Human-induced landscape change associated with habitat loss and fragmentation places wildlife populations at risk. One issue in these landscapes is a change in the prevalence of disease which may result in increased mortality and reduced fecundity. Our understanding of the influence of habitat loss and fragmentation on the prevalence of wildlife diseases is still in its infancy. What is evident is that changes in disease prevalence as a result of human-induced landscape modification are highly variable. The importance of infectious diseases for the conservation of wildlife will increase as the amount and quality of suitable habitat decreases due to human land-use pressures. We review the experimental and observational literature of the influence of human-induced landscape change on wildlife disease prevalence, and discuss disease transmission types and host responses as mechanisms that are likely to determine the extent of change in disease prevalence. It is likely that transmission dynamics will be the key process in determining a pathogen's impact on a host population, while the host response may ultimately determine the extent of disease prevalence. Finally, we conceptualize mechanisms and identify future research directions to increase our understanding of the relationship between human-modified landscapes and wildlife disease prevalence. This review highlights that there are rarely consistent relationships between wildlife diseases and human-modified landscapes. In addition, variation is evident between transmission types and landscape types, with the greatest positive influence on disease prevalence being in urban landscapes and directly transmitted disease systems. While we have a limited understanding of the potential influence of habitat loss and fragmentation on wildlife disease, there are a number of important areas to address in future research, particularly to account for the variability in increased and decreased disease prevalence. Previous studies have been based on a one-dimensional comparison between unmodified and modified sites. What is lacking are spatially and temporally explicit quantitative approaches which are required to enable an understanding of the range of key causal mechanisms and the reasons for variability. This is particularly important for replicated studies across different host-pathogen systems. Furthermore, there are few studies that have attempted to separate the independent effects of habitat loss and fragmentation on wildlife disease, which are the major determinants of wildlife population dynamics in human-modified landscapes. There is an urgent need to understand better the potential causal links between the processes of human-induced landscape change and the associated influences of habitat fragmentation, matrix hostility and loss of connectivity on an animal's physiological stress, immune response and disease susceptibility. This review identified no study that had assessed the influence of human-induced landscape change on the prevalence of a wildlife sexually transmi...

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Context. Global climate change will lead to increased climate variability, including more frequent drought and heatwaves, in many areas of the world. This will affect the distribution and numbers of wildlife populations. In south-west Queensland, anecdotal reports indicated that a low density but significant koala population had been impacted by drought from [2001][2002][2003][2004][2005][2006][2007][2008][2009], in accord with the predicted effects of climate change.Aims. The study aimed to compare koala distribution and numbers in south-west Queensland in 2009 with pre-drought estimates from 1995-1997.Methods. Community surveys and faecal pellet surveys were used to assess koala distribution. Population densities were estimated using the Faecal Standing Crop Method. From these densities, koala abundance in 10 habitat units was interpolated across the study region. Bootstrapping was used to estimate standard error. Climate data and land clearing were examined as possible explanations for changes in koala distribution and numbers between the two time periods.Key results. Although there was only a minor change in distribution, there was an 80% decline in koala numbers across the study region, from a mean population of 59 000 in 1995 to 11 600 in 2009. Most summers between 2002 and 2007 were hotter and drier than average. Vegetation clearance was greatest in the eastern third of the study region, with the majority of clearing being in mixed eucalypt/acacia ecosystems and vegetation on elevated residuals.Conclusions. Changes in the area of occupancy and numbers of koalas allowed us to conclude that drought significantly reduced koala populations and that they contracted to critical riparian habitats. Land clearing in the eastern part of the region may reduce the ability of koalas to move between habitats.Implications. The increase in hotter and drier conditions expected with climate change will adversely affect koala populations in south-west Queensland and may be similar in other wildlife species in arid and semiarid regions. The effect of climate change on trailing edge populations may interact with habitat loss and fragmentation to increase extinction risks. Monitoring wildlife population dynamics at the margins of their geographic ranges will help to manage the impacts of climate change.

Binding of radioactive thyroxine to proteins in the plasma of vertebrates was studied by electrophoresis followed by autoradiography. Albumin was found to be a thyroxine carrier in the blood of all studied fish, amphibians, reptiles, monotremes, marsupials, eutherians (placental mammals), and birds. Thyroxine binding to transthyretin was detected in the blood of eutherians, diprotodont marsupials, and birds, but not in blood from fish, toads, reptiles, monotremes, and Australian polyprotodont marsupials. Globulins binding thyroxine were only observed in the plasma of some mammals. Apparently, albumin is the phylogenetically oldest thyroxine carrier in vertebrate blood. Transthyretin gene expression in the liver developed in parallel, and independently, in the evolutionary lineages leading to eutherians, to diprotodont marsupials, and to birds. In contrast, high transthyretin mRNA levels, strong synthesis, and secretion of transthyretin in choroid plexus from reptiles and birds indicate that transthyretin gene expression in the choroid plexus evolved much earlier than in the liver, probably at the stage of the stem reptiles. NH2-terminal sequence analysis suggests a change of transthyretin pre-mRNA splicing during evolution.

Complete mortality of males after mating is known in several small dasyurid and didelphid species (up to 300g) and has previously been suggested to be a consequence of their small size and their inability to sequester sufficient fat reserves for an intense rut in the winter. Males of these species use increased corticosteroid levels to allow protein catabolism, enabling them to support their mating effort with other body reserves. However, increased corticosteroid levels have negative consequences such as anaemia, gastrointestinal ulceration, immune suppression and disease. The Australian dasyurid Dasyurus hallucatus shows complete male die off after mating in tropical savannah, yet males of this species may weigh as much as 1120 g and continue to eat during the rut. Die off in D. hallucatus shows many similarities to that in the smaller species including weight loss, fur loss, parasite infestation, increased testosterone levels and anaemia. However, in contrast to smaller species, there is no evidence of elevated corticosteroid levels or gastrointestinal ulceration. Consequently, the phenomenon of male die off after mating lacks a universal explanation.

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With 1 plate and 4 figures in the text) Breeding, population dynamics and seasonal changes in physical and physiological parameters were examined in the northern quoll (Dasyurus hallticatus) at Mitchell Plateau, Western Australia, between September 1981 and November 1982. Females gave birth to a single litter of young in July or August. Births were earlier on near-coastal sites than on inland sites. Litter size was greater on inland sites and litter size differed between years. By September all females were either carrying pouch young or were lactating. Lactation ceased by April. Testosterone levels in males peaked in July. There were significantly more male than female pouch young. However, in only one grid was the adult sex ratio different from parity, with an excess of females in September 1981 and 1982. Embryonic mortality was > 53% but loss of pouch young was small. Although males and females moved similar distances between successive recaptures, the extent of movement varied seasonally, being greatest in September. Males were generally larger and heavier than females. Seasonal variations were recorded for most physical and physiological parameters. The most pronounced changes occurred towards the end of the dry season (July to September) for both males and females. Over this period there was a significant decline in weight (males), haematocrit (males), plasma albumin (males) and leucocytes (both males and females) and significant elevations in values of haemoglobin and both free and protein-bound cortisol in both males and females. Few males survived the post-mating period from July to September. They appeared to decline in condition over this period more markedly than females: they lost more weight, their haematocrit and plasma albumin values declined to a greater extent, and they were more heavily infected with lice (Boopia uncinata). Males with lower testosterone and higher free and protein-bound cortisol had increased prospects of surviving the breeding season, which suggests that it is the dominant males that are less likely to survive the breeding season. Individuals in the three major populations at Mitchell Plateau differed greatly in their physiological values. The high-density population in a sandstone area had intermediate levels of free cortisol and higher haematocrit values than both the other populations, and higher levels of haemogl3bin than the population on laterite substratum.