A comparison of mark–release–recapture methods for estimating colony size in the wood ant Formica lugubris

AbstractAvian cholera, caused by the bacterium Pasteurella multocida, is a common and important infectious disease of wild birds in North America. Between 2005 and 2012, avian cholera caused annual mortality of widely varying magnitudes in Northern common eiders (Somateria mollissima borealis) breeding at the largest colony in the Canadian Arctic, Mitivik Island, Nunavut. Although herd immunity, in which a large proportion of the population acquires immunity to the disease, has been suggested to play a role in epidemic fadeout, immunological studies exploring this hypothesis have been missing. We investigated the role of three potential drivers of fadeout of avian cholera in eiders, including immunity, prevalence of infection, and colony size. Each potential driver was examined in relation to the annual real-time reproductive number (Rt) of P. multocida, previously calculated for eiders at Mitivik Island. Each year, colony size was estimated and eiders were closely monitored, and evaluated for infection and serological status. We demonstrate that acquired immunity approximated using antibody titers to P. multocida in both sexes was likely a key driver for the epidemic fadeout. This study exemplifies the importance of herd immunity in influencing the dynamics and fadeout of epidemics in a wildlife population.

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The Abundance of Microcystin-Producing Genotypes Correlates Positively with Colony Size in Microcystis sp. and Determines Its Microcystin Net Production in Lake Wannsee

Applied and Environmental Microbiology ◽

10.1128/aem.69.2.787-795.2003 ◽

2003 ◽

Vol 69 (2) ◽

pp. 787-795 ◽

Cited By ~ 150

Author(s):

Rainer Kurmayer ◽

Guntram Christiansen ◽

Ingrid Chorus

Keyword(s):

Growth Rate ◽

Colony Size ◽

Population Growth Rate ◽

Size Class ◽

Net Production ◽

Cell Numbers ◽

Size Classes ◽

Key Factor ◽

Genotype Composition ◽

Working Hypotheses

ABSTRACT The working hypotheses tested on a natural population of Microcystis sp. in Lake Wannsee (Berlin, Germany) were that (i) the varying abundance of microcystin-producing genotypes versus non-microcystin-producing genotypes is a key factor for microcystin net production and (ii) the occurrence of a gene for microcystin net production is related to colony morphology, particularly colony size. To test these hypotheses, samples were fractionated by colony size with a sieving procedure during the summer of 2000. Each colony size class was analyzed for cell numbers, the proportion of microcystin-producing genotypes, and microcystin concentrations. The smallest size class of Microcystis colonies (<50 μm) showed the lowest proportion of microcystin-producing genotypes, the highest proportion of non-microcystin-producing cells, and the lowest microcystin cell quotas (sum of microcystins RR, YR, LR, and WR). In contrast, the larger size classes of Microcystis colonies (>100 μm) showed the highest proportion of microcystin-producing genotypes, the lowest proportion of non-microcystin-producing cells, and the highest microcystin cell quotas. The microcystin net production rate was nearly one to one positively related to the population growth rate for the larger colony size classes (>100 μm); however, no relationship could be found for the smaller size classes. It was concluded that the variations found in microcystin net production between colony size classes are chiefly due to differences in genotype composition and that the microcystin net production in the lake is mainly influenced by the abundance of the larger (>100-μm) microcystin-producing colonies.

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