Large body size confers a competitive advantage in animal contests but does not always determine the outcome. Here we explore the trade-off between short-term achievement of high social status and longer-term life history costs in animals which vary in competitive ability. Using laboratory mice, Mus musculus, as a model system, we show that small competitors can initially maintain dominance over larger males by increasing investment in olfactory status signalling (scent-marking), but only at the cost of reduced growth rate and body size. As a result they become more vulnerable to dominance reversals later in life. Our results also provide the first empirical information about life history costs of olfactory status signals
SUMMARYNecrobacillosis occurs in man and animals. The typical forms of the disease in animals are caused by Fusobacterium necrophorum biovar A; biovar B strains are much less pathogenic. In this study the pathogenicity for mice of eight human isolates of F. necrophorum was compared with that of animal biovar A and B strains.By subcutaneous inoculation seven of the human strains differed from biovar A but resembled biovar B in (1) producing, at the most, mild local lesions that rapidly healed, and (2) Nonetheless, strain A2433 differed from biovar A, both in the nature of the lesions produced and in its failure to cause severe general signs of illness and rapidly fatal infection.By intravenous inoculation one of two biovar B strains and all except one of the eight human strains produced purulent lesions, often severe, in the liver and elsewhere, but infection was not usually associated with general signs of illness. In contrast, intravenous injection of a biovar A strain gave rise to a rapidly fatal infection, with severe lesions in the liver or elsewhere.The results suggest that the term 'necrobacillosis' as used in human and veterinary medicine refers to diseases that differ in important respects.
Forty-six strains of Fusobacterium necrophorum, 24 from animals and 22 of human origin, were examined by pathogenicity tests in mice, while the same strains were being examined in laboratories elsewhere by other methods. The pathogenicity tests consisted of (1) subcutaneous inoculation with a large dose of a pure culture, (2) subcutaneous inoculation with a small dose of E necrophorum mixed with a large but relatively harmless dose of Staphylococcus aureus, and (3) intravenous inoculation with a large dose of a pure culture. Fourteen strains, all of animal origin, showed the characteristic behaviour of biotype A. Twenty-eight strains, 10 of animal origin and 18 from man, were classified as biotype B. The remaining four strains, all from man, produced a distinct type of infection in mice; these strains were referred to as 'A2433-like' because of their resemblance to a strain described in an earlier study. It would appear that biotype A strains, responsible for classical necrobacillosis in animals, do not infect man; that biotype B strains occur in both man and animals; and that 'A2433-like' strains are probably confined to man.
Oral pretreatment of mice with either a mixture of kanamycin and erythromycin or metronidazole to modify the gut microflora greatly enhanced the faecal excretion of Fusobacterium necrophorum biovar A given by mouth. This lends support to the suggestion that disturbance of the gastrointestinal microflora in animals such as cattle, which often carry the organism in the rumen, may lead to intestinal multiplication and faecal excretion, thereby providing a source of infection that may lead to necrobacillosis of the body surface.
Only a small proportion of animals tested were found to be excreting Fusobacterium necrophorum biovar A, the causative organism of necrobacillosis, in the faeces (3 of 69 wallabies, 1 of 66 deer, 2 of 81 cattle). The two positive cattle belonged to a single group of calves on a farm with a history of necrobacillosis and the litter underfoot also readily yielded biovar A organisms. All attempts to demonstrate biovar A in litter on other farms and in soil from an area populated by wallabies and deer failed. Ruminal contents from young beef cattle proved a fertile source of F. necrophorum biovar A, 15 of 18 animals giving a positive result. It is suggested that disturbance of the gastrointestinal microflora leads to intestinal multiplication and faecal excretion of the organism, which may then give rise to necrobacillosis of the body surface.
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