Drug – bio-affecting and body treating compositions – Lymphokine
Patent
1986-08-05
1988-05-10
Schain, Howard E.
Drug, bio-affecting and body treating compositions
Lymphokine
424 88, 435 68, 530395, A61K 3900, G01N 3353
Patent
active
047434465
DESCRIPTION:
BRIEF SUMMARY
BACKGROUND OF THE INVENTION
1. Field of the Invention
This invention relates to antigens produced by the liver fluke organism Fasciola.
2. Brief Description of the Drawing
The accompanying drawing shows schematically the life cycle of Fasciola hepatica.
3. Description of Prior Art
Fasciola hepatica infections in cattle and sheep are reported to be responsible for losses due to poor growth and low milk yields valued in 1974 at (40 million per annum in the UK alone. It is also known that liver fluke increases susceptibility to salmonellosis in cattle. F. hepatica infections are also a serious problem in sheep, and increase susceptibility to "Black disease" caused by Clostridium oedematiens.
F. hepatica is a form of parasitic worm and has a complex life cycle involving more than one host which can more easily be understood from the accompanying drawing. The mature (adult) flukes reside in the bile ducts of a vertebrate host (cattle, sheep, etc.), from which eggs pass into the intestine and eventually onto pastures in faeces. After embryonation, miracidia are formed which hatch to infect certain species of snails (the second host). Asexual reproduction occurs in the snail and after some weeks the pre-infective form of fluke, known as cercariae, is released. A single miracidium typically gives rise to 200-600 cercariae. The cercariae anchor themselves to suitable substrates such as grass and secrete refractory coats or cysts. This process is called encystment. The encysted stage is known as a metacercaria and it is in this form that the parasite enters the vertebrate host, thereby infecting it. After ingestion by the vertebrate host, the juveniles emerge from their metacercarial cysts in the small intestine (a process known as excystment). The emergent free juveniles are hereinafter referred to as 0-day juveniles, to indicate the infective stage of the juveniles, at which they are ready to infect the animal. In this specification the "juvenile" stage means all stages from immediately before infection up to 4 days post infection (p.i.) in mice. (The length of the juvenile stage varies from one animal species to another). The juveniles migrate across the peritoneal cavity to the liver and thence to the bile duct, wherein they mature to adulthood.
Although there are many good chemotherapeutic agents available to combat liver flukes, the majority are ineffective against the earliest stages of a primary infection. Since primary infections often cause chronic, sometimes acute, disease, it would be advantageous to immunise the animals to protect against the earlier stages of primary infection. Dead adult flukes are ineffective, see K. B. Sinclair et al., Res. Vet. Sci. 16, 320-327 (1974). These observations have led to the hypothesis that a change in surface antigens occurs during the growth and development of F. hepatica. The juvenile and adult forms of fluke have a tegument, which includes a surface cytoplasmic layer connected to sub-muscular cellular regions by cytoplasmic tubes. The structure and cellular composition of the tegument changes with maturation of the fluke. The cytoplasmic layer has on its surface a plasma membrane which has on it a glycoproteinaceous surface layer which is known as the glycocalyx. The newly emerged 0-day stage juvenile flukes (NEJs) possess a glycocalyx specific to the juvenile stage, which is subsequently shed and exchanged for another type of glycocalyx before adulthood. The fluke replaces the shed layer after a short period by secretions from the tegument. It therefore changes the outermost surface which it presents to the vertebrate host and therefore the surface antigens which have stimulated an immune reaction in the host. It is thought that by this means the parasite evades immune attack, since by the time that the host has been stimulated to produce antibodies to the juvenile stage specific surface antigens presented, the fluke has changed its surface. In this way, a primary infection of fluke may evade the immune response for long enough to enter the liver parenchyma (a rel
REFERENCES:
patent: 4416866 (1983-11-01), Strand
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National Research Development Corporation
Schain Howard E.
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