Summary1. The risk of parasitism and infectious disease is expected to increase with population density as a consequence of positive density-dependent transmission rates. Therefore, species that encounter large fluctuations in population density are predicted to exhibit plasticity in their immune system, such that investment in costly immune defences is adjusted to match the probability of exposure to parasites and pathogens (i.e. densitydependent prophylaxis). 2. Despite growing evidence that insects in high-density populations show the predicted increase in resistance to certain pathogens, few studies have examined the underlying alteration in immune function. As many of these species show increased cuticular melanism at high densities, the aim of this study was to use a multivariate approach to quantify relative variation in the allocation of resources to immunity associated with both rearing density (solitary vs. crowded) and cuticular colour (pale vs. dark) in a phase-polyphenic Lepidopteran species ( Spodoptera littoralis Boisduval). 3. Relative to pale individuals, dark larvae (the high-density phenotype) exhibited higher haemolymph and cuticular phenoloxidase (PO) activity and a stronger melanotic encapsulation response to an artificial parasite inserted into the haemocoel. However, they also exhibited lower antibacterial (lysozyme-like) activity than pale larvae. Larval density per se had little effect on most of the immune parameters measured, though capsule melanization and antibacterial activity were significantly higher in solitary-reared than crowded larvae. 4. Correcting for variation in larval body condition, as estimated by weight and haemolymph protein levels, had little effect on these results, suggesting that variation in immune function across treatment groups cannot be explained by condition-dependence. These results are examined in relation to pathogen resistance, and the possibility of a trade-off within the immune system is discussed.

No abstract

To determine whether the portion of a vertebrate host population having specific immunity to tick-borne encephalitis (TBE) virus can participate in the TBE virus transmission cycle, natural hosts immunized against TBE virus were challenged with infected and uninfected ticks. Yellow-necked field mice (Apodemus flavicollis) and bank voles (Clethrionomys glareolus) were either immunized with TBE virus by subcutaneous inoculation of the virus, or they were exposed to virus-infected Ixodes ricinus ticks. One month later, when serum neutralizing antibody was detectable, the animals were infested with infected (donor) adult female ticks and uninfected (recipient) nymphal ticks; recipients were allowed to feed either in close contact (chamber 1) or physically separated (chamber 2) from the infected donor ticks. Following challenge with infected (and uninfected) ticks, viremia developed in all the control, nonimmune animals, whereas viremia was undetectable in all those animals naturally immunized by previous exposure to infected ticks. Despite the presence of neutralizing antibodies in all the immunized animals, 89% (24/ 27) immune animals supported virus transmission between infected and uninfected cofeeding ticks. Most transmission was localized, occurring within chamber 1; disseminated transmission from chamber 1 to chamber 2 was reduced. Immunization by tick bite was more effective than immunization by syringe inoculation in blocking cofeeding virus transmission. Nevertheless 76% (9/12) animals with "natural" immunity still supported transmission. The results demonstrate that natural hosts having neutralizing antibodies to TBE virus (and no detectable viremia) can still support virus transmission between infected and uninfected ticks feeding closely together on the same animal. These observations have important epidemiological implications relating to the survival of TBE virus in Nature.

No abstract

No abstract