Drug – bio-affecting and body treating compositions – Antigen – epitope – or other immunospecific immunoeffector
Reexamination Certificate
1998-12-18
2001-09-11
Nolan, Patrick J. (Department: 1644)
Drug, bio-affecting and body treating compositions
Antigen, epitope, or other immunospecific immunoeffector
C424S009100
Reexamination Certificate
active
06287564
ABSTRACT:
FIELD OF THE INVENTION
The invention relates to a method of identifying and breeding high immune response animals within a population of animals under stress, such as during peripartum.
BACKGROUND OF THE INVENTION
It has been found that there is an association between stress and disease occurrence in animals (T. Molitor and L. Schwandtdt, “Role Of Stress On Mediating Disease In Animals”, Proc. Stress Symposia: Mechanisms, Responses, Management. Ed., N. H. Granholm, South Dakota State University Press, Apr. 6-7, 1993). Further it has been suggested that stress can lead to a compromised immune system. (T. Molitor and L. Schwandtdt, “Role Of Stress On Mediating Disease In Animals”, Proc. Stress Symposia: Mechanisms, Responses, Management. Ed., N. H. Granholm, South Dakaota State University Press, Apr. 6-7, 1993/ Morrow-Tesch J. L. et al. 1996 J. Therm. Biol. 21(2):101-108) This can have significant effect on populations of animals such as commercial livestock including cattle, pigs, poultry, horses, and fish, wherein stress can be related to growth inhibition, infertility, and decreased milk or egg production (where applicable). It has been shown that the peripartum period or periparturition, in animals is a period of stress. (L. G. Johnson, “Temperature Tolerance, Temperature Stress, and Animal Development”, Proc. Stress Symposia: Mechanisms, Responses, Management. Ed., N. H. Granholm, South Dakaota State University Press, Apr. 6-7, 1993; J. J. McGloner, “Indicators Of Stress In Livestock And Implications For Advancements In Livestock Housing”, Proc. Stress Symposia, : Mechanisms, Responses, Management. Ed., N. H. Granholm, South Dakaota State University Press, Apr. 6-7, 1993; T. Molitor and L. Schwandtdt, “Role Of Stress On Mediating Disease In Animals”, Proc. Stress Symposia: Mechanisms, Responses, Management. Ed., N. H. Granholm, South Dakaota State University Press, Apr. 6-7, 1993; M. J. C. Hessing et al, “Social Rank And Disease Susceptibility In Pigs”, Vet Immunol. Immunopath 43:373-387, 1994; F. Blecha, “Immunoligcal Reactions Of Pigs Regrouped At Or Near Weaning”, Am. J. Vet. Res. 46(9): 1934-1937, 1985; D. L. Thompson et al., “Cell Mediated Immunity In Marek's Disease Virus-Infected Chickens Genetically Selected For High and Low Concentrations Of Plasma Corticosterone”, Am. J. Vet. Res. 41(1):91-96, 1980; Kehrli, H. E. et al., 1989a & b, Am. J. Vet. Res. 50(2):207 and 215).
Impairment of bovine host defense during the peripartum period may be associated with high concurrent disease occurrence. Impaired resistance may be due to endocrine factors associated with metabolic and physical changes occurring during gestation, parturition and lactation (Smith et al., 1973; Guidry et al., 1976; Burton et al., 1993). Infectious diseases of the peripartum period include mastitis, metritis and pneumonia. Metabolic and some reproductive diseases also predominate during this period and include retained placenta, milk fever, ketosis, and displaced abomasum. Mastitis is the most economically relevant disease. Estimated annual losses from mastitis are $35 billion (U.S) worldwide (Giraudo et al. 1997), $2 billion (U.S.) in the United States (Harmon, 1994) and $ 17 million (Can.) in Canada ($140-300 Can./cow) (Zhang et al., 1993).
Mastitis is an inflammation of the mammary gland characterized by local and systemic responses (Burvenich et al., 1994). Mastitis can be clinical or subclinical, when signs are not directly observable, but somatic cell counts in milk (SCC) increase and overall production performance decreases. Mastitis is caused by a number of Gram positive and Gram negative bacteria which are either major or minor pathogens. Major pathogens induce the greatest compositional changes in milk and have the greatest economic impact (Harmon, 1994). They include
Staphylococcus aureus, Escherichia coli, Streptococcus agalactiae
, Klebsiella spp., and others, while minor pathogens include coagulase negative staphylococci, and
Corynebacterium bovis
. The incidence of udder infection and clinical mastitis is usually highest at parturition and during early lactation (Smith et al., 1985). Coliforms such as
E. coli
and Klebsiella are the most common major pathogen during this period. Since coliform mastitis is difficult to treat, natural defence mechanisms of the mammary gland have been investigated in pursuit of control procedures (Burvenich et al., 1994). Coliform mastitis may be peracute and fatal, or subclinical. Most commonly it is acute clinical mastitis, with local and systemic signs of disease. Coliforms are Gram-negative microorganisms from the family Enterobacteriaceae which include important species from the genera Escherichia, Klebsiella, Enterobacter, Citrobacter and Proteus (Harmon, 1994; Kremer et al., 1994). The structure of the cell wall of coliform bacteria plays an important role in the virulence of the bacteria and subsequently in the pathogenesis of mastitis. The cell wall of
E. coli
has an inner cytoplasmic membrane, a peptidoglycan layer, an outer membrane that consists of two layers: a phospholipid protein layer and an outer lipopolysaccharide layer (LPS), and finally some strains possess an additional capsular polysaccharide layer. The LPS layer has three components: the O-specific polysaccharide chain, a polysaccharide core, and lipid A. Lipid A mediates the biological properties of LPS (endotoxin). Endotoxemia causes clinical signs of disease including high fever, drowsiness, appetite loss, dehydration, loss in milk production, cardiovascular failure, shock and often death (Kremer et al., 1994; Burvenich et al., 1994). Factors which contribute to susceptibility to mastitis include the complex environment (pasture, bedding, cleanliness of holding areas), management (milking practices, antibiotic therapy during lactation and dry-off) and physical trauma to the teat and/or udder (Cullor, 1995).
Various attempts have been made to develop vaccines against
S. aureus
as a treatment for mastitis, but without success. Vaccines have included toxoid, protein A, capsule and fibronectin in varying combinations and concentrations (reviewed by Sordillo, 1995). While these preparations may reduce the severity and duration of mastitis, new infections are not prevented. Inclusion of capsular polysaccharide in vaccine preparation slightly reduced the rate of new infection (Watson and Schwartskoff, 1990). More recently, the combination of a crude extract of
S. aureus
exopolysaccharides and inactivated unencapsulated
S. aureus
and Streptococcus spp. in a vaccine decreased incidence of intramammary infections caused by
S. aureus
(Giraudo et al., 1997). Newer vaccines against environmental coliforms contain rough or R-mutants of
E. coli
or
Salmonella typhimurium
. The surface core antigens of these mutants induces formation of cross-protective antibody that provides protection against various gram-negative diseases of animals including mastitis and calf scours. (Parker et al., 1994). These vaccines decrease incidence and severity of clinical disease but do not affect prevalence of coliform infections (Sordillo, 1995).
Direct selection for disease resistance may be done either by selecting the most disease-resistant breeding stock under normal environmental conditions, or by challenging the breeding stock with specific pathogens (Hutt, 1959). Indirect selection is based on identification of reliable indirect markers of disease resistance (Detilleux et al., 1993). Phenotypic indicators include morphological markers (eg. eye margin pigmentation in bovine infectious keraconjunctivitis), physiological markers (eg. hemoglobin type in malaria), and innate or immune response traits (eg. PMN function, antibody response and CMI). Genotypic indicators include candidate genes (eg. MHC genes, Ig genes, TcR genes), and anonymous molecular genetic markers (eg. RFLPs, tandem repeats loci, microsatellite loci) (Detilleux et al., 1993).
Experiments using immune response variation as selection criteria have been successful at directing response to be high or low (Biozzi et al., 1968;
Mallard Bonnie
Wagter-Lesperance Lauraine
Bereskin & Parr
Gravelle Micheline
Nolan Patrick J.
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