The objective of the present study was to determine the effects of rumen-protected choline (RPC) supplementation on body condition, milk production and milk choline content during the periparturient period. Thirty-two Holstein cows were allocated into two groups (RPC group -with RPC supplementation, and control group -without RPC supplementation) 28 days before the expected calving. Cows were fed the experimental diet from 21 days before expected calving until 60 days of lactation. The daily diet of the RPC group contained 100 g of RPC from 21 days before calving until calving and 200 g RPC after calving for 60 days of lactation, which provided 25 g and 50 g per day choline, respectively. Body condition was scored on days 221, 7, 35 and 60 relative to calving. Milk production was measured at every milking; milk fat, protein and choline content were determined on days 7, 35 and 60 of lactation. Body condition was not affected by RPC supplementation. Milk yield was 4.4 kg higher for the group of cows receiving supplementary choline during the 60 days experimental period and 4% fat-corrected milk production was also increased by 2.5 kg/day. Milk fat content was not altered by treatment, but fat yield was increased by 0.10 kg/day as a consequence of higher milk yield in the RPC-treated group. Milk protein content tended to increase by RPC supplementation and a 0.18 kg/day significant improvement of protein yield was detected. Milk choline content increased in both groups after calving as the lactating period advanced. However, milk choline content and choline yield were significantly higher in the RPC group than in the control group. The improved milk choline and choline yield provide evidence that some of the applied RPC escaped ruminal degradation, was absorbed from the small intestine and improved the choline supply of the cows and contributed to the changes of production variables.

We evaluated the lactation performance, liver lipid content and plasma metabolites indicating the energy balance of dairy cows supplemented with conjugated linoleic acid (CLA) pre- and post-partum (PP) vs. only PP. A total of 60 cows were divided into three groups (n = 20). Daily diet of cows was supplemented with 14 g of CLA (7 g cis-9, trans-11 and 7 g trans-10, cis-12 isomers) from week 3 before the expected date of calving (group CLA1), or from the day of calving (group CLA2) until 77-91 days PP. Control cows were fed an isocaloric, isonitrogenous and isolipidic diet without CLA. Between week 3 and week 6 PP, the milk yield of cows in both CLA-treated groups was approximately 4.5 kg higher (p < 0.05) than in control. Milk fat concentrations decreased from week 3 and were lower in both CLA groups than in control (p < 0.01). Body condition score loss was lower (p < 0.05) in the CLA1 than in the control group on week 5 PP. By week 11 PP, the body condition of both CLA1 and CLA2 groups exceeded that of control. Plasma non-esterified fatty acid was lower in CLA1 compared to CLA2 and control during the early PP period (p < 0.05), while this difference faded away by the late PP period. Beta-hydroxybutyrate (BHBA) increased rapidly in all groups following calving. In CLA1 group, it began to decrease sooner than in CLA2 and control. The prevalence of subclinical ketosis (BHBA > 1.2 mm) was lower in CLA1 group than in CLA2 and control (p < 0.05). Liver biopsy analyses showed that CLA1 treatment decreased (p < 0.05) the total lipid content of liver compared to control at week 5 after calving. Our results show that CLA supplementation is more efficient in alleviating body mass mobilization and decreasing the incidence of subclinical ketosis when applied as early as 3 weeks before calving than started feeding after calving.

Rumen-protected choline (RPC) was evaluated for effects on the lipid and glycogen content of the liver and metabolic variables in the blood plasma of dairy cows. Thirty-two Holstein cows were allocated into two groups (RPC group with RPC supplementation and control group without RPC supplementation) 28 days before the expected calving. Cows were fed the experimental diet from 21 days before calving until day 60 of lactation. The diet of the RPC group was supplemented with 100 g/day of RPC from 21 days prepartum until calving and 200 g/day of RPC for 60 days postpartum, providing 25 and 50 g of choline, respectively. Liver samples were taken by percutaneous needle biopsy, then analysed for total lipid (TLl), triglyceride (TGl) and glycogen (GLYl) contents on days -21, +7, +35 and +60 relative to calving. Blood was collected on the same sampling days and 21 days after calving. Glucose, non-esterified fatty acid (NEFA), β-hydroxybutyrate (BHBA), triglyceride (TGp), total cholesterol (TCh), urea, ammonia and aspartate aminotransferase (AST) were determined from blood samples. The TLl and TGl contents were 25.0 ± 4.3 g and 25.3 ± 3.8 g per kg wet weight (mean ± SEM), respectively, lower in the RPC group than in the control animals. No significant differences were observed in the GLYl concentrations between the two groups. However, a lower TGl: GLYl ratio was shown in the liver of cows fed the RPC diet as compared to the controls. RPC supplementation decreased BHBA while increasing TGp concentrations were shown in the blood of cows fed the RPC diet, possibly as a consequence of improved lipoprotein synthesis in, and triglyceride excretion from, the liver, together with a reduced rate of ketogenesis.

In calves reared free of Oesophagostomum radiatum and given a single infection of this helminth, the third ecdysis in the life cycle was completed in the gut wall in 5-7 days. The fourth stage larva moved into the gut lumen between the seventh md 14th days, where the fourth ecdysis occurred between 17 and 22 days. The prepatent period was 32-42 days. Egg production reached its peak usually during the sixth to 10th weeks, and in most calves this rate of production persisted for only 1-4 weeks. The subsequent decline in the egg count to low levels was very rapid, and was accompanied by the elimination of most of the adult worms. Reinfection with large doses of larvae, either during the period of peak egg production or some weeks later when the egg count was at low levels, did not produce any increase in the egg count, except on rare occasions. In these instances only a small increase was detected. Egg counts of calves given daily doses of larvae showed a trend similar to that resulting from a single dose, and attempts at reinfection with massive doses when the egg count had declined to low levels were also unsuccessful in producing any appreciable rise in the egg count. The failure of the egg count to respond to a challenge dose of larvae is regarded as evidence that a resistance to reinfection had been acquired. Resistance was apparent following a single dose as low as 1000 larvae and a daiIy dose as low as 50 larvae. Necropsies confirmed this conclusion and indicated that, whereas the host resistance mechanism could be responsible for the encapsulation of some reinfecting larvae in the gut tissues and their subsequent death, such mechanism was directed mainly against fourth stage larvae shortly after they had moved back to the gut lumen. The reaction here resulted in the elimination of all or most of the larvae and was accompanied by diarrhoea. While some reinfecting larvae survived in nodules for many weeks in the third or fourth stage, it would seem that the majority of those successfully penetrating the tissues completed the histotrophic phase within the normal period. The few reinfecting larvae which survived to maturity in the gut lumen completed their development also within the normal period. Infection was followed by the production of circulating antibodies detectable by both the haemagglutination and complement fixation tests. With calves infected with a single dose of larvae, all developed haemagglutinins, but complement-fixing (C. F.) antibodies were detected only in some, and these had become infected with Cooperia spp. prior to the experiment. Levels of both types of antibody were low, only exceeding in a few calves a titre of 1/80 for haemagglutinins and of 1/20 for C. F. antibodies. Following reinfection, C. F. antibodies were detected in all animals. They appeared simultaneously with haemagglutinins and there was little evidence that reinfection had stimulated any significant secondary rise in either type of antibody. The available data gave no definite indication of any effect of these antibodies in host-parasite reactions. They suggest, however, that haemagglutinins may be indicative merely of a state of infection, and that C.F. antibodies are stimulated more readily after reinfection.

The reaction to helminth infection was studied in calves grazing natural pasture in an area of south-eastern Queensland. Calves raised worm-free were exposed each month to natural infections with Cooperia punctata, C. pectinata, Trichostrongylus axei, Haemonchus placei, and Oesophagostomum radiatum. The observations extended over 2 years. Calves first exposed during the months of higher rainfall (December–April) suffered a mortality of 93%, whereas the mortality was 63% in those placed on the pasture during the drier months. Weight loss and death of calves during the first 8 weeks' grazing was associated with a pasture larval contamination of more than 50 larvae of the above species per sq yd. Evidence was obtained that O. radiatum was the main pathogen during the experimental period, and egg counts of this species greater than 380 eggs per gram of faeces were associated with clinical signs of infection. Some calves, which were initially exposed to infection shortly after seasonal rains had fallen, acquired the highest worm burdens and survived for less than 10 weeks. Calves which survived for 11–22 weeks were on a better than average pasture, and were first exposed to infection at least 4 weeks after suitable rains when the larval population had commenced to decline. These calves acquired approximately half the worm burden recorded for the calves which did not survive beyond 10 weeks. Calves surviving for longer than 22 weeks were first exposed to infection 2–3 months after seasonal rains, and showed a mean maximum O. radiatum egg count less than two-thirds of that recorded for the animals which survived for 11–22 weeks. Body weights in the group surviving for more than 22 weeks did not increase until after 20 weeks, when the egg counts had decreased to consistently low levels. Infective larvae of O. radiatum ingested after the first week did not contribute significantly to the adult population found at necropsy. Despite the inability of these larvae to complete their development, pathogenic effects of the continuous intake continued until about the 20th week. No evidence was found that the presence of haemagglutinating and complement fixing antibodies was correlated with the survival of calves.

The histopathological aspects of the host response to Oesophagostomum radiatum were studied in calves, reared worm-free, following a single dose of 5000–10,000 infective larvae. The penetration of larvae caused mainly productive changes in the gut tissue and was not followed by overt clinical symptoms. Five to seven days after infection, obliteration of small blood-vessels by endothelial proliferation and perivascular accumulation of histiocytes and lymphocytes occurred, \ particularly in the vicinity of the histotropic larvae, resembling a delayed type hypersensitivity reaction. The ensuing inflammation appeared to facilitate the termination of the histotropic phase by disorganizing the tissue produced around the third-stage larva during its development. The migration of fourth-stage larvae to the colon and subsequent moult to the fifth stage was accompanied by infiltration of eosinophil leucocytes into the gut tissue with accumulation of these cells around and within the mucosal glands, particularly in the colon. The resultant crypt abscessi, which resembled the active lesions found in ulcerative colitis, showed protracted healing, with formation of granulomas containing giant cells. Plasma cell production characteristic of a secondary response occurred only in the lymph nodes draining inflamed sections of the large intestine where adult worms were located. Healing of the acute enteritis resulted in fibrosis and hyperplasia of the gut wall.

The histopathological aspects of the host response to Oesophagostomum radiatum were investigated following the reinfection of previously exposed calves. The elimination of third-stage larvae 18–22 hr after administration of the reinfecting dose was associated with oedema, hyperaemia, and hypersecretion in the intestine and was followed by a transient but intense diarrhoea. The infiltration of the oedematous intestinal tissues with eosinophil and neutrophil leucocytes and the vasculitis in the vicinity of the histotropic larvae indicated an Arthus type reaction. During the development of the third-stage larvae the exudative hyperergic inflammation changed to a proliferative granulomatous type. The moulting of the larva to the fourth stage was associated with a recurrence of oedema and vasculitis, and was followed by isolation and elimination of the larva and surrounding necrotic host tissue. If the larva was not discharged the healing was delayed and the nodular lesion persisted. The diarrhoea during the elimination of fourth-stage larvae was associated with oedema of the gut wall, hypertrophy, and profuse secretion of the mucosal glands. These changes developed to an excessive degree in the proximal 2 ft of the colon following the termination of the histotropic phase. The varying course of the enteric process was accompanied by simultaneous changes in the regional lymphatic tissue. Cell destruction, phagocytosis, and depletion of follicles during the acute phases alternated with lymphopoiesis during the proliferative reparative periods. The tissue damage from the exaggerated response to reinfection of a sensitized host resulted in anorexia and weight loss.

Calves raised worm-free were exposed to natural infection on unimproved pasture infected with Trichostrongylus axei, Haemonchus placei, Ostertagia ostertagia, Cooperia punctata and C. pectinata, and Oesophagostomum radiatum. Some calves received, in addition, experimental infections of O. radiatum and H. placei. All calves showed depressed body weight gains. Haematocrit, haemoglobin, and serum protein levels were reduced, returned to normal after 15–18 weeks' grazing in calves that survived, but continued to fall and reached lower levels in those that died. Calves killed in extremis showed emaciation, oedema, degenerated fat tissue, inflammatory and degenerative changes in the gastrointestinal tract, and atrophy of the lymphatic tissues and thymus. These symptoms are reminiscent of a "wasting syndrome".