Volume 6, Issue 3
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645



Cortisone was administered to 40 of a total of 60 rats, starting on the day when all animals were infected with larvae by stomach tube. Twenty animals were treated for a total of 30 days; the other 20 received cortisone for 60 days. Five months after the primary infections, approximately half of each group of rats was reinfected. Five weeks later, all animals were killed; serum was taken for serologic studies and larval counts were made to determine the numbers of larvae encysted in the musculature. Animals treated for 30 days with cortisone developed slightly greater numbers of encysted larvae than their untreated controls; those treated for 60 days were found to contain very much larger numbers of larvae in the muscles. Upon reinfection, the untreated controls failed to develop additional larvae in the musculature, while the animals treated for 30 and 60 days developed large (and approximately equal) numbers of larvae.

Serologic studies, using lyophilized larvae as the source of antigen for a microflocculation test, demonstrated the presence of a measurable amount of circulating antibody in the untreated controls after primary infections. More of the animals demonstrated higher titers of antibody upon reinfection. Animals treated with cortisone for 30 days developed a high titer of circulating antibodies, while those treated for 60 days largely failed to develop any demonstrable antibodies.

To explain the lack of immunity to reinfection on the part of both 30 and 60-day treated animals, in spite of the presence of a high titer of circulating antibodies in the 30-day group, it is suggested that resistance to adult worms may be brought about by a specific delayed tissue hypersensitivity of the infectious variety, involving the intestinal mucosa. There is some evidence that such hypersensitivity may be masked by the action of cortisone.


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