By Dr. Ben Golas, V.M.D.
Colorado State University
Fort Collins, Colorado
White-nose syndrome (WNS) is a disease affecting cave-dwelling bats caused by the fungus Pseudogymnoascus destructans (Pd). WNS first appeared in New York during 2006 and has since spread across the eastern half of the United States and Canada (Figure 1), killing over 6 million bats in the past decade. This is devastating for North American ecosystems; a female little brown bat can eat her weight in bugs in a single night, which doesn’t sound like much but can mean as many as 300 to 3,000 insects per day! By consuming mosquitoes, beetles, and moths that can be pests for people and agricultural crops, bats are estimated to save the United States as much as 3.7 BILLION dollars per year in pest suppression, and this is a service that we are losing through their demise. So how can we promote bat survival in the face of such a deadly threat? Our research group is trying to identify the conditions that allow bats to survive WNS so we can identify and potentially support at-risk populations.
To save bats, the first thing we need to do is find out why some survive, and to answer that question, it behooves us to ask, how does fungal infection similar to athlete’s foot turn deadly? The WNS fungus only grows at low temperatures, between about 0 and 20 degrees Celsius. Bats lower their metabolism when they hibernate, which causes their body temperature to drop to match the cold temperatures of their hibernation roosts, which might mean just above freezing for some. When their body temperature dips low enough, the fungus makes its move, growing into them (Figure 2) and leading to increased arousal from hibernation. This could be due to itchy lesions needing grooming, evaporative water loss from fungus opening thin skin membranes, or other unknown reasons, but in any case, increased arousal means increased energy loss. An arousing bat uses as much as 67 times as much energy as it does in a full day of hibernation, so increasing the frequency of arousal can really take a toll on a bat that can only store a limited payload of fat before hibernation begins. When those fat stores run low in the middle of winter, bats may die of starvation or arouse and attempt to find food. Seeing as there are not many bugs flying around in the dead of winter, these bats die of starvation or exposure outside the roost.
Given this reason for death, our group is trying to identify how some bats can live with WNS. Despite heavy casualties in some species like the little brown bat, others, such as the big brown bat, do not appear to suffer great mortality by WNS, and even of those badly-affected species, there are still remnant populations that survive in areas where the fungus has been around for years. How is it that some bats are part of the millions of dead, but others persist? In 2016, an energetics model was published that starts to get at this phenomenon. It suggests that the microclimates (temperature and humidity) where bats hibernate can influence whether they survive or perish from infection. Bats start the winter with a certain amount of energy, and fungal growth increases the amount of energy needed to survive the winter through increased arousal. The more growth, the more energy used, with both fungal growth and the bat’s regular energy use in hibernation being dependent on local microclimate. The fungus tends to prefer warmer, wetter ends of this spectrum, so the bats that hibernate in warm wet sites are going to have more energy sapped compared to bats using colder, drier roosting areas. Some bats, like the little brown bat, require the warm, wet areas in general, making them more susceptible to mortality, while others, such as the big brown bats, have a larger range of microclimates in which they can hibernate, such that they can avoid the areas where the WNS fungus would flourish.
The exciting thing about this new energetic model is that it seemed to hold true on a species-wide, continental scale, explaining why little brown bats across North America suffer so much more mortality than big brown bats. We are interested in taking this a step further and exploring this hypothesis in individual bats. Do bats that survive in areas where WNS is common choose to use hibernation roosting areas that are not ideal for fungal growth? To explore this idea, we plan to measure microclimates in these roosts (Figure 3) and see if bats are utilizing “survival space,” areas with microclimates that are suitable for bat hibernation but not fungal growth, such that the bat is able to survive winter. We can also look for ecological traps, areas that were commonly used for hibernation before the fungus appeared but are now deadly due to fungal presence. If we can identify survival spaces and ecological traps, we may be able to artificially create environments wherein bats can safely roost, or we might even be able to dissuade bats from hibernating in areas that could be tempting but deadly ecological traps.
Bats are a great asset to us and the natural ecosystems we all share. They have already suffered terribly as WNS has spread across the continent, and likely there is much more death to come, but hope remains in those remnant populations we see persisting in the WNS death zones. By finding out how these populations are surviving, we may be able to help promote their growth as well as potentially protect those that are yet to be exposed. There are many questions yet to be answered, but I at least am optimistic that not all is lost for our North American bats, and there are many brilliant people working hard to try to find solutions for a devastating situation. If you have questions about WNS or our work, please leave them in the comments section, and thank you for reading!
By Danny L. Bryan, Ph.D.
Associate Professor of Biology
The timber rattlesnake (Crotalus horridus) is facing serious threats throughout the United States, with population studies indicating a decreasing trend throughout its range. Once considered a vile and deadly reptile, sentiment toward the snake is changing as further details of its life history are determined. Timber rattlesnakes are not aggressive and rely on camouflage as their primary defense. Timber rattlesnakes are found in the eastern United States from New England to northern Florida and eastern Texas to Minnesota. Originally found in 34 states, the species has been extirpated from Delaware, Maine, and Rhode Island. It is listed as endangered in Connecticut, Indiana, Massachusetts, New Hampshire, New Jersey, Ohio, Vermont, and Virginia. The species is considered threatened in Illinois, Minnesota, New York, and Texas. Timber rattlesnakes are protected in Arkansas, Kansas, Maryland, Tennessee, and Wisconsin and are partially protected in Mississippi, Missouri, Nebraska, and Pennsylvania. In Tennessee, it is listed as a species of Greatest Conservation Need and protected from take.
Cumulative effects of land clearing for timber and agriculture, habitat alteration for road construction, residential and commercial development, fragmentation of foraging habitat, destruction of hibernacula, vehicular mortality, natural predation, and collection from the wild have all contributed to decline of the species, with future extinction not outside of the realm of possibility. Roads and development fragment habitat, creating barriers to movement and decreasing successful migration through habitat patches. Habitat fragmentation also isolates populations, thereby reducing gene flow and possibly leading to inbreeding depression. Roads serve as ecological traps for rattlesnakes because the animals are more conspicuous when crossing roads and thus are more easily exposed to depredation or killing by humans.
Because of the fate of timber rattlesnakes in other states, the species became my subject of study in Tennessee as early as 1990. In 2000, I became the Tennessee representative for a group of scientists involved in developing the Timber Rattlesnake Conservation Action Plan for the United States Fish and Wildlife Service. Little was known about timber rattlesnakes in Tennessee during that time, so the natural history and survivability of the species became my dissertation topic.
I was working on a translocation project when a wildlife officer from Bear Hollow Wildlife Management Area brought me a nuisance timber rattlesnake on August 27th, 2005. The snake was using a resident’s driveway culvert for cover and the resident wanted the snake relocated for the safety of his family. After inspecting the snake, I noticed several large masses along the body of that snake and decided it was not a good candidate for translocation. I contacted the University of Tennessee Veterinary College to inquire about the tumors. Initially we suspected it was a mycobacterial infection, caused by a relative of the bacterium causing tuberculosis in humans. The snake died the following day with no definitive diagnosis and no necropsy was performed.
I was tracking a male timber rattlesnake on August 7th, 2007, and during this time I discovered a new female timber rattlesnake. This female was utilizing habitat that would be more appropriate for gravid females than foraging females during this stage of the active season. After I captured the snake, I noticed she was extremely lethargic, anorexic, and in need of a shed. As I was returning to base to process the snake, she died and clear fluid began draining from her nares. I strongly believe these were my first two encounters with Snake Fungal Disease.
On August 13th, 2012, I was invited, along with the Tennessee Wildlife Resources, to assist the United States Army Corps of Engineers in capturing and moving wildlife as the Corps was cleaning debris from a designated work site. A large male timber rattlesnake was discovered at the site and captured. I immediately noticed the snake was lethargic, had discolored scutes, and a mass above the left eye. I had recently read an article by Dr. Matt Allender on a disease infecting massasaugas in Illinois. I observed too many similarities associated with the timber rattlesnake and the snakes in his study. I took samples from the timber rattlesnake and sent them to Dr. Allender to test for Snake Fungal Disease. The tests confirmed presence of the disease and this was the first confirmed case in Tennessee.
Snake Fungal Disease (SFD), caused by Ophidiomyces ophiodiicola, is an emerging threat to rattlesnake populations. This fungus was first confirmed in an infected eastern rat snake (Pantherophis spiloides) in Sparta, Georgia in 2009 and has been linked to declines in the eastern massasauga (Sistrurus catenatus catenatus). The infection has a high mortality rate and has been linked to a 50% decline in the timber rattlesnake population in New Hampshire. The first confirmed case of SFD in Tennessee was from the timber rattlesnake I collected at Center Hill Lake on August 13th, 2012.
To date, the disease has been confirmed in at least 18 states: Illinois, Florida, Massachusetts, Minnesota, New Jersey, New York, Ohio, Tennessee, Wisconsin, South Carolina, North Carolina, Georgia, Connecticut, Arkansas, New Hampshire, Virginia, and Michigan. It has also been detected in southern Canada. The spread of the disease appears to be following a path very similar to that of White Nose Syndrome in our bat populations. Snake species that have been confirmed with the disease so far include: northern watersnakes (Nerodia sipedon), eastern racers (Coluber constrictor), rat snakes (Pantherophis spiloides), timber rattlesnakes (Crotalus horridus), mud snakes (Farancia abacura), pigmy rattlesnakes (Sistrurus miliarius), massasaugas (Sistrurus catenatus), copperheads (Agkistrodon contortix), milksnakes (Lampropeltis Triangulum), cottonmouths (Agkistrodon piscivorous), ribbon snakes (Thamnophis sauritus), corn snakes (Pantherophis guttatus), indigo snakes (Drymarchon couperi), kingsnakes (Lampropeltis getula), and ringneck snakes (Diadophis punctatus).
Clinical signs of the disease include cellulitis, oral swelling, cutaneous abscessation, ocular swelling, respiratory distress, scabs, crusty scales, subcutaneous nodules, abnormal molting, cloudiness of the eyes, hyperkeratosis, skin ulcers, swelling of the face, anorexia, and nodules in deep tissues and facial regions. The disease can begin at any time, but tends to be observed more frequently at emergence from hibernation. Not all hibernation sores are SFD. Other skin infections can resemble SFD and include fungal species of Trichophyton (ringworm), Epidermophyton, Cladosporium, Fusarium, and bacterial keratitis. The only way to confirm the causative agent of an infection is through clinical diagnosis. Snakes may shed out of these infections without difficulty.
The fungal disease begins as a dermatitis, and in the early stages, some snakes may effectively shed free of the disease. However, if the disease is able to take hold, it penetrates through the dermal layers into muscle and bone and may subsequently become systemic. Mortality rates are very high in this phase of the disease. I have noticed timber rattlesnakes that have tested positive for the disease in Tennessee have abnormal loreal pits. The loreal pit is a deep depression behind the nostril which serves to thermoregulate and also opens to a sensitive infrared detecting organ. These pits may serve as an entry point for infection. The disease can also change the behaviors of the snake, which may increase opportunities for depredation. Snakes may come out of hibernation during mild winter days to bask. Basking raises the temperature of snakes in order to stimulate an immune response. However, in winter months, the temperature increase from basking does not raise temperatures enough to illicit an effective immune response. Conversely, basking-induced temperature increases during winter will actually stimulate additional fungal growth.
Snakes have been treated for SFD with an approximate 50% success rate. The process involves surgically removing fungal masses, treatment with anti-fungal drugs given intramuscularly, and housing in elevated temperatures. Anti-fungal drugs are administered for approximately six months. These drugs can have an adverse effect on the individual’s organ systems, not to mention the added stress placed on confining wild animals. At a population level, this type of treatment is not feasible and the laws of various states may deem it illegal to house venomous snakes for treatment and also to release the snakes once they have been held in captivity.
The timber rattlesnake in the photographs above also experienced neurological disorders. The snake’s side-to-side head movements were not smooth, but rather erratic and jerky – one might say the movements were reminiscent of those associated with Parkinson’s disease. This is a clear indication that the central nervous system was affected by SFD. This 137 cm male timber rattlesnake was found killed by a predator within 24 hours of its release, but was not consumed. It appeared a violent death for the rattle was broken off, the skin stripped from the neck as he was likely shaken, and sharp punctures covered the entire body
Snakes can spread the disease through direct contact; however, as snakes crawl through their habitat prodding and probing rock crevices and rodent holes, they often develop micro-abrasions. These openings in the skin allow entry of fungal spores from ground contact. Due to climate change, the winters in Tennessee are milder and wetter. These conditions can facilitate active fungal growth during hibernation when the snakes are most vulnerable.
There is still much to learn about SFD. The ecology of the fungus, the transmission of the disease, potential variants of Ophidiomyces, the effects on snake populations, and timing of morbidity and death are all questions yet to be answered about this emerging disease.
About the Author
Dr. Danny L. Bryan is Program Director and Assistant Professor of Biology at Cumberland University in Lebanon, TN and serves as a scientific and species review expert for the Tennessee State Wildlife Action Plan. Dr. Bryan is currently conducting research on the distribution, natural history and conservation of the timber rattlesnake in Tennessee and has spent the past several years studying the impact of development in Middle Tennessee on the Timber Rattlesnake population. Prior to Professor Bryan's study, which is in conjunction with the Tennessee Wildlife Resource Agency and the U.S. Fish & Wildlife Service, very little was known about the Timber Rattlesnake population in the state. The species is currently listed as a "Species of Greatest Conservation Need " in Tennessee; however, Bryan's study - which focuses on the Timber Rattlesnakes' population movements and repopulation - suggests the species may be endangered due to encroaching development and habitat loss. Bryan was also the first to identify the fungal disease, Ophidiomyces ophiodiicola, in Tennessee which may add an additional threat to the species.
By Justin Kaiser
3rd year Veterinary Student
Colorado State University
Many people have heard of the frequent and recurring problems that numerous wildlife species in the world face in this day and age. More species are considered endangered than ever before by the International Union for the Conservation of Nature and the list just continues to grow. The main culprits for this struggle are frequently cited as habitat encroachment and poaching, but there exists a less frequently discussed area that damages wildlife species increasingly more in today’s world: infectious disease.
More specifically, infectious diseases originating in domestic animals and spilling into wildlife species that were previously naïve to these pathogens are creating a stir in wildlife news and conservation groups. As efforts increase to preserve natural habitats, civilization begins to surround and hug the borders of these natural areas. With this border-sharing comes the interactions of species that do not normally comingle. When these interactions occur, pathogens are exchanged and wildlife is threatened by a hazard arguably as harmful as poaching and habitat loss. This reverse transmission of disease from domesticated animals into wildlife populations is often termed 'spillback'.
There have been multiple documented examples of spillover and spillback in recent years, including pneumonia in bighorn sheep, tuberculosis in several species (for example - deer, opossums, and badgers), brucellosis in bison, and many others. Some of these have larger impacts than others on wildlife, environmental, and even human health. As such, it can be incredibly complicated to understand and control disease dynamics and transmission patterns once an outbreak begins due to wildlife acting as permanent reservoirs.
One particular area of research that I have chosen to focus in on as of late is global big cat conservation. Big cats have been battling the odds due to the previously mentioned effects of human encroachment and habitat loss. Now, threats have begun to emerge that standard conservation efforts may not be suited to address. One of these threats, canine distemper virus (CDV), is proving to be a greater risk to some of the planet’s most threatened and beloved animals than originally anticipated.
Belonging to the same genus of viruses as Rinderpest and Measles, CDV has a wide range of documented mortality and morbidity, depending on the species in question. In dogs and many other carnivores, the disease manifests as gastrointestinal, respiratory, and neurologic signs often resulting in death. If the animal does survive, lasting neurologic problems are often present. One aspect of the virus that is becoming more apparent, however, is its importance as one of the biggest infectious threats to carnivore species, second only to rabies.
Big cats have shown a particular susceptibility to the virus and first proved its lethal potential on the Serengeti plains in Africa, where it is believed to be responsible for the deaths of 1/3 of the wild lion population in the 1990s. The death toll was estimated to be over 1000 animals, and was characterized by grand mal seizures (warning: links to graphic video) and eventual death. Investigations suggested that the strain of CDV present in the lion populations matched that of the domestic and feral dogs surrounding the area. Vaccination programs were put into place for these dog populations, and though unclear its long term affects, it seemed to quell the source of CDV in the lion populations.
Recent research in Russia and some Asian countries has revealed a very similar problem in the Amur tiger (the largest cat in the world), the Bengal tiger, and several other large felid species of concern throughout the world. With habitat borders fighting to withstand the encroachment of human activity, domestic species interaction with big cats is becoming more common. In many situations, the buffer zones of national parks harbor animals associated with local people, and disease control in these populations is nearly nonexistent. For example, some areas in the US and other countries have nearly eradicated canine distemper with routine vaccination (however, we deal with the disease in raccoons and other wild carnivores in these areas which tend to act as reservoirs). As big cats predate smaller animals, both domestic and feral, they bring the diseases of their prey into the parks and ignite the spread of these infections that are difficult to measure in such naturally elusive species as the tiger.
Though vaccination is a possibility in big cats, it is not always practical to execute. New vaccine strategies are recommended, such as the use of oral bait vaccines such as those used to control rabies in the eastern US. Though an obvious area of growing concern, the complete impact of CDV on big cat populations has not been thoroughly studied. Research for vaccine implementation is currently underway for big cats, but without effective deployment strategies, vaccination of the cats will prove very difficult. Another more sustainable approach would be to implement vaccine programs for the feral and domestic animals that are in close proximity to big cat habitats. As the constant fight for natural space for wildlife continues, buffer zones to national parks must be kept clear of development and other anthropomorphic (caused by human) pressures that may cross the borders of the parks and silently kill the species within.
Packer, C., S. Altizer, M. Appel, E. Brown, J. Martenson, S. J. O'brien, M. Roelke-Parker, R. Hofmann-Lehmann, and H. Lutz. "Viruses of the Serengeti: Patterns of Infection and Mortality in African Lions." Journal of Animal Ecology J Anim Ecology 68.6 (1999): 1161-178.
Gilbert, Martin, Svetlana V. Soutyrina, Ivan V. Seryodkin, Nadezhda Sulikhan, Olga V. Uphyrkina, Mikhail Goncharuk, Louise Matthews, Sarah Cleaveland, and Dale G. Miquelle. "Canine Distemper Virus as a Threat to Wild Tigers in Russia and across Their Range." Integrative Zoology 10.4 (2015): 329-43.
Sharon L. Deem, Lucy H. Spelman, Rebecca A. Yates, and Richard J. Montali. Canine Distemper In Terrestrial Carnivores: A Review." Journal of Zoo and Wildlife Medicine 31.4 (2000): 441-51.
Photos acquired from Veterinary Initiative for Endangered Wildlife, a nonprofit organization dedicated to the conservation and veterinary care of endangered species worldwide.
About the author: Justin Kaiser is in his third year of veterinary school at Colorado State University. His passion is big cat conservation and it's currently focused on studying canine distemper in tigers. He may be reached at email@example.com.
By Jonathan E. Kolby
National Geographic Explorer
PhD Candidate, James Cook University
As the world witnesses catastrophic biodiversity loss, amphibian species are among those most at risk. Already burdened by habitat destruction and pollution, hundreds of amphibian species around the world are now threatened with extinction by an emerging infectious disease. The culprit is amphibian chytrid fungus (Batrachochytrium dendrobatidis), an often highly virulent aquatic pathogen that causes the skin disease chytrdiomycosis. Severe infection often damages vital skin function and interferes with the ability to regulate electrolytes, resulting in cardiac arrest. Before this planet loses some of its most fascinating and unique creatures for good, my team of biologists, zoologist, artists and conservationists seek to give these animals a boost in their battle against chytrid.
Chytrid has now been detected in approximately 60 countries and on every continent except Antarctica. Unfortunately, this pathogen demonstrates low host species specificity and many of the worlds’ 7000+ amphibian species appear to be susceptible. Response to infection and time until death varies considerably between species, and those that do tolerate infection can act as reservoir hosts, aiding in its persistence and spread. This pathogen knows virtually no boundaries. It has been found in amphibian habitats from sea level upwards to alpine mountain peaks in remote wilderness areas, and continues to spread between countries and continents.
For the past 5 years, I’ve been studying global chytrid dispersal and exploring opportunities to reduce its spread. Chytrid is transmitted through direct skin contact between amphibians and by exposure to materials contaminated with zoospores shed from infected animals. These non-living infectious materials, also known as fomites, can include things such as water, soil, shipping containers, and footwear. Part of the reason why chytrid is an especially difficult pathogen to control is because it can survive for weeks and potentially months in the absence of a host. The international wildlife trade transports millions of amphibians annually, and my PhD thesis research has shown this to be a frequent contemporary pathway of international chytrid dispersal in the absence of targeted biosecurity regulations.
Unfortunately, no attempt to stop an advancing wave of chytrid has yet been successful and once established, it cannot be eradicated. Halting this globally emerging disease event now poses one of the greatest conservation challenges in modern times. Despite the strong link between amphibian commerce and chytrid spillover, even countries that don’t commercially import amphibians continue to become exposed, for example Madagascar. It’s possible that hitchhiking alien amphibian invaders or even tropical storms might have introduced chytrid to this island nation, but the exact source remains a mystery.
As we struggle to control the spread of chytrid, time is running out for many species on the brink of extinction, especially those in Latin America. For the past 10 years, I’ve been monitoring the long-term impact of chytrid in the cloud forest of Cusuco National Park in Honduras. In this high-elevation rainforest, I found that chytrid severely threatens three endangered frog species with extinction: 1) the Cusuco spike-thumb frog (Plectrohyla dasypus), 2) the Exquisite spike-thumb frog (Plectrohyla exquisita), and 3) the Mossy red-eyed frog (Duellmanohyla soralia). A growing number of species around the world may soon become extinct without some form of conservation intervention, but few long-term rescue methods have been successfully demonstrated. Therefore, I’m proud to announce the establishment of the Honduras Amphibian Rescue and Conservation Center (HARCC), a new platform my frog rescue team has launched from which to combat chytrid-driven extinction in Central America.
The greatest challenge to keeping amphibians alive in the wild with chytrid is that treatment for infection must be administered in a controlled environment, most often via the administration of an itraconazole bath. Even following successful treatment, amphibians do not appear to develop a significantly greater resistance to subsequent chytrid infection. After studying how chytrid affects certain endangered amphibians in Honduras, my team is fortunate to have identified a method likely to prevent extinction while allowing them to remain in their natural chytrid-positive habitat.
Chytrid appears to consistently infect younger amphibians both more frequently and severely than adults, and a large proportion of these young amphibians are unlikely to survive to adulthood. Conversely, my surveys have also shown that the “lucky” survivors that dodged the chytrid bullet as juveniles are often able to tolerate infection as adults and persist in a chytrid-positive environment. Did these animals survive because they possessed superior innate resistance to disease and if so, might this be transferred to offspring? Or could these animals have instead simply escaped chytrid exposure longer, despite equivalent susceptibility? This is an area still under investigation, but most importantly, our field data agree with recent studies that show a clear age-related association between the timing of chytrid exposure and frog survival: adult frogs survive more often than young recently metamorphosed frogs. Thus, it may be possible to protect some species from extinction in the wild by loosening this bottleneck and protecting young animals from disease through a head-start and reintroduction program based at HARCC.
HARCC is a frog rescue laboratory that we are constructing inside two ocean shipping containers in Honduras. Once fully operational, our frog rescue head-start program at HARCC will entail collecting large numbers of baby frogs from the rainforest before they die from chytridiomycosis and transporting them to our biosecure HARCC facility where we can manage their infections and boost survival. We will continue caring for them inside this safe environment until they become healthy adults with mature immune systems, at which time they will be reintroduced back into the rainforest to supplement the population of wild adults. We expect these adult frogs to survive and reproduce in the wild, and create a greater pool of offspring that will help offset the chytrid-elevated death rate of juvenile frogs. This process of collection, protection, and reintroduction year after year will help buffer against extinction. In addition, natural selection can continue searching for frogs that might be genetically resistant to chytridiomycosis and potentially build innate immunity within the populations over time. This head-start conservation method has previously been successful in assuring the survival of a variety of other wildlife species, but has infrequently been explored as a potential tool to combat chytrid.
The spread of chytrid represents one of the greatest conservation challenges the world is currently facing. Developing an effective solution will require a strong network of international communication, collaboration, and capacity building. I’m extremely hopeful that what my frog rescue team is learning in a small rainforest in Honduras may eventually save amphibians around the world from this frightening fungal foe!
My team is currently raising funds to finish building the HARCC frog rescue facility, train our Honduran staff, and begin frog rescue operations by summer 2017. If you’d like to learn more and help support this effort, please visit our project page here: Save Frogs From Extinction.
To follow our progress and read more about this exciting conservation effort, subscribe to our updates at www.FrogRescue.com and view the HARCC FrogRescue YouTube video channel here: HARCC FrogRescue. Please also follow us on Facebook and Instagram/Twitter (@MyFrogCroaked).