A number of
distressed and dead turtles were found by canoeists in the Bellinger River on
the north coast of New South Wales on Wednesday February 18 2015. At that time,
it was reported by NSW National Parks and Wildlife rangers, NSW Wildlife
Information, Rescue and Education Service (WIRES) volunteers and local
residents that 30 turtles were affected. Several days later, the tally
increased to 52 and within a month 500 turtles were confirmed as dead ().
But the real toll is far greater, with many more washed away during a flood in
late February.
The peril of this one turtle species is more than an
isolated issue. It gives us a window into the health of the entire ecosystem
around the Bellinger River, and suggests something is very wrong. It may also
be a window into what may still occur in similar river systems up and down the east
coast of Australia.
The dead turtles are all from one species, the Bellinger
River Snapping Turtle (Myuchelys georgesi),
which is a species that only exists in a 25-kilometre stretch of the Bellinger
River. The risk of extinction is high. Ill turtles display symptoms of blindness, growths around
the eye (septicemic cutaneous ulcerative disease, or SCUDs) and are extremely
lethargic and emaciated. The mortality rate of infected animals is 100% (Moloney et al. 2015). High
mortality combined with an extremely limited range means that this is quite
possibly a rapid extinction event. The disease has been identified as a virus,
yet no more detail about the type of virus has been released (ABC Online 2015).
Pathogens can be transmitted directly between animals
or indirectly through intermediate “hosts,” such as infected prey or biting
insects. Indirect transmission cycles are often affected by environmental
conditions such as temperature and rainfall. Higher temperatures
associated with climate change may contribute to an increase in pathogens
within intermediate hosts and vectors, or increased survival of animals
that harbor disease. For example, warmer summer temperatures in
the Arctic now allow the lung nematode larvae often found in muskoxen
to develop to the infectious stage within the intermediate host, the marsh
slug, at a rate that has reduced the parasite’s life cycle from 2 years to
1 year (Kutz and others, 2005).
Survival of another nematode, the brain worm of white-tailed
deer, may also be increased by recently warmer temperatures and milder winters in the north-central United States and southern Canada. The
parasite, which overwinters as larvae in snails and is accidentally eaten
with plants, causes neurological disease in moose. Moose are already
heat stressed by climate change (Lenarz and others, 2009) and may be
more susceptible to parasitic and infectious diseases (Murray and others,
2009), including the brain worm of white-tailed deer (fig. 5).
Changes in precipitation patterns also have a significant potential
to affect patterns of wildlife disease through survival of disease agents
or vectors and through effects on host parasite relationships. In the
example of the brain worm of deer, increased precipitation also may
result in increased survival of the snail populations, resulting in more
exposure of deer to infected snails.
Climate change is also having a detrimental effect on microhabitats. Amphibian and reptilian populations have declined in the lowland forests in Costa Rica in part through the effect of climate change on the humid leaf litter microhabitat of the forest floor (Whitfield and others, 2007). Weather conditions also significantly affect the microclimates for nests and burrows. For example, in sea turtles, elevated temperatures may lead to altered sex ratios or loss of nesting beaches secondary to sea level rises. Temperatures outside the range of those that turtles can tolerate result in the death of the developing sea turtle embryos (Morreale and others, 1982). At an organism level, enviornmental change not only affects endocrine disruptions, sex-ratio changes and decreased reproductive parameters (Reusch & Wood 2007) , but also include teratogenic and genotoxic effects, immunosuppression and other immune-system impairments that can lead directly to disease or increase the risk of acquiring disease (Selgrade 2007).
Identifying the cause of wildlife diseases is difficult because rarely can a single factor be identified as responsible, a concept commonly termed the ‘epidemiological triad’. In addition to immune suppression related to exceeded stress responses and pollutant exposure, environmental change can impinge directly on wildlife health and survival and, consequently, affect the viability of their populations in various intricate ways. For example, climate-related shifts in pathogen and host ranges and pathogen spillover from humans and domestic animals can both increase exposure to new diseases (reviewed in Smith et al. 2009). Similarly, changes in habitat size or quality might lead to a reduction in prey population sizes and increased competition for resources (Ryall & Fahrig 2006), which in turn might augment starvation and lead to disease and/or death. Effects will be further complicated if the genetic makeup of the affected populations has been compromised owing to reduced gene flow or inbreeding, as low levels of genetic diversity tend to be correlated with reduced fitness and lowered evolutionary potential (Spielman et al. 2004).
Infectious disease was infrequently listed as a contributing factor to species extinction or endangerment. The IUCN Red List (IUCN 2004) reports that in the past 500 years, 100 plant and 733 animal species are known to have gone extinct. Whereas multiple causal factors are typically listed as having contributed to a species’ extinction, the most common causes appear to be habitat loss and overexploitation (IUCN 2004). Of these 833 known species extinctions, only 31 cases (3.7%) have been attributed, at least in part, to infectious disease. Whereas some forces, such as habitat loss or overexploitation, are listed as the single causal driver of a species’ extinction, in no case is infectious disease listed alone (IUCN 2004). This raises the possibility that infectious disease is less likely than other drivers of species extinction to act in isolation. It is critical that we combine evidence with theory to discern the circumstances under which infectious disease is most likely to serve as an agent of extinction. This can occur when a pathogen is evolutionarily novel to a susceptible host species, when a pathogen utilizes a reservoir (biotic or abiotic), and when hosts have small pre-epidemic population sizes (de Castro & Bolker 2005; Gerber et al. 2005).
Climate change is also having a detrimental effect on microhabitats. Amphibian and reptilian populations have declined in the lowland forests in Costa Rica in part through the effect of climate change on the humid leaf litter microhabitat of the forest floor (Whitfield and others, 2007). Weather conditions also significantly affect the microclimates for nests and burrows. For example, in sea turtles, elevated temperatures may lead to altered sex ratios or loss of nesting beaches secondary to sea level rises. Temperatures outside the range of those that turtles can tolerate result in the death of the developing sea turtle embryos (Morreale and others, 1982). At an organism level, enviornmental change not only affects endocrine disruptions, sex-ratio changes and decreased reproductive parameters (Reusch & Wood 2007) , but also include teratogenic and genotoxic effects, immunosuppression and other immune-system impairments that can lead directly to disease or increase the risk of acquiring disease (Selgrade 2007).
Identifying the cause of wildlife diseases is difficult because rarely can a single factor be identified as responsible, a concept commonly termed the ‘epidemiological triad’. In addition to immune suppression related to exceeded stress responses and pollutant exposure, environmental change can impinge directly on wildlife health and survival and, consequently, affect the viability of their populations in various intricate ways. For example, climate-related shifts in pathogen and host ranges and pathogen spillover from humans and domestic animals can both increase exposure to new diseases (reviewed in Smith et al. 2009). Similarly, changes in habitat size or quality might lead to a reduction in prey population sizes and increased competition for resources (Ryall & Fahrig 2006), which in turn might augment starvation and lead to disease and/or death. Effects will be further complicated if the genetic makeup of the affected populations has been compromised owing to reduced gene flow or inbreeding, as low levels of genetic diversity tend to be correlated with reduced fitness and lowered evolutionary potential (Spielman et al. 2004).
Infectious disease was infrequently listed as a contributing factor to species extinction or endangerment. The IUCN Red List (IUCN 2004) reports that in the past 500 years, 100 plant and 733 animal species are known to have gone extinct. Whereas multiple causal factors are typically listed as having contributed to a species’ extinction, the most common causes appear to be habitat loss and overexploitation (IUCN 2004). Of these 833 known species extinctions, only 31 cases (3.7%) have been attributed, at least in part, to infectious disease. Whereas some forces, such as habitat loss or overexploitation, are listed as the single causal driver of a species’ extinction, in no case is infectious disease listed alone (IUCN 2004). This raises the possibility that infectious disease is less likely than other drivers of species extinction to act in isolation. It is critical that we combine evidence with theory to discern the circumstances under which infectious disease is most likely to serve as an agent of extinction. This can occur when a pathogen is evolutionarily novel to a susceptible host species, when a pathogen utilizes a reservoir (biotic or abiotic), and when hosts have small pre-epidemic population sizes (de Castro & Bolker 2005; Gerber et al. 2005).
In the Bellinger River Snapping Turtle, First reports are that the virus detected is novel to
turtles, however no detail has been provided thus far. However, whether the host species was particularly susceptible because pre-epidemic populations sizes were low is worth investigating. The
distribution of the Bellinger River Snapping Turtle is restricted to the
Bellinger River catchment and numbers have been estimated at 4500 (Blamires et
al 2005), however, density estimates from surveys in 2007 (Spencer et al. 2007;
Spencer et al. 2013) suggest that population size may have been half of that.
Regardless, small populations sizes and a severely restricted distribution may
have combined to make the Bellinger River Snapping Turtle susceptible to a novel pathogen, particularly if
populations were under stress leading up to infection.
This study explores the epidemiology of the disease and explores whether the Bellinger River Snapping turtle were particularly susceptible by exploring how environmental and climatic factors have created unsuitable conditions to support the population. ie. were turtles possibly stressed and possibly immune-compromised prior the disease outbreak.
The Event: Epidemiology of the Disease
The Event: Epidemiology of the Disease
This section is a summary of Moloney et al.'s 2015 report: Bellinger River Snapping Turtle Mortality
Event 2015. A severe mortality event in Bellinger River Snapping Turtles (Myuchelys georgesi) was investigated on February 18, 2015 by Bellingen Shire Council (BSC), Environment Protection Authority (EPA), and National Parks and Wildlife Service (NPWS) following a report of dead or dying turtles on the side of the River from local kayakers. Over the course of the investigations an estimated 432 M. georgesi were observed with symptoms of a disease or dead since February 14, 2015. They were described as slow moving and unable to see.
Fig. 1. Map indicating sick, dead or healthy animals captured during initially surveys after the disease was first recorded. February 16th-April 7th 2015 (Map reproduced from Moloney et al. 2015).
Sick turtles were initially treated by veterinarians, however after high rates of mortality and potential biosecurity risk, ill turtles were humanely euthanased (Moloney et al. 2015). The Australian Registry of Wildlife Health at Taronga Conservation Society Australia conducted gross and histological examinations of affected animals and coordinated the diagnostic investigation that spanned multiple state agencies and academic institutions. Initial presenting signs included swollen eyes and the turtles were thin. Many had slight clear nasal discharge, and some animals had hind limb paresis. At necropsy, animals were thin, had bilateral swollen eyelids and anterior uveitis, and some animals had tan foci on the skin of the ventral thighs. Fibrin plaques were observed within the vitreous humour, haemorrhage into the eye, and inflammation extending into the periorbital tissues and possibly extending into the sinuses.
Histopathology showed inflammation extended from the eyelids, peri-orbital tissues, and
sinuses, sometimes extending along the olfactory/optic nerve into the meninges. There was also histological evidence of fibrinonecrotising splenitis and nephritis with multisystemic fibrinoid vasculopathy. All turtles had acute lesions but the severe emaciation suggests an undetermined event preceded and possibly predisposed to the development of the acute inflammatory changes. Bacteria were evident in the lesions in some animals, with a pattern of inflammation in the internal organs most consistent with embolic spread - showering in blood or lymphatic vessels including the spleen, kidney, and more recent inflammation in the liver, oral cavity and other tissues.
A range of infectious agents have been tested for and excluded as the primary pathogen for the including Ranavirus, adenovirus, paramyxovirus (ferlavirus), herpesvirus, mycoplasma, chlamydia and trichomonas. No known toxins or environmental toxins have been detected. Electron microscopy results have been negative. Scientists at the Elizabeth MacArthur Agricultural Institute (EMAI) Virology Laboratory have recently (July 2015) detected a novel virus in tissues of affected turtles (Moloney et al. 2015). Extensive testing has shown very high levels of the virus in tissues in which the most severe lesions were observed, suggesting a major role for this virus. Further work is being undertaken on the characterisation of the virus and determining its significance in the pathogenesis of this disease.
The disease was first observed in the mid-lower sections of the River and surveys involving 2-8 people snorkelling or kayaking (February 18th- March 25th) suggested that the disease was propagating upstream (Molaney et al. 2015). Surveys began in the upper sections of the River to remove healthy individuals from 8th-12th April. Seventeen healthy individuals of a range of sizes and sexes were removed and relocated to a quarantine facility for holding and breeding.
Fig. 3. Proportion of sick or dead animals captured during surveys in February/March 2015 in two lower catchment (light grey), two mid catchment (grey) and two upper catchment (dark grey) sites (Adopted from Moloney et al. 2015).
Changes in Body Condition
Historical data on the species stems from a range of studies that have occurred inconsistently since 2000. The last systematic survey was conducted in 2007 (Georges et al. 2011, Spencer et al. 2014) and we compared changes in size structure (population comparisons) and body size (individual changes) from this survey to the diseased population in 2015. The trend of the disease appears to support was for increasing susceptibility with body size, with very sick or dead juveniles captured in 2015 (Fig. 4). In support of this theory was the fact that the majority of the catch during a survey in November 2015 were juveniles (20- Bellinger Courier Sun. Nov. 17, 2015).
Fig. 4. Population changes in body size. Histograms (percentage of animals) of (a) juveniles and females and (b) males captured in 2007 (light grey) and 2015 (dark grey).
Individual turtles also grew by an average of 10.4% +/- 2.1% (n=18). The body condition of snapping turtles brought into captivity for breeding was below that of Emydura maquarii captured at the same time in April 2015 (Fig. 5). However in October 2015, body condition of captive Bellinger River Snapping Turtle's had significantly increased (Fig. 5). In captivity, turtles were maintained in 2000L ponds at 21C on a diet of fish, plants (Valisnaeria spp) and commercial turtle mixes. Turtles were fed a combination of dietary items three times a week and remaining food was removed from ponds within 12 hours of offering. Health checks and weighing was performed fortnightly. Body condition scores were generated by the following formula Mass (g) divided by the cube of midline plastron length (mm), and multiplied by 10,000 (Chessman pers. com.)
Fig. 6. Annual changes from the mean in water course levels from 1983 to 2014 in the Bellinger River at (a) Thora (lat.-30.4259 ,lon. 152.7809) and (b) the Manning River at Killawarra lat:-31.9175 lon: 152.3117)
Fig. 9(a). Cumulative differences from mean daily maximum
temperatures over the last five decades and (b) Cumulative differences from
mean daily maximum temperatures over the last five years- South West Rocks BOM Site
number: 059030 (~60km from Thora).
Discussion
The three years of heating and drying in the region, prior to the disease outbreak, is significant. Mean river levels at Thora from 2012-2014 were the lowest that they have ever been since recording began (Fig. 6). Thora is where the outbreak first occurred and the period 2012-2015 is the longest period without a flood occurring (Fig. 7). This decline in river levels is not directly associated with rainfall, with only below average rainfall occurring in 2014 (Fig. 8) over this period. Over a much longer period, but certainly magnified in 2013-2014, was significant warming in the region (Fig. 9). As air temperatures rise, water temperatures do also, and in the upper stretches of the River, where turtle predominantly reside (Spencer et al. 2014), the River is a series of riffles and water holes and warming would be increased in shallow stretches of rivers and surface waters of water holes. Warming of upper layers in deeper water holes slows down air exchange, a process that normally adds oxygen to the water (REF). In a turtle species that relies on cloacal bursae (Cann 1998) for signficant gas exchange, "dead zones", or areas of depleted of oxygen may significantly impact survival. Persistent dead zones can produce toxic algal blooms, foul-smelling water, and result in massive fish kills (REF).
the same period
Other diagnostic exclusions included:
Event 2015. A severe mortality event in Bellinger River Snapping Turtles (Myuchelys georgesi) was investigated on February 18, 2015 by Bellingen Shire Council (BSC), Environment Protection Authority (EPA), and National Parks and Wildlife Service (NPWS) following a report of dead or dying turtles on the side of the River from local kayakers. Over the course of the investigations an estimated 432 M. georgesi were observed with symptoms of a disease or dead since February 14, 2015. They were described as slow moving and unable to see.
Fig. 1. Map indicating sick, dead or healthy animals captured during initially surveys after the disease was first recorded. February 16th-April 7th 2015 (Map reproduced from Moloney et al. 2015).
Sick turtles were initially treated by veterinarians, however after high rates of mortality and potential biosecurity risk, ill turtles were humanely euthanased (Moloney et al. 2015). The Australian Registry of Wildlife Health at Taronga Conservation Society Australia conducted gross and histological examinations of affected animals and coordinated the diagnostic investigation that spanned multiple state agencies and academic institutions. Initial presenting signs included swollen eyes and the turtles were thin. Many had slight clear nasal discharge, and some animals had hind limb paresis. At necropsy, animals were thin, had bilateral swollen eyelids and anterior uveitis, and some animals had tan foci on the skin of the ventral thighs. Fibrin plaques were observed within the vitreous humour, haemorrhage into the eye, and inflammation extending into the periorbital tissues and possibly extending into the sinuses.
Histopathology showed inflammation extended from the eyelids, peri-orbital tissues, and
sinuses, sometimes extending along the olfactory/optic nerve into the meninges. There was also histological evidence of fibrinonecrotising splenitis and nephritis with multisystemic fibrinoid vasculopathy. All turtles had acute lesions but the severe emaciation suggests an undetermined event preceded and possibly predisposed to the development of the acute inflammatory changes. Bacteria were evident in the lesions in some animals, with a pattern of inflammation in the internal organs most consistent with embolic spread - showering in blood or lymphatic vessels including the spleen, kidney, and more recent inflammation in the liver, oral cavity and other tissues.
Fig. 2. External symptoms of the disease.
A range of infectious agents have been tested for and excluded as the primary pathogen for the including Ranavirus, adenovirus, paramyxovirus (ferlavirus), herpesvirus, mycoplasma, chlamydia and trichomonas. No known toxins or environmental toxins have been detected. Electron microscopy results have been negative. Scientists at the Elizabeth MacArthur Agricultural Institute (EMAI) Virology Laboratory have recently (July 2015) detected a novel virus in tissues of affected turtles (Moloney et al. 2015). Extensive testing has shown very high levels of the virus in tissues in which the most severe lesions were observed, suggesting a major role for this virus. Further work is being undertaken on the characterisation of the virus and determining its significance in the pathogenesis of this disease.
The disease was first observed in the mid-lower sections of the River and surveys involving 2-8 people snorkelling or kayaking (February 18th- March 25th) suggested that the disease was propagating upstream (Molaney et al. 2015). Surveys began in the upper sections of the River to remove healthy individuals from 8th-12th April. Seventeen healthy individuals of a range of sizes and sexes were removed and relocated to a quarantine facility for holding and breeding.
Changes in Body Condition
Historical data on the species stems from a range of studies that have occurred inconsistently since 2000. The last systematic survey was conducted in 2007 (Georges et al. 2011, Spencer et al. 2014) and we compared changes in size structure (population comparisons) and body size (individual changes) from this survey to the diseased population in 2015. The trend of the disease appears to support was for increasing susceptibility with body size, with very sick or dead juveniles captured in 2015 (Fig. 4). In support of this theory was the fact that the majority of the catch during a survey in November 2015 were juveniles (20- Bellinger Courier Sun. Nov. 17, 2015).
Fig. 4. Population changes in body size. Histograms (percentage of animals) of (a) juveniles and females and (b) males captured in 2007 (light grey) and 2015 (dark grey).
Individual turtles also grew by an average of 10.4% +/- 2.1% (n=18). The body condition of snapping turtles brought into captivity for breeding was below that of Emydura maquarii captured at the same time in April 2015 (Fig. 5). However in October 2015, body condition of captive Bellinger River Snapping Turtle's had significantly increased (Fig. 5). In captivity, turtles were maintained in 2000L ponds at 21C on a diet of fish, plants (Valisnaeria spp) and commercial turtle mixes. Turtles were fed a combination of dietary items three times a week and remaining food was removed from ponds within 12 hours of offering. Health checks and weighing was performed fortnightly. Body condition scores were generated by the following formula Mass (g) divided by the cube of midline plastron length (mm), and multiplied by 10,000 (Chessman pers. com.)
Fig. 5. Body condition score of Myuchelys georgesi and Emydura macquarii at capture in April 2015 (dark grey) and after 6 months in captivity (light grey)
Environmental Conditions
Average water course levels at Thora were well below average for the last three years (Fig. 6), with water levels almost 30% below average in 2014. Deaths were recorded less than a week after a minor-moderate flood in February 2015 (Fig. 7). Over the 32 year period, average water course height at Thora was ~2m, however from Spring 2011-April 2015, water course levels average ~1.5m (Fig. 7). During this period, only one moderate-major flood occurred in the River until the flood surrounding the disease outbreak in February 2015. It is likely that low River levels negated two minor flood levels in 2013/2014 (Fig. 7). Low River levels were not directly related to rainfall, with only 2014 having significantly reduced rainfall levels (Fig. 8).
Fig. 6. Annual changes from the mean in water course levels from 1983 to 2014 in the Bellinger River at (a) Thora (lat.-30.4259 ,lon. 152.7809) and (b) the Manning River at Killawarra lat:-31.9175 lon: 152.3117)
Fig. 7.Monthly averages of water course levels at Thora from 1982-2015. Solid black line is average levels over the same time period. Dotted lines represent minor (3m), moderate (4.5m) and major (5.8m) flood levels in the River. Deaths we first observed just after a minor-moderate flood in February 2015. Thora (lat.-30.4259 ,lon. 152.7809)
Fig. 8. Difference to
mean in annual rainfall totals at Thumb Creek (Figtree-Lat: -30.68 Lon:152.61) from
1961-2014.
Significant warming has occurred in the region since 1965.Cumulative differences from mean daily maximum temperatures were calculated for each decade and the degree of warming in the region has been 8-9 times greater in the last decade compared to 1965-1974 (Fig. 9a). Looking specifically at the last five years, the degree of heating in the rgion in 2014 was almost twice as large as compared to 2010.
Discussion
Disease outbreak is uncommon but not rare in turtles. Ranaviruses (genus Ranavirus) have been observed in disease epidemics and mass mortality events in free-ranging amphibian, turtle, and tortoise populations worldwide. Reports of outbreaks in wild turtles have largely involved box turtles in North America (Devoe et al. 2004; Kimble et al. 2014) Infection is highly fatal in turtles, and the potential impact on endangered populations could be devastating. While Ranavirus has been ruled out in the current disease outbreak (Moloney et al. 2015), this analyses critically combines long-term population and environmental data to discern the circumstances under which a novel virus has possibly served as an agent of extinction in the Bellinger River Snapping Turtle. Scientists at the Elizabeth MacArthur Agricultural Institute (EMAI) Virology Laboratory have
recently (July 2015) detected a novel virus in tissues of affected turtles (Moloney et al. 2015) but the question of why turtles were susceptible in February 2015 is not known.
Low genetic diversity reduces species' fitness and the ability to respond to pathogens (Spielman et al. 2004; Allendorf and Luikart 2007). The consequences of low genetic diversity for emerging wildlife diseases is no better displayed in the devastating effects of Tasmanian Devil facial tumor (Lafferty and Kuris 2002). Genetic variability among specimens of Myuchelys georgesi is exceptionally low, and order of magnitude lower than in the sympatric Emydura macquarii (Georges 2015), which were unaffected by the disease outbreak. This result is consistent with the mitochondrial data which identified 7 mt haplotypes in Emydura macquarii from the Bellinger River, but only one for Myuchelys georgesi (Georges et al., 2011). Hence low genetic diversity in Myuchelys georgesi may have increased its susceptibility to a novel virus.
Similarly, susceptibility may have increased because turtles were immunocompromised because of the direct and indirect effects of climatic changes. Our analyses indicates that while over a 7-8 year period turtles of all sizes grew by ~10%, however, the body condition of turtles at the time of the disease was ~15% lower than Emydura maquarii captured at the same time and ~18% lower than their same scores after six months in captivity. Several dietary studies on Myuchelys georgesi indicate that they are dietary specialist (relative to other short-neck turtles- See Spencer et al. 2014). Their diet consists predominantly of insect larvae and things that fall on the surface, like berries, figs and insects.
Low genetic diversity reduces species' fitness and the ability to respond to pathogens (Spielman et al. 2004; Allendorf and Luikart 2007). The consequences of low genetic diversity for emerging wildlife diseases is no better displayed in the devastating effects of Tasmanian Devil facial tumor (Lafferty and Kuris 2002). Genetic variability among specimens of Myuchelys georgesi is exceptionally low, and order of magnitude lower than in the sympatric Emydura macquarii (Georges 2015), which were unaffected by the disease outbreak. This result is consistent with the mitochondrial data which identified 7 mt haplotypes in Emydura macquarii from the Bellinger River, but only one for Myuchelys georgesi (Georges et al., 2011). Hence low genetic diversity in Myuchelys georgesi may have increased its susceptibility to a novel virus.
Similarly, susceptibility may have increased because turtles were immunocompromised because of the direct and indirect effects of climatic changes. Our analyses indicates that while over a 7-8 year period turtles of all sizes grew by ~10%, however, the body condition of turtles at the time of the disease was ~15% lower than Emydura maquarii captured at the same time and ~18% lower than their same scores after six months in captivity. Several dietary studies on Myuchelys georgesi indicate that they are dietary specialist (relative to other short-neck turtles- See Spencer et al. 2014). Their diet consists predominantly of insect larvae and things that fall on the surface, like berries, figs and insects.
It is critical that we combine evidence with theory to
discern the circumstances under which infectious disease is most likely to
serve as an agent of extinction. This can occur when a pathogen is
evolutionarily novel to a susceptible host species, when a pathogen utilizes a
reservoir (biotic or abiotic), and when hosts have small pre-epidemic
population sizes (de Castro & Bolker 2005; Gerber et al. 2005). Myuchelys georgesi are insectivore specialists (Fig. 10) and the food that they eat are highly sensitive to pollution, increased sedimentation or general water conditions. In a River, that changes significantly because of rainfall (Figs. 8 and 10), insect populations are also going to respond rapidly and be affected by natural changes. Bellinger River Snapping Turtles are probably adapted to 'boom-bust' cycles of the River and resilient to natural shortages of food for periods. However, if there are chronic issues with the food supply, then the turtles will begin to be impacted. In 2001, a season after a major flood, very few females were gravid in Spring. Aquatic vegetation, such as Ribbon weed (Valisnaeria spp) were scoured by the flood and had not returned (Spencer 2001). The food supply of the turtles had been impacted before winter and they likely forwent breeding that year (Spencer 2001). A reproductive cycle like this is common with 'boom-bust' organisms and being long-lived, skipping a breeding season is no big deal. The problem comes when there is long-term disruption of the food cycle and being a clear-water water specialist (Spencer et al. 2014), changes to water quality are magnified.
Fig. 10. Proportion of diet that consists of aquatic insects
of three short necked species that inhabit clear East Coast River or Lake
systems in Australia. Data obtained from Spencer et al. 2014.
The three years of heating and drying in the region, prior to the disease outbreak, is significant. Mean river levels at Thora from 2012-2014 were the lowest that they have ever been since recording began (Fig. 6). Thora is where the outbreak first occurred and the period 2012-2015 is the longest period without a flood occurring (Fig. 7). This decline in river levels is not directly associated with rainfall, with only below average rainfall occurring in 2014 (Fig. 8) over this period. Over a much longer period, but certainly magnified in 2013-2014, was significant warming in the region (Fig. 9). As air temperatures rise, water temperatures do also, and in the upper stretches of the River, where turtle predominantly reside (Spencer et al. 2014), the River is a series of riffles and water holes and warming would be increased in shallow stretches of rivers and surface waters of water holes. Warming of upper layers in deeper water holes slows down air exchange, a process that normally adds oxygen to the water (REF). In a turtle species that relies on cloacal bursae (Cann 1998) for signficant gas exchange, "dead zones", or areas of depleted of oxygen may significantly impact survival. Persistent dead zones can produce toxic algal blooms, foul-smelling water, and result in massive fish kills (REF).
the same period
Other diagnostic exclusions included:
- PCR and other tests including virus isolation in a number of cell cultures have excluded a wide range of infectious agents including Ranavirus, adenovirus, paramyxovirus (ferlavirus), herpesvirus, mycoplasma, chlamydia and trichomonas.
- No known toxins or environmental toxins have been detected.
- Electron microscopy results have been negative
Observation analysis did not identify any contamination impacting the river at these sites at the time of sampling. The EPA collected water samples at four separate sites on the 18/2/15 for toxicology, pesticide, herbicide and hydrocarbon testing. The pesticides included organochlorines, organophosphates and pyrethroids. All results were negative. The EPA also inspected the road works being conducted by the Roads and Maritime Service (RMS) upstream of the affected area at Myers Bluff. No significant environmental issues were identified at this site.
During the surveys, no other aquatic species were observe to be affected, including observations of small numbers of healthy freshwater turtles including the Murray River Turtle (Emydura macquarii).
Other animals observed during the surveys included eels, water dragon, goanna, snake and
multiple species of fish.
Figure
References
ABC Online 2015. http://www.abc.net.au/news/2015-09-02/mystery-virus-killing-rare-freshwater-turtles-identified/6744476. Accessed 18 Nov 2015.
Bellinger Courier Sun. Nov. 17, 2015. Spring brings hope to Bellingen's turtles. http://www.bellingencourier.com.au/story/3496851/spring-brings-hope-to-bellingens-turtles/?cs=483 Accessed. November 22, 2015
Bellinger Courier Sun. Nov. 17, 2015. Spring brings hope to Bellingen's turtles. http://www.bellingencourier.com.au/story/3496851/spring-brings-hope-to-bellingens-turtles/?cs=483 Accessed. November 22, 2015
Moloney B. Britton S. Matthews S. 2015. Bellinger River Snapping Turtle Mortality Event 2015: Epidemiology Report. NSW Department of Primary Industries. http://www.bellingen.nsw.gov.au/sites/bellingen/files/public/images/documents/bellingen/Environment/BRST_Mortality_Event_DPI_Epidemiology_Report_2015_Final%20Copy.pdf
http://rstb.royalsocietypublishing.org/content/364/1534/3429 (for references)
http://www.nwhc.usgs.gov/publications/fact_sheets/pdfs/Climate_Change_and_Wildlife_Health.pdf
http://rstb.royalsocietypublishing.org/content/364/1534/3429 (for references)
http://www.nwhc.usgs.gov/publications/fact_sheets/pdfs/Climate_Change_and_Wildlife_Health.pdf
Comments
Post a Comment