. free from bacterial contamination. Analyses of the Idootl were made immediately and after 3, 6 and 24 hours. Potassium oxalate was employed as a n anti-coagulant for the whole I)lood. The amount of the potassium oxalate used was roughly O.O67C, oi the blooct. The specimen was cultured at the end o f 24 hours amt. thus Iiacterial contamination was excluded.Andyticnl ProcetJzivcs: 13rehnie ant1 Erahdy' have recently tlescribed a comparatively simple and accurate method for t.he estimation of the lactic acid of I>lood. Hence we employed their method for the determination o f lactic acid in the blood. The sugar of blood we determined by the Shaff er-Hartmann method.;' Discussion of Keszdts: 'The results are presented in Table I. The findings for 10 subjects showed that the i i i xpitro process of glycolysis, the sugar gradually clecrease4 \vith a parallel rise in the lactic acid. All instances except one (subject 2) showed that the difference between the amount of disappeared sugar and the increased lactic acid during 23 hours lies lvithin 12 mg. I n subject 2 the difference between these 2 sul-stances was 20.5 mg.IBrehme, T., and Brahdy, B., Biochcm. Z., 1926, clxxv, 348.
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