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History. The method of artificial insemination was first applied to dogs by Lazzaro Spallanzani, an Italian physiolo­gist as early as 1780. At that time the method aroused only scientific interest. Some practical use of artificial insemi­nation was made in horse breeding about 1890. Wide use of artificial breeding for improvement in farm animals was first made in the USSR through the work by Ivanov. He started the program with horses about 1900 and soon in­cluded cattle and sheep; by 1938 this method of breeding had been in common practice for breeding mares (a female horse), cows and ewes.

Importance of Artificial Insemination. The method of artificial insemination is now applied to all classes of farm animals, especially to dairy cows. By artificial insemination the maximum results are obtained from the best sires. The number of cows bred by one bull can be increased from the normal number of between 30 and 50 per year by natural service, up to between 300 and 700 and in some cases up to 10,000 or more.

 

 

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Supplementary reading

Avian influenza

Avian influenza (Fowl Plague) in chickens is characterized by a high morbidity and mortality rate with respiratory and nervous signs. The characteristic lesions include subcu­taneous hemorrhages, cyanosis of the head region, edema of various parts of the body, and hemorrhages in the pro-ventricles.

Incidence. Avian influenza virus, associated with highly fatal disease, has been isolated in a number of countries. Less pathogenic types are frequently associated with respiratory disease in turkeys. Infection is probably widespread in wild bird populations.

Susceptibility. Influenza virus naturally infects ducks, however, chickens, turkeys, geese, quail, and a wide variety of wild birds are susceptible to the infection.

Cause. The causative agent is a virus which belongs to the influenza group of viruses. There are a number of sero­types isolated from avian species which differ widely in their pathogenicity. The virus is readily destroyed in the poultry environment.

Transmission.

Contact spread readily occurs among pen mates.

Aerosol spread of the virus has been reported to occur between flocks.

The possibility of vertical transmission should always be considered, especially with less pathogenic types.

Mechanical means of transfer of infection include peo­ple, equipment, and artificial insemination.

Clinical signs. In susceptible chickens following an incu­bation period of 2-4 days the signs of the disease may appear suddenly. The course of the disease is usually short and the virus spreads rapidly within a flock.

Following the onset of signs, birds may only live a few hours. In field outbreaks morbidity may be 100 per cent and mortality may vary from 50 per cent to 100 per cent. The flock is generally depressed. Individual birds have ruffled feathers, inappetence and drop in egg production. The eye­lids may be closed and the conjunctiva is red and swollen. Characteristically edema and cyanosis develop around the head region involving the comb, wattles and the area sur­rounding the eyes. The edema may extend down the neck and breast. Edema of the glottis may occur causing diffi­culty in breathing resulting in suffocation. When respiratory signs are present a grey to blood-tinged mucus exudes from the nostrils. There may be hemorrhages in the mouth. In most outbreaks varying degrees of di­arrhea may be observed.

Affected birds usually die within 2 days of the onset of signs. Birds surviving the acute phase of the disease deve­lop nervous signs including excitation, convulsions, or cir­cling movements and ataxia.

 

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