On Breeding Chicks Resistant to Pullorum Disease Without Exposure Thereto

Pullo~um disease, once more graphically labelled as bacillary white diarrhoea, is a disease, primarily of voung chiclts, caused by the bacterium, Snlnzonelln pzrllorz~m. ~ f f e c t e d chiclts show symptoms within a few days after hatching and thc peak of mortality is usually passed by nvo weelts of age. Resistance is lowered by chilling, especially during the first weelt of life. Because the causative organism can be transmitted from infected hens through their eggs to the next generation, the orthodox method of control is to exclude from breeding floclts all birds that react to agglutination tests for S. pzlllorznn. Another method, unorthodox but effective, is mentioned later. Evidence that chiclts differ genetically in resistance to pullorum disease has recently been reviewed elsewhere (Hutt, 1958). I t will suffice here to state ( I ) that Leghorns have been shown to be more resistant than Rhode Island Reds and other heavy breeds (Hut t and Scholes, 1941), ( 2 ) that the natural resistance of ~ e ~ h o i n s can be enhanced by selection, as Roberts and Card (1935) have shown and (3) that equally resistant stock can be developed similarly even in Rhode Island Reds (De Volt et nl., 1941). Some yeass ago the senior author began a search for any detectable difference between birds resistant to pullorum disease and those susceptible t o it. Followino the discovery that chiclts of a resistant breed (White Leghorn) 9 are able to r a m body temperature Inore rapidly during the first 10 days after hatching than Rhode Island Reds (Hutt, 1935; Lamoreux and Hutt; 1939), further investigations showed that this samc difference distinguishes resistant chiclts and resistant families from susceptible ones within a pure breed. Eventually, from the studies of Scholcs and Hut t (1912) and Ram and Hut t (1955), recently reviewed by Hut t ( 1958), it was concluded that genetic resistance to S. ~ Z L ~ ~ O T Z L ~ J ~ is associated wit11 superior control of the thermoregulatory mechanism. That superiority is shown not only (1) by a sustained febrile reaction after infection, but also ( 2 ) , in chiclts not infected, by more rapid transition from the poiltilothermic state of the embryo during incubation to thc 1~omoiothermic one of thc ten-day-old chick. Thc ratc of that transition can be measured by thc avcragc tcmpcrature of thc chick up to 10 days of agc, or even to 6 days of dgc. I n ,211 optimum environment, the a\7erage temperature of uninfectcd chiclts at 10 davs of age is 105 to 107°F. Sincc 1,amoreus (1935) has found tcmpcratbrcs over 109°F. in adult rvactors (prcsumably infcctcd), it was recognizcd that defence in the chiclt did not lic in attaining the thermal dcath point for S. pzdlori1~17, but more liltcly in the acceleration by higher temperatures of such dcfencc mechanisms as pl~agocytosis, bacteriolj~sis and the production of anti,l~odics.