Recovery of Mycoplasma agalactiae from the ears of goats experimentally infected by the intramammary route.

The role of inapparent carriers of Mycoplasma agalactiae and the strategies used to colonise the external ear canal in goats remain unclear. This study examined the ability of M. agalactiae to colonise the ears of goats infected experimentally by the intramammary route. The right mammary glands of 15 lactating goats were inoculated with 10(10) colony forming units (cfu) of M. agalactiae. The goats were randomly assigned to three groups of five animals each and sampled at slaughter at 5, 15 or 45 days post-infection (dpi). A further four goats served as uninfected controls. Right and left ear swabs were collected for detection of M. agalactiae by culture before and after sacrifice. M. agalactiae was detected in 19/20 (95%) ear swabs from goats sampled at 15 and 45dpi, whereas all ear swabs collected before inoculation, ear swabs collected from the group sampled at 5dpi and ear swabs from control goats at the time of sacrifice were negative for M. agalactiae. Blood samples collected at 6, 12, 24, 48 and 72h post-infection for detection of M. agalactiae by culture were also negative. There were differences in the antigenic profiles of isolates recovered from the ears compared to the 7MAG strain used to inoculate the animals and most isolates from the mammary gland, milk and supramammary lymph nodes.

Suitability of electronic mini-boluses for the early identification of goat kids and effects on growth performance and development of the reticulorumen.

A total of 60 twin-goat kids (30 male and 30 female) of the Canary Island Majorera dairy breed were used in 2 experiments to evaluate 2 types of electronic identification mini-boluses and their effects on rearing performances and reticulorumen development. Electronic identification mini-boluses were cylindrical and made of ceramic materials (B1, 9.0 g and 38.5 × 9.5 mm; B2, 16.3 g and 42.2 × 12.2 mm), contained a 32-mm half-duplex passive transponder, and were administered to kids at different BW. In Exp. 1, treatments were 1) control, without bolus (n = 15) and 2) identified with B1 at 4.8 kg of BW (n = 15). In Exp. 2, treatments were 1) control, without bolus (n = 15) and 2) identified with B2 at 5.6 kg of BW (n = 15). Kids were penned separately, according to mini-bolus treatments, fed a milk replacer daily, and slaughtered at 10 kg of BW. Milk replacer intake was recorded individually twice weekly and boluses read weekly until slaughter. The full and empty stomach complex was measured immediately after slaughter, and mini-bolus location was recorded. Samples of the reticulum and rumen wall were taken to measure the number and length of the papillae and crest. Despite the light BW of kids at time of mini-bolus treatment, no negative effects (P > 0.05) of B1 and B2 mini-boluses were observed on milk intake, growth rate, or G:F in either experiment. No kid mortality or mini-bolus losses were observed during either experiment. All mini-boluses were retained until slaughter, and all were found in the rumen upon dissection, except one B2, which was found in the reticulum. Mini-bolus treatment did not affect (P > 0.05) the weight of full and empty reticulorumen or the number of papillae and crest size of the reticulum epithelium. Moreover, the B1-treated kids showed a greater number of papillae in the rumen wall than the control kids (22.4 +/- 1.0 vs. 18.9 +/- 0.9 papillae/cm, respectively; P < 0.05) in Exp. 1. In conclusion, the use of mini-boluses was suitable for the electronic identification of growing kids from early ages (wk 2 to 5 of age and 5 to 6 kg of BW) and did not produce negative effects on their growth performances or on reticulorumen development. These results support the use of properly designed boluses as a unique identification device for the entire lifespan of goats.

Correlating the immune response with the clinical-pathological course of persistent mastitis experimentally induced by Mycoplasma agalactiae in dairy goats.

To correlate the clinical course of mycoplasma mastitis with its immune response, right mammary glands of 15 lactating goats were inoculating with 10(10) colony-forming units (cfu) of Mycoplasma agalactiae (Ma). Before sacrificing the animals at 5, 15 or 45 days post-inoculation (dpi), blood Ma antibody titres and milk mycoplasma colony and somatic cell counts were monitored. Ma colonised the mammary gland and milk counts increased to over 10(12)cfu/ml within 5 dpi. During this period, an innate immune response involving neutrophils and macrophages was observed, and Ma antigen appeared in the degenerated acinar epithelium. From 7 dpi, a specific antibody response coincided with reduced viable mycoplasmas in milk. The humoral immune response was limited; by 37 dpi, all animals scored negative for anti-Ma antibodies, and around 10(8)cfu/ml were shed. Results indicate an early immune response to Ma inoculation unable to control mycoplasmal invasion. An ensuing humoral response, despite reducing the mycoplasma burden, leads to chronic, persistent infection.

Short communication: apoptosis regulates passive immune transfer in newborn kids.

Ten newborn kids were used to evaluate the relationship between apoptosis and passive immune transfer in neonatal enterocytes. Kids were slaughtered in groups of 2 at birth, 1, 2, 3, or 60 d postpartum, and samples of duodenal epithelium collected from each animal. Samples were fixed, dehydrated, and embedded in paraffin wax. Sections were assessed for apoptotic cells and immunostained for IgG. Our results suggest that IgG absorption is mediated by apoptotic enterocytes. Thus, delaying apoptosis may improve the success of passive immune transfer.