136 



Scotland particularly, leaves practically no doubt in our minds as 

 to the infective nature of this disease. The results recorded show 

 that extinction after known contact with the disease is more frequent 

 in winter than in summer. This is doubtless because in large 

 measure loss in summer is compensated by production of bees ; at 

 the same time the closer association as a cluster in winter probably 

 fosters the disease. Also, as the ventilation of the hive in winter 

 is usually much more restricted, this has probably the same effect. 



With regard to those cases in which the disease did not 

 develop after contact within the working period, e.g. No. 5 (p. 128), 

 but in which at a later season it appeared, we have observed that 

 occurrences of this nature are not infrequent. We have in common 

 with various bee-keepers of experience found that in stocks which 

 have been associated in a particular area with sick bees, e.g. those 

 taken to heather in summer, the disease often appears in the 

 following working season. In these cases infection was not con- 

 veyed to the bees which were actually in contact with the disease, 

 for with the exception of the queen these had completed their 

 normal life without showing any signs of the disease before it 

 appeared in the stock. And these bees which actually developed 

 the disease were never in the infected area at all. 



The readiest explanation in such cases, and one which must 

 hold the field in the meantime, is that in these instances we have an 

 infection from an independent source, and that original contamina- 

 tion was merely assumed. We acknowledge, however, that cases of 

 this nature are fairly numerous, and that we cannot set aside 

 entirely the possibility of another explanation. In the experiment 

 quoted above. No. 5, contamination did take place, and no disease 

 followed in the bees in the hive at the time, whilst it developed in 

 the summer following. The assumption of a latent non-infective 

 period for the causal organism would explain all such cases ; so also 

 would the absence in the first season of the conditions necessary 

 for its development in the bees. These views imply a prolonged 

 vitality for the organism outside the bee. 



From the results recorded under brood experiments it would 

 appear that the queen from an Isle of Wight diseased stock does 

 not transmit the disease hereditarily. This is corroborated by the 

 general results obtained in the above described cases where such 

 queens were transferred from their sick stocks to healthy, in which 

 they produced bees over prolonged periods covering usually full 

 working seasons without the appearance of disease. 



We have further obtained some evidence that such queens do 

 not produce bees which are specially susceptible, i.e. of inferior 

 racial quality. Brood from such queens removed from the infected 

 stock and transferred to hives in the immediate neighbourhood did 

 not develop the disease on reaching the adult stage, although the 

 opportunities for infection were very favourable. 



In none of our experiments, with the possible exception of No. 

 3 (p. 134), did the queen convey the disease by contagion. 



From the fact that the queen in a diseased stock invariably 

 survives to the last, it is generally assumed that she is immune to 

 this dsease. Such an assumption is not altogether warranted. It 

 must be borne in mind that she is constitutionally adapted to a 



