In seven cynomolgus monkeys, ascorbic acid deficiency was experimentally produced by feeding with a compressed diet containing no ascorbic acid for 20 weeks. Then, these monkeys were challenged with 0.02mg (viable count: 7.1×10
6) of
Shigella flexneri 2a strain 5503 by the oral route, resulting in the development of pronounced clinical dysentery in 3 out of 7 deficient monkeys 4, 6 and 12 days after the challenge. On the contrary, none of 4 control healthy monkeys challenged with the same dose of the homologous strain exhibited any signs of clinical dysentery.
By the near end of the period producing experimental ascorbic acid deficiency, however, the other 2 animals destined for the use in experimental challenge had succumbed to natural infection with
S. flexneri 2a. And some of the animals in both the experimental and the control groups harbored
S. flexneri 2a or
S. flexneri var. Y on the day of challenge. Thus, it should not be neglected that the present experimental challenge with a relatively small dose of
S. flexneri 2a may be regarded as having been carried out under the situation that an inapparent natural infection with
Shigella was occurring among the monkeys used.
In any event, these results seem to indicate that the ascorbic acid deficient monkey has, more or less, a lowered resistance to
Shigella infection.
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