The effects of different beak trimming techniques on plasma corticosterone and performance criteria in Single Comb White Leghorn hens.

DeKalb XL chicks were given a beak trim at 6 d of age (6DP) with a 2.8-mm gauge and a beak trim at 11 wk (11WB) with a block cut approximately 2 mm anterior to the nasal openings. Corticosterone (CS) levels of the 6DP treatment were (P < or = 0.01) elevated above nontrimmed CS levels at 2 h posttrim; and BW and feed consumption (FC) of the 6DP were depressed until 8 wk of age. At 11 wk of age, CS of the 11WB treatment was (P < or = 0.02) elevated above controls at 1, 2, 8, and 5 wk posttrim. The 11WB treatment resulted in a decrease in FC and a reduction in BW at 12, 14, and 16 wk of age, whereas there were no differences among treatments in livability during the pullet phase. At 72 wk of age, FC of the nontrimmed controls was greater than both beak trimmed treatments, and both beak trimmed treatments had greater hen housed eggs, percentage hen day egg production, and percentage livability. Both beak trimmed treatments resulted in better egg income, feed cost per hen, and net income (NI). The 6DP and 11WB beak trim treatments resulted in an improvement of NI per hen of 1.48 dollars and 1.86 dollars, respectively. In addition, both beak trimmed treatments exhibited better feather score and Hansen's test (fearfulness). It was concluded that pullets and hens could adapt to the physiological stress of beak trimming and out perform, during a lay phase, controls whose beaks were not trimmed.

Novel responses of human skin to intradermal recombinant granulocyte/macrophage-colony-stimulating factor: Langerhans cell recruitment, keratinocyte growth, and enhanced wound healing.

Recombinant granulocyte/macrophage-colony-stimulating factor (rGM-CSF), prepared from Chinese hamster ovary (CHO) cells and Escherichia coli, was administered to 35 patients with the borderline and polar lepromatous forms of leprosy by the intradermal and subcutaneous routes at doses of 7.5-45.0 micrograms/d for 10 d. With each of these doses and routes, increases in the number of circulating eosinophils were noted. After the intradermal injection, the local skin sites demonstrated zones of roughening and micronodularity that appeared within 24-48 h and persisted for more than 6 d. Reinjection of sites led to enhanced areas of epidermal reaction. GM-CSF prepared from CHO cells was a more potent inducer of this effect. GM-CSF given by the subcutaneous route, at higher doses, failed to initiate these changes. At the microscopic level, the epidermis became thickened (+75%) with increased numbers and layers of enlarged keratinocytes. These contained increased numbers of ribosomes and prominent nucleoli, and were imbedded in a looser meshwork of the zona Pellucida. The modified keratinocytes remained MHC class II antigen negative throughout the course of the response. A major change in the dermis was the progressive accumulation of CD1+, Birbeck granule-positive cells. These Langerhans were recognizable at 48 h after intradermal injection and reached maximum numbers by 4 d. During this period the number of epidermal Langerhans cells remained relatively constant. No increment in dermal Langerhans cells occurred when GLM-CSF was injected by the subcutaneous route. No appreciable increase in the numbers of T cells and monocytes was noted, and granulocytes and eosinophils were largely present within the dermal microvasculature. 4-mm punch biopsies taken from injected sites and adjacent controls were compared in terms of the rapidity of wound healing. 22 of 26 sites demonstrated more rapid filling and hemostasis, whereas four were equivalent to controls. We conclude that rGM-CSF, when introduced into the skin, leads to enhanced keratinocyte growth, the selective recruitment of Langerhans cells into the dermis, and enhanced wound healing of the prepared site. There was no evidence of an enhanced cell-mediated response to Mycobacterium leprae, and bacillary numbers remained unchanged.

Inflammation induced by a glycolipid fraction from Mycobacterium leprae.

1. The inflammatory properties of a glycolipid fraction isolated from human recovered Mycobacterium leprae were investigated. The inflammatory reaction induced in mouse lung by the inoculation of the glycolipid fraction adsorbed to charcoal particles was characterized by a large influx of macrophages at various stages of maturation and of epithelioid cells around the particles. 2. When injected as an aqueous emulsion into the footpad of mice, the same fraction evoked a dose-dependent massive influx of mononuclear (MN) cells. The inflammatory reaction reached a peak at 6 days. The minimal effective dose of glycolipid was 0.1 micrograms. 3. The kinetics of inflammatory cell migration was studied by total and differential counts of leucocytes that migrated to the peritoneal cavity of mice inoculated intraperitoneally with the glycolipid fraction. This fraction initially induced intense polymorphonuclear (PMN) migration, which was later reduced, with a simultaneous increase in MN cells. 4. Adherent peritoneal cells (APC) incubated with glycolipid released one or more soluble factor(s) which induce active PMN and MN cell chemotaxis in vivo as well as in vitro. Thus, the MN cells may be attracted to the site of glycolipid inoculation by factor(s) released through the interaction of macrophages with the glycolipid fraction. 5. The present results demonstrate that a glycolipid containing trehalose and mycolic acid isolated from M. leprae reproduces some aspects of the fundamental lesion of leprosy.

Inflammation induced by a glycolipid fraction from Mycobacterium leprae

1. The inflammatory properties of a glycolipid fraction isolated from human recovered Mycobacterium leprae were investigated. The inflammatory reaction induced in mouse lung by the inoculation of the glycolipid fraction adsorbed to charcoal particles was characterized by a large influx of macrophages at various stages of maturation and of epithelioid cells around the particles. 2. When injected as aqueous emulsion into the footpad of mice, the same fraction evoked a dose-dependent massive influx of mononuclear (MN) cells. The inflammatory reaction reached a peak at 6 days. The minimal effective dose of glycolipid was 0.1 microng. 3. The kinetics of inflammatory cell migration was studied by total and differential counts of leucocytes that migrated to the peritoneal cavity of mice inoculated intraperitoneally with the glycolipid fraction. This fraction initially induced intense polymorphonuclear (PMN) migration, which was later reduced, with a simultaneous increase in MN cells. 4. Adherent peritoneal cells (APC) incubated with glycolipid released one or more soluble factor9s) which induce active PMN and MN cell chemotaxis in vivo as well as in vitro. Thus, the MN cells may be atracted to the site of glycolipid incolulation by factor(s) released through the interaction of macrophages with the glycolipid fraction. 5. the present results demonstrate that a glycolipid containing trehalose and mycolic acid isolated from M. leprae reproduces some aspects of the fundamental lesion of leprosy

Evaluation of bacteraemia in leprosy patients.

Thirty five patients of leprosy have been screened for bacteraemia by haemolysis (HL), leucocyte adherence (LA) and buffy coat (BC) methods and the results have been compared. The HL method has yielded not only higher number of acid-fast bacilli (AFB) but also has detected more frequently AFB in blood of leprosy patients as compared to other methods. Further, it has been established that the skin over the cubital fossa does not play any significant role in contaminating blood samples while sampling blood by venepuncture.