Temporal dynamics and spatial patterns of Galliform birds in Trentino – Italy.

This study examines the population dynamics of 5 species of closely related galliform birds in the Dolomites, north-east Italian Alps. The aim was to assess the dynamics of these populations at the edge of their European distribution and to investigate the patterns of spatial synchrony. Three main types of data sets were used in the analysis. First, the hunting statistics collected from 210 hunting areas between 1965 and 1994 for each of the 5 galliform species. Second, rock partridge count data from 29 sample areas during the period 1994 to 1998. Third, guts helminths collected from rock partridge shot between 1995 and 1998. Tetraonid populations at the edge of their southern European distribution exhibited a weak tendency to cycle. These cycles only showed significant negative autocorrelation at half the cycle period and were classified as phase-forgetting quasi-cycles contrasting with the more regular oscillations recorded in the same species in Finland. Cycles were not found in time series of black grouse Tetrao tetrix or capercaillie Tetrao urogallus. Rock partridge Alectoris graeca saxatilis exhibited a higher tendency to fluctuate. Rock partridge populations declined between 1965 and 1975 with populations in the western province declining earlier. Total winter loss and spring to summer loss of adults were the most important population parameters influencing the year to year change in numbers. There was some compensation to hunting mortality. The hypothesis that macroparasites may be of significance in destabilising partridge abundance and generating cyclic oscillations was examined by investigating the intensity of parasite infection in cyclic and non cyclic populations. Ascaridia compar and Heterakis tenuicauda were prevalent in the rock partridge populations and significantly greater in cyclic populations than non-cyclic populations. There were large variations in synchrony both within and between species and only weak negative relationships between synchrony and distance. Species in neighbouring habitats were more likely to be in synchrony than species separated by several habitats. A detailed spatial analysis on rock partridge populations found an increase in synchrony with scale from the population to meta-population level. Rock partridge clustered in two groups DRY and WET and synchrony was stronger in populations in the same habitat with populations in the dry habitat showing a higher tendency to cycle. The modelling of the long term dynamics of spatially structured populations indicated that environmental stochasticity was the main cause of synchrony although there is also some dispersal between populations and the importance of this varied between species. Population viability analysis of the grey partridge Perdix perdix in populations in Britain between 1930-1960 and the "declining" continental populations from 1970 to 1994 confirms that the UK populations prior to 1960 were more resilient than the continental populations. Even very small harvesting cannot be tolerated by the present continental populations and this may indicate that the persistence of hunting activity, although with a limited effort, has contributed to the extinction of many sub-populations and is critically threatening the remaining ones

Variation in host susceptibility and infectiousness generated by co-infection: the myxoma-Trichostrongylus retortaeformis case in wild rabbits. JR Soc Interface

One of the conditions that can affect host susceptibility and parasite transmission is the occurrence of concomitant infections. Parasites interact directly or indirectly within an individual host and often these interactions are modulated by the host immune response. We used a free-living rabbit population co-infected with the nematode Trichostrongylus retortaeformis, which appears to stimulate an acquired immune response, and the immunosuppressive poxvirus myxoma. Modelling was used to examine how myxoma infection alters the immune-mediated establishment and death/expulsion of T. retortaeformis, and consequently affects parasite intensity and duration of the infection. Simulations were based on the general T H 1-T H 2 immunological paradigm that proposes the polarization of the host immune response towards one of the two subsets of T helper cells. Our findings suggest that myxoma infections contribute to alter host susceptibility to the nematode, as co-infected rabbits showed higher worm intensity compared with virus negative hosts. Results also suggest that myxoma disrupts the ability of the host to clear T. retortaeformis as worm intensities were consistently high and remained high in old rabbits. However, the co-infection model has to include some immune-mediated nematode regulation to be consistent with field data, indicating that the T H 1-T H 2 dichotomy is not complete. We conclude that seasonal myxoma outbreaks enhance host susceptibility to the nematode and generate highly infected hosts that remain infectious for a longer time. Finally, the virus-nematode co-infection increases heterogeneities among individuals and potentially has a large effect on parasite transmission

Immune regulation of a chronic bacteria infection and consequences for pathogen transmission

<p>Abstract</p> <p>Background</p> <p>The role of host immunity has been recognized as not only playing a fundamental role in the interaction between the host and pathogen but also in influencing host infectiousness and the ability to shed pathogens. Despite the interest in this area of study, and the development of theoretical work on the immuno-epidemiology of infections, little is known about the immunological processes that influence pathogen shedding patterns.</p> <p>Results</p> <p>We used the respiratory bacterium <it>Bordetella bronchiseptica </it>and its common natural host, the rabbit, to examine the intensity and duration of oro-nasal bacteria shedding in relation to changes in the level of serum antibodies, blood cells, cytokine expression and number of bacteria colonies in the respiratory tract. Findings show that infected rabbits shed <it>B. bronchiseptica </it>by contact up to 4.5 months post infection. Shedding was positively affected by number of bacteria in the nasal cavity (CFU/g) but negatively influenced by serum IgG, which also contributed to the initial reduction of bacteria in the nasal cavity. Three main patterns of shedding were identified: i- bacteria were shed intermittently (46% of individuals), ii- bacteria shedding fell with the progression of the infection (31%) and iii- individuals never shed bacteria despite being infected (23%). Differences in the initial number of bacteria shed between the first two groups were associated with differences in the level of serum antibodies and white blood cells. These results suggest that the immunological conditions at the early stage of the infection may play a role in modulating the long term dynamics of <it>B. bronchiseptica </it>shedding.</p> <p>Conclusions</p> <p>We propose that IgG influences the threshold of bacteria in the oro-nasal cavity which then affects the intensity and duration of individual shedding. In addition, we suggest that a threshold level of infection is required for shedding, below this value individuals never shed bacteria despite being infected. The mechanisms regulating these interactions are still obscure and more studies are needed to understand the persistence of bacteria in the upper respiratory tract and the processes controlling the intensity and duration of shedding.</p

Evolutionary History and Attenuation of Myxoma Virus on Two Continents

The attenuation of myxoma virus (MYXV) following its introduction as a biological control into the European rabbit populations of Australia and Europe is the canonical study of the evolution of virulence. However, the evolutionary genetics of this profound change in host-pathogen relationship is unknown. We describe the genome-scale evolution of MYXV covering a range of virulence grades sampled over 49 years from the parallel Australian and European epidemics, including the high-virulence progenitor strains released in the early 1950s. MYXV evolved rapidly over the sampling period, exhibiting one of the highest nucleotide substitution rates ever reported for a double-stranded DNA virus, and indicative of a relatively high mutation rate and/or a continually changing selective environment. Our comparative sequence data reveal that changes in virulence involved multiple genes, likely losses of gene function due to insertion-deletion events, and no mutations common to specific virulence grades. Hence, despite the similarity in selection pressures there are multiple genetic routes to attain either highly virulent or attenuated phenotypes in MYXV, resulting in convergence for phenotype but not genotype. © 2012 Kerr et al

Variation in host susceptibility and infectiousness generated by co-infection: the myxoma–Trichostrongylus retortaeformis case in wild rabbits

One of the conditions that can affect host susceptibility and parasite transmission is the occurrence of concomitant infections. Parasites interact directly or indirectly within an individual host and often these interactions are modulated by the host immune response. We used a free-living rabbit population co-infected with the nematode Trichostrongylus retortaeformis, which appears to stimulate an acquired immune response, and the immunosuppressive poxvirus myxoma. Modelling was used to examine how myxoma infection alters the immune-mediated establishment and death/expulsion of T. retortaeformis, and consequently affects parasite intensity and duration of the infection. Simulations were based on the general TH1–TH2 immunological paradigm that proposes the polarization of the host immune response towards one of the two subsets of T helper cells. Our findings suggest that myxoma infections contribute to alter host susceptibility to the nematode, as co-infected rabbits showed higher worm intensity compared with virus negative hosts. Results also suggest that myxoma disrupts the ability of the host to clear T. retortaeformis as worm intensities were consistently high and remained high in old rabbits. However, the co-infection model has to include some immune-mediated nematode regulation to be consistent with field data, indicating that the TH1–TH2 dichotomy is not complete. We conclude that seasonal myxoma outbreaks enhance host susceptibility to the nematode and generate highly infected hosts that remain infectious for a longer time. Finally, the virus–nematode co-infection increases heterogeneities among individuals and potentially has a large effect on parasite transmission

Comparative analysis of the complete genome sequence of the California MSW strain of myxoma virus reveals potential host adaptations

Myxomatosis is a rapidly lethal disease of European rabbits that is caused by myxoma virus (MYXV). The introduction of a South American strain of MYXV into the European rabbit population of Australia is the classic case of host-pathogen coevolution following cross-species transmission. The most virulent strains of MYXV for European rabbits are the Californian viruses, found in the Pacific states of the United States and the Baja Peninsula, Mexico. The natural host of Californian MYXV is the brush rabbit, Sylvilagus bachmani. We determined the complete sequence of the MSW strain of Californian MYXV and performed a comparative analysis with other MYXV genomes. The MSW genome is larger than that of the South American Lausanne (type) strain of MYXV due to an expansion of the terminal inverted repeats (TIRs) of the genome, with duplication of the M156R, M154L, M153R, M152R, and M151R genes and part of the M150R gene from the right-hand (RH) end of the genome at the left-hand (LH) TIR. Despite the extreme virulence of MSW, no novel genes were identified; five genes were disrupted by multiple indels or mutations to the ATG start codon, including two genes, M008.1L/R and M152R, with major virulence functions in European rabbits, and a sixth gene, M000.5L/R, was absent. The loss of these gene functions suggests that S. bachmani is a relatively recent host for MYXV and that duplication of virulence genes in the TIRs, gene loss, or sequence variation in other genes can compensate for the loss of M008.1L/R and M152R in infections of European rabbits.This work was funded in part by grant R01 AI093804 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health. E.C.H. was supported by an NHMRC Australia Fellowship, and D.C.T. was supported by an ARC Future Fellowship

Peste des petits ruminants virus transmission scaling and husbandry practices that contribute to increased transmission risk: an investigation among sheep, goats, and cattle in Northern Tanzania

Peste des petits ruminants virus (PPRV) causes an infectious disease of high morbidity and mortality among sheep and goats which impacts millions of livestock keepers globally. PPRV transmission risk varies by production system, but a deeper understanding of how transmission scales in these systems and which husbandry practices impact risk is needed. To investigate transmission scaling and husbandry practice-associated risk, this study combined 395 household questionnaires with over 7115 cross-sectional serosurvey samples collected in Tanzania among agropastoral and pastoral households managing sheep, goats, or cattle (most managed all three, n = 284, 71.9%). Although self-reported compound-level herd size was significantly larger in pastoral than agropastoral households, the data show no evidence that household herd force of infection (FOI, per capita infection rate of susceptible hosts) increased with herd size. Seroprevalence and FOI patterns observed at the sub-village level showed significant spatial variation in FOI. Univariate analyses showed that household herd FOI was significantly higher when households reported seasonal grazing camp attendance, cattle or goat introduction to the compound, death, sale, or giving away of animals in the past 12 months, when cattle were grazed separately from sheep and goats, and when the household also managed dogs or donkeys. Multivariable analyses revealed that species, production system type, and goat or sheep introduction or seasonal grazing camp attendance, cattle or goat death or sales, or goats given away in the past 12 months significantly increased odds of seroconversion, whereas managing pigs or cattle attending seasonal grazing camps had significantly lower odds of seroconversion. Further research should investigate specific husbandry practices across production systems in other countries and in systems that include additional atypical host species to broaden understanding of PPRV transmission

Genome scale evolution of myxoma virus reveals host-pathogen adaptation and rapid geographic spread

The evolutionary interplay between myxoma virus (MYXV) and the European rabbit (Oryctolagus cuniculus) following release of the virus in Australia in 1950 as a biological control is a classic example of host-pathogen coevolution. We present a detailed genomic and phylogeographic analysis of 30 strains of MYXV, including the Australian progenitor strain Standard Laboratory Strain (SLS), 24 Australian viruses isolated from 1951 to 1999, and three isolates from the early radiation in Britain from 1954 and 1955. We show that in Australia MYXV has spread rapidly on a spatial scale, with multiple lineages cocirculating within individual localities, and that both highly virulent and attenuated viruses were still present in the field through the 1990s. In addition, the detection of closely related virus lineages at sites 1,000 km apart suggests that MYXV moves freely in geographic space, with mosquitoes, fleas, and rabbit migration all providing means of transport. Strikingly, despite multiple introductions, all modern viruses appear to be ultimately derived from the original introductions of SLS. The rapidity of MYXV evolution was also apparent at the genomic scale, with gene duplications documented in a number of viruses. Duplication of potential virulence genes may be important in increasing the expression of virulence proteins and provides the basis for the evolution of novel functions. Mutations leading to loss of open reading frames were surprisingly frequent and in some cases may explain attenuation, but no common mutations that correlated with virulence or attenuation were identified.This work was funded in part by grant R01 AI093804 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health. E.C.H. is funded by an NHMRC Australia Fellowship. D.C.T. is funded by an ARC Future Fellowship

Network model of immune responses reveals key effectors to single and co-infection dynamics by a respiratory bacterium and a gastrointestinal helminth

Co-infections alter the host immune response but how the systemic and local processes at the site of infection interact is still unclear. The majority of studies on co-infections concentrate on one of the infecting species, an immune function or group of cells and often focus on the initial phase of the infection. Here, we used a combination of experiments and mathematical modelling to investigate the network of immune responses against single and co-infections with the respiratory bacterium Bordetella bronchiseptica and the gastrointestinal helminth Trichostrongylus retortaeformis. Our goal was to identify representative mediators and functions that could capture the essence of the host immune response as a whole, and to assess how their relative contribution dynamically changed over time and between single and co-infected individuals. Network-based discrete dynamic models of single infections were built using current knowledge of bacterial and helminth immunology; the two single infection models were combined into a co-infection model that was then verified by our empirical findings. Simulations showed that a T helper cell mediated antibody and neutrophil response led to phagocytosis and clearance of B. bronchiseptica from the lungs. This was consistent in single and co-infection with no significant delay induced by the helminth. In contrast, T. retortaeformis intensity decreased faster when co-infected with the bacterium. Simulations suggested that the robust recruitment of neutrophils in the co-infection, added to the activation of IgG and eosinophil driven reduction of larvae, which also played an important role in single infection, contributed to this fast clearance. Perturbation analysis of the models, through the knockout of individual nodes (immune cells), identified the cells critical to parasite persistence and clearance both in single and co-infections. Our integrated approach captured the within-host immuno-dynamics of bacteria-helminth infection and identified key components that can be crucial for explaining individual variability between single and co-infections in natural populations