Lysozyme in calves

Relatively high lysozyme concentrations, depending on age, were recorded from intestinal content, spleen, liver, kidney, lung, lymph nodes, and mucosa of calves. Yet, only minor quantities of lysozyme were found in blood serum or plasma and in granulocytes. Physicochemical characterisation, precipitation, using polyclonal antisera, and crosswise neutralisation of lysis reaction were likely to suggest occurrence of immunological relationship reactions as well as differences between organ lysozymes, on the one hand, and intestinal lysozymes, on the other.     

Salmonellosis in calves

Despite the efforts of both physicians and veterinarians, the number of cases of salmonellosis per year has held steady or risen. The ability of the organism to live in many different animal species and under inhospitable environmental conditions is likely responsible for Salmonella's prevalence today. Diverse clinical signs occur in salmonellosis; they range from unthriftiness to explosive, necrotizing diarrheas with high mortality. Secondary complications of pneumonia, bone and joint infections, and meningoencephalitis can result from calfhood infections. Treatment of enteric salmonellosis is chiefly aimed at maintaining fluid, acid-base, and electrolyte balance. Bacteremic or septicemic calves also require systemic antibiotics. The control measures for salmonellosis are based on sanitation and management. Individual calf hutches or pens provide adequate isolation if sufficient spacing and good sanitation are maintained. The Salmonella vaccines presently available provide limited protection; however, live vaccines made from auxotrophic strains of Salmonella appear to be more efficacious.     

Anencephaly in calves

Anencephaly occurred in four calves and was characterized by cranioschisis, absence of the diencephalon with the cerebral hemispheres and rostral midbrain, various forms of eye defects, and relatively normal development of caudal brain stem, cerebellum and spinal cord. Amorphous dysplastic vestiges of the cerebral tissue protruded into the cranial defects. Morphologic features varied but were essentially similar. The cerebellum was absent in one case. Anencephaly in calves at least those we observed and defined in this study is localized defect confined to the brain, eye and skull. No spinal defect was observed in the calves.     

Citrullinaemia in Friesian calves

Six Friesian calves from a pedigree herd died or were killed within 1 week of birth because of progressive central nervous disease in which the only consistent lesion was cerebral oedema. The cause was citrullinaemia, resulting from an autosomally inherited dysfunction of the urea cycle enzyme arginosuccinate synthetase. Citrullinaemia was diagnosed by demonstrating markedly elevated concentrations of citrulline in the blood of one calf and in the cerebral spinal fluid of another. One of two sires used in the herd was a heterozygous carrier of the disease. Heterozygocity was demonstrated using a polymerase chain reaction/restriction endonuclease test designed to detect the genetic mutation that causes citrullinaemia in cattle.     

D-lactate-induced neurotoxicity in calves

D-lactic acidosis occurs as a complication of short-bowel syndrome in humans and in a variety of other gastrointestinal disorders in monogastrics and ruminants. It is associated with signs of impaired central nervous system (CNS) function including ataxia and coma. The objective of this experiment was to determine if either acidification of nervous tissue or D-lactic acid is responsible for decreased neurological function. Eight Holstein calves (32 ± 11 d) were surgically catheterized with indwelling intravenous jugular and atlanto-occipital space cerebrospinal fluid (CSF) catheters and infused for 6 h in random order with iso-molar DL-lactic acid (DL-LA), L-lactic acid (L-LA), hydrochloric acid (HCl) or saline. DL-LA induced ataxia after 4 h of infusion and produced the greatest obtunding of CNS function (at 7 h, score 8.0 ± 0.4), whereas, the other infusions caused neither ataxia nor scores over 1.5 (p < 0.01 from DL-LA). After 6 h, DL-LA induced significantly less acidemia than HCl (pH 7.13 ± 0.06 and 7.00 ± 0.04, base excess −16 ± 1 and −23 ± 3 mmol/l, bicarbonate 11 ± 1 and 8 ± 1 mmol/L respectively, all p < 0.01), but greater than L-LA and saline (p < 0.01). CSF changes followed a similar but less pronounced pattern. Although HCl infusion produced a severe acidemia and CSF acidosis, only minor effects on neurological function were evident suggesting that D-lactate has a direct neurotoxic effect that is independent of acidosis. Conversely, L-LA produced only minor neurological changes.     

Neomycin toxicosis in calves

Calves (n = 4) were given neomycin (2.25 or 4.5 mg/kg) twice daily IM and were compared with 2 calves given penicillin IM. The 2 hallmarks of aminoglycoside toxicosis, nephrotoxicosis and ototoxicosis, were seen with both dosages of parenterally administered neomycin. Nephrotoxicosis was confirmed by abnormal findings in urinalysis (granular casts, proteinuria, low specific gravity), renal biopsy results (tubular degeneration and necrosis), and increased 24-hour amounts of urinary enzymes (alanine aminopeptidase and gamma-glutamyltranspeptidase). Azotemia, decreased creatinine clearance, polyuria, and polydipsia also were documented in calves given neomycin. Clinically, deafness was suspected in 2 calves and was documented by electrical auditory-evoked response tests. Abnormalities in partial thromboplastin times and renal residues of neomycin were seen in all 4 calves that were given neomycin, but not in calves that were given penicillin.     

Enterotoxemia in neonatal calves

The incidence, bacterial characteristics, disease syndromes, diagnosis, treatment, and prevention of enterotoxemia of neonatal calves caused by Clostridium perfringens (Types A, B, C, D, and E) are reviewed.     

D-Lactic acidosis in calves

Metabolic acidosis has long been known as a frequent and potentially severe complication of neonatal calf diarrhoea. It has also been described in 'acidosis-without-dehydration' syndrome in calves and was suspected to occur during ruminal drinking. Clinical signs of central nervous impairment, particularly changes in behaviour and posture, progressing to coma and recumbency, were originally attributed to this metabolic disturbance. The loss of bicarbonate in the faeces was regarded as the main cause of acidosis in this context. During the past decade, however, evidence has accumulated that d-lactic acidosis is a more common occurrence in calves with neonatal diarrhoea. The most probable source of D-lactataemia is bacterial fermentation of undigested substrate that reaches the large intestine due to damage to small intestinal mucosal epithelium. Recent research has shown that most of the clinical signs that were formerly attributed to acidosis were in fact due to elevated blood levels of D-lactate. The aim of this review is to provide a current overview of d-lactic acidosis.     

Study on diarrhea in young calves. 2. Pathomorphological studies in clinically healthy calves and in calves with diarrhea

Pathological-anatomical and histological investigations were performed in 49 calves aged from 1 to 18 days, 26 of them being affected by diarrhoea, 23 being without clinical signs. In both the groups above all rhinitis, gastritis and typhlocolitis could be observed, thus the affection could be characterized as rhinogastrocolitis. Significant differences only existed between diarrhoea affected and clinical incospicuous calves concerning the macroscopic signs of the colon, periportal infiltrates of the liver and thymus in involution. The peak of inflammatory reaction is in general reached at the 7. to 10. day of life. In concordance with bacteriological findings the results refer to an affection not due to coli infection. Virus etiology may not be excluded and has to be examined in further studies.