Following intravenous administration of an oxytetracycline-HC1 and an oxytetracycline-dihydrate formulation to dairy cows, no statistical difference could be found between the pharmacokinetic parameters, derived from the three-compartment model, of these preparations. Urinary recovery was continued for a period of 72 h following intravenous or intramuscular OTC administration. The recovery of OTC in the urine in the 72-h period was in the range of 73% to 96% of the available dose administered. The renal OTC clearance, the renal creatinine clearance, the urinary flow, and the interrelationships of these were determined on the basis of urine and plasma data. The mean OTC renal clearance ranged from 482 to 1050 ml/min and the creatinine clearance from 651 to 1304 ml/min. The OTC and creatinine clearances were significantly correlated to the urine flow up to 30 ml/min. The total body clearance and renal clearance values were of the same order of magnitude, and along with the urine recovery data they provided evidence of predominantly renal route of OTC elimination in dairy cows. The renal OTC elimination is the net result of mainly glomerular filtration, partly tubular secretion, minus reabsorption in the urogenital tract.
The clinical and pathological findings after a natural intra-uterine infection with BVD-virus in a Friesian dairy herd are described. The virological and serological aspects will be discussed in a separate paper (30). In a period of 4 years, 11 calves were born with the following nervous symptoms: more or less serious incoordination, tremor, oscillating nystagmus, and a negative blinking reflex. The pupillary and sucking reflexes were normal. No ocular defects, such as lenticular opacity or retinal atrophy were observed. The first calf was born in 1979. Within 6 months the symptoms disappeared. After a normal conception and pregnancy this animal gave birth to 2 clinically normal calves in 1981 and 1982. The second calf died at the age of 2 months, due to an ulcerating enteritis. In 1980, again 8 calves with the same nervous symptoms were born within a period of 3 months. Two calves died at the age of 3 days and 5 weeks respectively; 2 calves were sold when 10 days and 3 weeks old; one calf did not improve and was necropsied at the age of 17 days. The remaining 3 calves showed only a slight hypermetria when examined after 6 months. At that time nystagmus was only visible with ophthalmoscopy. Two calves were slaughtered when 10 months old. The last one, a bull, proved to be sterile and was necropsied at the age of 1 1/2 year. A calf, born in 1981, recovered within a week and was necropsied at the age of 15 days. The last calf, born in 1982, did not improve at all and was necropsied at the age of 14 days. During these 4 years none of the other animals in the herd showed any symptoms due to an acute or chronic BVD-virus infection. At post mortem examination of 6 animals no macroscopically visible malformations were found. Hypomyelination and abnormal glial cells were evident in 5 cases, especially in the two youngest calves which did not show any improvement. One of them had had an obvious thymic hypoplasia. The calf which recovered within a week showed only very slight changes. In one of the calves slaughtered at 10 months, inflammatory lesions were found in the brain. The diagnosis was confirmed by virological investigations. Clinically as well as pathologically there was a close resemblance to Border disease in lambs and congenital tremor in piglets after prenatal exposure to Hog cholera virus.
The influence of the leukotoxin of Pasteurella haemolytica on the generation of arachidonic acid metabolites by bovine polymorphonuclear leukocytes (PMNs) was investigated. PMNs released 5-, 12-, and 15-hydroxyeicosatetraenoic acids (5-, 12-, and 15-HETE) and leukotriene B4 (LTB4) upon stimulation with arachidonic acid. The leukotoxin preparations dose dependently enhanced the release of the 5-lipoxygenase products 5-HETE and LTB4 in arachidonic acid-stimulated PMNs, whereas the release of 12-and 15-HETE was not affected. The enhanced release of LTB4 and 5-HETE was not due to a decreased cellular retention of the 5-lipoxygenase products. In addition, leukotoxin preparations by themselves were also able to induce LTB4 and 5-HETE production in the absence of exogenous arachidonic acid. Generation of 5-lipoxygenase products by PMNs stimulated by leukotoxin may represent an important cellular event that occurs during infections with P. haemolytica.
The influences of a stress situation on the phagocytic cell function before and after infection with Pasteurella haemolytica were measured in calves. No differences in phagocytic and metabolic activity of alveolar macrophages (AMs) were observed in vitro between cells isolated from stressed and nonstressed animals. The uptake of bacteria and the migration of polymorphonuclear leukocytes (PMNs) did not differ. However, the production of superoxide by PMNs isolated from stressed animals was significantly diminished as compared to control PMNs. The stressed and six of the nine control calves were then infected intrabronchially with P. haemolytica. Phagocytic cell function was again evaluated after three days. The lavage fluid obtained from the lungs of the infected animals contained about three times more PMNs and six times more AMs as compared to the lavage fluid of the control calves. However, the increase in phagocytic cell numbers was less by half in the calves infected after the stress period. No differences were detected in phagocytic and metabolic activity of PMNs and AMs among control, infected, and stressed and infected calves. However, the chemotactic activities of PMNs obtained from infected stressed and infected nonstressed animals were diminished as compared to control PMNs. In conclusion, the metabolic responsiveness of PMNs is diminished and the accumulation of phagocytic cells at a site of infection is reduced after a stress period.
SUMMARY The results are described of virological and serological research carried out in a Dutch dairy herd during a number of years. The motive was the birth of a number of calves with neurological disorders pointing at an intra-uterine infection with BVD-virus in 1980. Also in the previous and in both the following years a calf was born with similar symptoms. The clinical signs and the course of the affection in these eight calves were described in a previous paper (2). The diagnosis was confirmed through virus isolation from pre-colostral blood of one calf and from autopsy material from four aberrant calves. During the investigation three clinically normal animals with a persistent virus infection were found. The clinically recovered animal of 1979 also proved to be a virus carrier. In addition, in two animals a transient viremia in the presence of specific antibodies was found. The four virus carriers conceived normally. The second pregnancy of the oldest animal also passed normally. Their five calves proved to be BVD-virus carriers as well. One calf, born in 1982, showed nervous disturbances to a serious extent. Of the four other clinically normal animals, one calf was euthanasized because of a serious necrotizing enteritis. The remaining calves stayed healthy and grew up normally. One of the two animals with a transient viremia wasfive months pregnant at that moment. At birth in 1981 her calf showed nervous disorders, but both the virological and the serological examinations of the pre-colostral blood were negative.
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