F. NEGROPHORUS 481 



variable. Mannitol and lactose are not fermented. A soft clot is formed in 4-14 days 

 in litmus milk. Indole +. HjS +. Nitrate reduction — . M.R. — . V.P. — . Methyl- 

 ene blue reduction +. Catalase weakly positive. 



Antigenic Structure. — Antigenic relationships exist within the group, and in some 

 sm-veys the strains examined have fallen into a relatively few groups. As a whole, how- 

 ever, the species is antigenically heterogeneous (see Orcutt 1930, Beveridge 1934, Dack, 

 Dragstedt and Heinz 1937, Henthorne, Thompson and Beaver 1936, Walker and Dack 

 1939). 



Pathogenicity. — F.necrophorus appears to be responsible for several necrotic and gan- 

 grenous lesions in animals, such as calf diphtheria, labial necrosis of rabbits, and foot-rot of 

 sheep, and occasionally for necrotic lesions in man. Organisms identical with or closely 

 simulating F. necrophorus have been described by Harris and Brown (1927) in puerperal 

 fever, by Dack, Dragstedt and Heinz (1936) in chronic ulcerative colitis, by Thompson 

 and Beaver (1931) and Cohen (1932) in human lung abscesses, by Beaver, Henthorne and 

 Macy (1934) in hepatic abscesses, and by Lemierre (1936) as a cause of pyaemia and septi- 

 caemia (see also Necrobacillosis, Chapter 79). 



Experimentally, the organism is pathogenic for rabbits and mice. It is non-pathogenic 

 for guinea-pigs, dogs, cats, pigeons, and hens, 

 though McCullough (1938) succeeded in infect- 

 ing guinea-pigs deficient in vitamin C with \ 

 human strains of F. necrophorus. Inoculated \ ^ 

 subcutaneously into the lower lip of rabbits, it > \ 

 gives rise to the typical necrotic disease (see \ \ 

 p. 1788), and causes death in 4—12 days. In- \ 

 jected intraperitoneaUy into rabbits, it proves \ 

 fatal in about the same time ; p.m. the per- \^ 

 itoneum is covered with large white masses, •. ^ ^ 

 sticking the two layers of serosa together ; X. \ 

 similar masses of caseous material occur between X \ » 

 the intestinal loops. Cultures can be obtained \ ^ 

 from the peritoneum. Intravenous inoculation \ 

 into rabbits is fatal in about 8 days ; post 

 mortem, there is a fibrmo-piu"ulent pleurisy, 



a caseous bronchitis, and disseminated lobular Fig. 88. — Fusiformis fusifortnis. 



pneumonia ; the bacilU can be cultiu-ed from the From a surface culture on serum agar, 

 affected organs. Histologically, the organisms anaerobically 2 days, 37° C. (X 1000), 



give rise to intense inflammation, followed by a 



rapid necrosis not only of the fixed tissue cells but also of the cells of the exudate ; no 

 liquefaction of the necrotic material occurs. 



Mice inoculated subcutaneously at the root of the tail die after about 12 days in an 

 emaciated condition. Two days after the inoculation, the local site is covered with a 

 dry brownish crust ; later a yeUowish-grey discoloration of the borders of the inoculation 

 wound becomes visible, and gradually spreads till at the time of death the whole of the 

 lower third of the back is involved. A purulent conjunctivitis develops, and the lids 

 are stuck together. Post mortem, the subcutaneous tissue around the wound and over 

 the lower part of the back is converted into a tough, dryish, yellowish-white necrotic 

 mass ; the caseation involves the back muscles as well. The whole area is surrounded 

 by oedema. Numerous organisms are found in the caseous material. The internal organs 

 appear normal. 



In both rabbits and mice the organism is said to be found only in the affected parts, 



never in the blood or in those internal organs that are free from lesions, but on this 



question there is some doubt. The ability of the organism to produce lesions seems to 



be largely due to its production of a necrotizing endotoxin (Beveridge 1934). There 



P.B. B 



