834 BRUCELLA 



(1934) prepares a mixture of 60 per cent, egg yolk and 40 per cent, rabbit serum 

 sterilized at 70°-75° C. on 3 successive days. Liquid media can ako be used 

 (Tamura and Gib by 1943) ; Steinhaus, Parker and McKee (1944) recommend for 

 this purpose a medium containing 1 per cent, dextrose, 0-15 per cent, cystine, 

 and 0-5 per cent, haemoglobin. Br. ttilarensis grows weU in the developing chick 

 embryo, multiplying particularly in the ectodermal epithelial cells. When inocu- 

 lated on to the chorio-aUantoic membrane, it leads to the death of the embryo 

 in 3-4 days. In both these respects it resembles Br. melitensis (Buddingh and 

 Womack 1941, Ransmeier 1943). Under suitable conditions the organism is said 

 to produce acid in glucose and glycerol, and usually in maltose, mannose and 

 Isevulose (Downs and Bond 1935, Francis 1942) ; but the acid produced seems 

 to be very slight, and may possibly be of the order of that formed by melitensis 

 and American suis strains. 



Moist heat at 55°-60° C. is fatal in 10 minutes. Antigenically Br. tularensis is 

 allied to the other members of the Brucella group. Francis and Evans (1926) found 

 that a serum prepared against Br. tularensis agglutinated Br. melitensis and Br. 

 abortus to about J or ^ of the titre. Neither organism was able, however, to absorb 

 the homologous agglutinins from a tularensis serum. Br. tularensis was agglutinated 

 to a low titre by anti-melitensis and anti-abortus sera, but was luiable to absorb 

 the homologous agglutinins from these sera. The 3 strains oiBr. tularensis examined 

 appeared to be antigenically homogeneous. 



Under natural conditions it gives rise to tularaemia in rodents — especially ground- 

 squirrels and jack-rabbits — and occasionally in man. Sheep are sometimes affected 

 (Parker and Dade 1929). Experimentally the disease can be reproduced in ground- 

 squirrels, gophers, guinea-pigs, rabbits, mice, and monkeys ; rats are more resistant 

 (Dieter and Rhodes 1926) ; cats, dogs, and pigeons appear to be immune. Feeding, 

 nasal instillation, cutaneous, subcutaneous, intraperitoneal, and conjunctival 

 infection are all successful. After subcutaneous infection of the guinea-pig, death 

 occurs in 5 to 8 days. Post mortem there is a whitish membrane-like area at the 

 site of inoculation ; the regional lymphatic glands may be enlarged and caseous ; 

 the spleen is enlarged, very dark in colour, and contains discrete, yellowish-white, 

 caseous granules up to 1 mm. in diameter, projecting shghtly above the surface ; 

 there are numerous granules in the liver ; focal necrotic areas are sometimes present 

 in the bone marrow (Lilhe and Francis 1933) ; the lungs are rarely involved. The 

 baciUi are present in large numbers in the blood and organs ; as little as 0-000,000,1 

 ml. of the heart's blood may prove infective for fresh animals. The virulence of 

 the organism may decline in culture, so that instead of causing an acute or subacute 

 disease in guinea-pigs, it gives rise to a chronic disease from which the animal often 

 recovers (McCoy 1912, Foshay 1932). Strains of lowered virulence have also been 

 isolated directly from ticks (Davis et al. 1934). The organism is extremely dangerous 

 to handle in the laboratory, and large numbers of workers have contracted the 

 infection. 



REFERENCES 



Alessandbini, a. and Sabatucci, M. (1931) Ann. Igiene (Sper.), 41, 29, 852. 



Antoni, V. DE. (1929) Boll. 1st. sieroter. Milano, 8, 651. 



Bang, B. (1897) Z. Thiermed., 1, 241. 



Bang, 0. (1931) 2me Congr. int. Path, comp., i. 95. 



Bau, K. H. and Wang, K. (1935-36) Z. Hyg. InfektKr., 117, 399. 



Beattie, C. p. and Rioe, R. M. (1934) J. Amer. med. Ass., 102, 1670. • 



Beller, K. and Stookmaybr, W. (1933) Dtsch. tierdrztl. Wschr., 41, 551. 



Bee, a. (1933) Z. InfektKr. HausL, 44, 129; (1936) C. R. Soc. Biol., 122, 845. 



Bevan, L. E. W. (1930) Brit. med. J., ii. 267. 



Bieling, R. (1930) Z. Hyg. InfektKr., Ill, 728. 



BoswoETH, T. J. (1938) J. comp. Path., 50, 345. 



Bruce, D. (1887) Practitioner, 39, 161; (1893) Ann. Inst. Pasteur, 7, 289. 



