Professional Dog Behavioral Therapist & Trainer OBEDIENCE- TRACKING- PROTECTION- SOCIALIZATION- SCHUTZHUND. IPO. IGP.
(15)
AKC Canine Good Citizen Evaluator
Animal Behavior College Certified Dog Trainer ID ABC119222
I was member & Certified Club and Regional Trial Helper of the GSDCA-Working Dog Association
Member and Certified Trial Helper of USA United Schutzhund Clubs of America
Work as Vet-tech at Veterinary Hospital
ABSTRACT. The ability to detect the direction of a track is of vital importance to animals of prey and is retained in many modern breeds of dogs. To study this ability, four trained German shepherd tracking dogs, equipped with head microphones to transmit sniffing activity, were video-monitored afte...
Socialization of puppies is vital to their health and well-being and can help prevent behavior problems later in life. Although this important developmental stage is critical to establishing appropriate social behaviors, it is also a period of increased disease risk. Discover how to incorporate a mo...
El sentido del olfato de tu perro es entre 1000 y 10 000 veces más sensible que el tuyo. Los perros tienen entre 125 000 000 y 300 000 000 de glándulas odoríferas (varía según la raza) en comparación con nuestras míseras 5 000 000. Los perros pueden detectar olores en partes por billón, por ejemplo, podrían detectar una manzana podrida en dos millones de barriles (que son aproximadamente 752 000 000 de manzanas)
La Foto es todos los vasos sanguíneos en la nariz de los perros.
Dogs with an enlarged esophagus benefitted from liquid sildenafil in a small new study.
https://www.cfsph.iastate.edu/FastFacts/pdfs/leptospirosis_F.pdf
Due to the increase in reports of canine leptospirosis, appropriate biosecurity, biosurveillance, and prevention measures are more imperative now than ever. Discover effective prevention measures that have been shown to be effective against urinary shedding and to decrease mortality associated with....
A balanced diet provides nourishment. However, patients with food allergy develop an aberrant immune response to what typically are common dietary components and may exhibit dermatological and gastrointestinal clinical signs. Dive into this roundtable of experts as they discuss the impact of ad...
Lyme Lowdown
¿Es un error que el perro lleve la boca abierta durante el rastreo? ¿pierde eficacia? Karl Zuschneid descubrió la respuesta
*First broadcast on April 30, 2019. There are 6 dog breeds native to Japan, including Akita and Shiba Inu. Each has adapted to the region of its origin, but they all have pointy ears, a curved tail, and an unwavering loyalty to their owner. This time on Japanology Plus, our theme is Japanese dog bre...
https://www.ada.gov/service_animals_2010.htm
The ADA Home Page provides access to Americans with Disabilities Act (ADA) regulations for businesses and State and local governments, technical assistance materials, ADA Standards for Accessible Design, links to Federal agencies with ADA responsibilities and information, updates on new ADA requirem...
Cooling down an overheating patient in the backcountry is often an insurmountable challenge. Now, researchers are testing a strategy from the endurance sports world for use on the trail.
5 Mitos sobre displasia de cadera en caninos
MV Ana Robles Fuente: Laboratorios Mayors, Argentina.
La gran mayoría de las razas grandes o gigantes pueden estar afectadas por Displasia de Cadera Canina (DCC), Sin embargo, raza puede ser afectada, de hecho puede aparecer en razas medianas y pequeñas (en menor proporción), mayormente con menos consecuencias para el animal (al ser más livianos) y también se encuentra en razas grandes de gatos, con las mismas características que en los perros.
En los perros, si bien la Displasia de Cadera Canina (DCC) es altamente heredable, no es congénita y al nacimiento no está presente. La gran mayoría de perros, tenidos como mascotas y reproducidos sin control presentan una incidencia mayor de la enfermedad que los controlados en los clubes de razas.
☑Mito 1
"Sólo las articulaciones de la cadera y los tejidos circundantes se ven afectados"
No solo la cadera puede ser afectada por cambios degenerativos – artrosis – en los cartílagos , por el contrario, es frecuente que los hombros , las rodillas y las articulaciones intervertebrales puedan mostrar cambios similares, como la pérdida de cartílago, la inflamación de la cápsula articular y la proyección de la enfermedad al hueso subcondral. La Displasia de cadera canina es simplemente la más notable – y más dolorosa – de las manifestaciones de este tipo de artrosis.
☑Mito 2
"La ausencia de displasia de cadera en los padres es garantía de libre displasia para los cachorros"
La probabilidad de tener un perro con Displasia de Cadera Canina (DCC) es del 25%, incluso si ambos padres tienen “buena” o “excelente” conformación de sus caderas. Este porcentual de aparición de la enfermedad sube mucho si cualquiera de los padres tiene displasia, si ambos tienen displasia o si los hermanos de los reproductores la presentan. La enfermedad es poligénica, es decir concurren un conjunto de genes que determinarán las característica de cada uno de los componentes de las articulaciones (ilion, isquion, p***s, acetábulos, cabezas y cuerpos femorales) Los genes anormales pueden no aparecer o expresarse por algunas generaciones, haciendo que el control y eliminación de la enfermedad sea aún más difícil. Se considera que la influencia genealógica es directa en por lo menos 3 generaciones (padres, abuelos y bisabuelos) y un poco menor hasta por 7 generaciones anteriores.
☑Mito 3
"Una dieta abundante ayuda a evitar la displasia de cadera"
En un estudio realizado en la Universidad de Davis (USA) a partir de las ocho semanas de edad, a las crías que se les disminuyó en un 24 % el peso de la ración, tuvieron un 46 % menor incidencia de displasia de cadera que las crías que pudieron comer libremente. Se considera hoy que no se debería estimular el crecimiento y el peso en los primeros meses de vida para que la influencia negativa ambiental sea mínima, en los perros predispuestos genéticamente, a la displasia de cadera. Por lo tanto, perros secos, delgados pero bien alimentados, crecen mejor, desarrollan mejor sus radios y sus articulaciones, que los cachorros gorditos, “hermosos” que solemos elegir como mascotas.
☑Mito 4
"Los ovejeros alemanes tienen mucha displasia y se “descaderan” cuando son viejitos"
Es común escuchar que los ovejeros alemanes son los que más sufren de Displasia de Cadera Canina (DCC) y luego cuando llegan a una edad avanzada “se descaderan” o quedan paralíticos. Hay que tener en cuenta que la raza Ovejero Alemán, hasta el día de hoy, es la raza más estudiada con respecto a Displasia, es la raza de la que tenemos más información con respecto a la incidencia de la enfermedad. Por esto decimos que estos perros son los más afectados, sin embargo estudiando conscientemente a otras razas de crecimiento rápido, nos encontramos que la displasia puede encontrarse en mayor proporción todavía. En el ovejero, gracias al control y a la selección realizada por displasia, el % de casos ha disminuido en los últimos años.
Entonces…. ¿En qué casos aparecen las parálisis de las patas traseras?
Los signos clínicos de la Displasia de Cadera Canina (DCC) incluyen: rengueras, pasos cortos y rígidos, lentitud para incorporarse o para echarse, dificultad para subir escaleras o saltar, mayor rigidez por la mañana y mejora “en caliente” durante el día. Estos síntomas empeoran con el aumento del ejercicio o se manifiestan al día siguiente de un ejercicio pesado. Suelen empeorar los días fríos y húmedos. Todos estos signos clínicos rara vez aparecen de repente y empeoran lentamente a lo largo de meses o años, además los signos rara vez son graves y la mayoría de los perros muestran solo una leve o moderada renguera o dolor. Hay que considerar que la gran mayoría de los perros no muestran signos de la enfermedad, ya que solo un 30 o 40 % manifiesta signos clínicos y se da principalmente en animales muy jóvenes. Cuando los perros llegan a una edad avanzada, muchos muestran signos de dolor, dificultad para incorporarse, tambaleo al caminar, disminución de las masas musculares y hasta parálisis de sus patas traseras (entre otros signos) y esto puede suceder tengan o no tengan displasia.
En la mayoría de los casos se trata de artrosis o enfermedad de los discos intervertebrales de la columna lumbar o dorso lumbar. El tratamiento debe ser particularmente enérgico en estos casos, para lograr una sobrevida satisfactoria y mejorar la calidad de vida del paciente. Esto puede ocurrir en todas las razas, siendo las más predispuestas las razas grandes.
☑Mito 5
"Los perros con displasia deben ser eutanasiados"
Hoy en día los perros pueden vivir muchos años con buena calidad de vida, con displasia de caderas.
Es una enfermedad grave funcional pero no es grave vital. Solo nombrarla asusta, pero una vez detectada es factible de ser tratada. Hace años, en la gran mayoría de los animales de compañía, las enfermedades de la cadera se diagnosticaban sólo, cuando los perros mostraron signos avanzados de dolor.
Hoy, el diagnóstico radiográfico es sencillo y con el aumento del conocimiento sobre las enfermedades del crecimiento, las mismas pueden ser diagnosticadas y tratadas muy precozmente. Las opciones de tratamiento disponibles en la actualidad pueden garantizar una vida larga y “normal”, incluso para los perros con enfermedad avanzada.
Learn what to look for
Índice cefálico.
La forma de la cabeza, y en especial la región facial, está determinada en gran medida por el cráneo. Dentro del espectro de conformación del cráneo, generalmente se reconocen tres amplias categorías que se corresponden con el concepto de biotipo cefálico definido por el antropólogo sueco Anders Retzius (1796-1860) y en cuya determinación interviene el concepto del Índice Cefálico Total. El concepto Índice cefálico fue utilizado por primera vez en el Siglo XIX, para clasificar restos humanos antiguos hallados en Europa.
Estos tres biotipos cefálicos, establecidos por Retzius para los humanos son: El Braquiocefálico, mesaticefálico y dolicocefálico.
Posteriormente Paul Broca (1824-1880), fundador de la sociedad antropóloga francesa, extrapoló los métodos craneométricos humanos a los animales con el propósito de realizar ciertas comparaciones y estableció las siguientes definiciones:
Dolicocéfalo (del griego antiguo kephalê, "cabeza" y dolikhos, "largo y delgado") en donde la porción facial del cráneo es más larga y estrecha, Braquiocéfala (del griego antiguo kephalê, "cabeza" y brakhys, "corto") en donde la porción facial del cráneo es más corta y ancha y Mesocéfala (del griego antiguo kephalê, "cabeza" y mesos, "medio") en donde la porción facial del cráneo es aparentemente igual a su ancho, es decir de proporciones intermedias.
Según Sisson y Grossman, Getty e König, plantean que las distintas razas caninas presentan numerosas variaciones en la forma y tamaño de la cabeza ósea. Las que tienen un cráneo estrecho y largo se designan como ☑dolicocéfalos (p. ej., galgos, collie). Otros perros tienen cráneos cortos y anchos y se denominan ☑braquicéfalo (p. ej., Bulldog inglés y francés, pequeños spaniels, pekinés, pug, shih tzu ) y las formas intermedias (p. ej., fox terrier, labrador) son ☑mesocéfalos.
Según Sisson y Grossman y Getty, los valores de índice cefálico que determinan el biotipo cefálico son:
☑Dolicocéfalo: Índice Cefálico inferior a 55
☑Mesocéfalo: Índice Cefálico entre 55 y 80
☑Braquicéfalo: Índice Cefálico superior a 80
El índice cefálico es la relación entre la anchura y la longitud, siempre que sea igual a 100.
La formula seria:
🔹Índice cefálico= ancho x 100/longitud
La longitud de la calavera, normalmente, se mide desde la cresta de la nuca al extremo rostral de la sutura interincisiva y la anchura, entre los somitos de los arcos cigomáticos.
📚Bibliografía: Determinación del índice cigomático y biotipo cefálico en perros mestizos cubanos y su importancia.
Gerardo cañete B y Gretchen Bravo M.
🤓Investigación: REMEVET
The German Shepherd is a breed of medium to large-sized working dog that originated in Germany. The breed's officially recognized name is German Shepherd Dog...
Don't Look Away - This coyote has sarcoptic mange. These suffering coyotes are showing up increasingly throughout Colorado's suburban communities. The reason? Wide spread use of rodenticides.
We encourage you to read the following article by Will Falk for more information about this horrible human caused ailment which is killing Colorado's wildlife:
https://prairieprotectioncolorado.org/lesson-from-a-mangy-coyote
Lessons From a Mangy Coyote: Why Anticoagulant Rodenticides Must Go
"The first time I saw a coyote with mange my heart broke. Most of her fur was gone. Her skin, covered with scabs and lesions, had a sickly pink pallor. Her tail seemed stuck between her legs. And, her movements, as she stumbled through a ditch next to a Colorado country road, were lethargic and listless. Just the sight of her made my own skin chafe and itch. As I hugged myself to ward away the horror, my fingernails dug into my own skin, scratching at the backs of my arms. The experience educated me in the realest ways about what the phrase “it made my skin crawl” truly means.
After witnessing this, I had to know more about what I had seen. I learned that this coyote was suffering from what scientists call sarcoptic mange, which is caused by mites who live in the skin of many wild canids. In burrowing into the animals’ skin to lay their eggs, these mites cause intense irritation and itchiness, scabbing, and hair loss. An animal affected by mange can develop secondary bacterial skin infections, too. Worst of all, mange can be fatal for animals if left untreated. With the loss of their fur, animals affected by mange often freeze to death. And, if the cold doesn’t kill them, those secondary bacterial skin infections exacerbated by excessive scratching will.
While mange does occur naturally, recent research suggests that the widespread use of anticoagulant rodenticides – a type of rat poison – weakens the immune systems of animals and makes them more susceptible to mange. A 2017 study linked anticoagulant exposure to mange in bobcats, for example.
Notoedric mange – which affects felines and is closely related to the sarcoptic mange that affects coyotes – ravaged the population of urban bobcats at Santa Monica Mountains National Recreation Area in southern California from 2002-2005. After mange was detected in 2001, the average annual survival of these bobcats plummeted by 49%. Mange-infected bobcats were necropsied and 98% of infected individuals had been exposed to anticoagulant rodenticides. These bobcats also had greater amounts of anticoagulant rodenticides than bobcats who did not die with mange.
After reading the results of the bobcat study, and against my better judgment, I was compelled to find images of bobcats with mange. I was met with the stares of blue-eyed bobcats, stripped of fur and looking like hairless, Sphynx cats. Unlike Sphynx cats, these bobcats weren’t bred selectively to be hairless. Their hair had been stripped and their skin ravaged by mites because they had eaten rodents who had eaten too many anticoagulant rodenticides.
And, what exactly are anticoagulant rodenticides? Anticoagulant rodenticides are widely used as a cheap and effective means for killing rodents. These rodenticides disrupt coagulation and cause fatal hemorrhaging. In simple terms, rodenticides cause the creatures who eat them to bleed more easily. Similar to the way a minor wound to a human taking a blood-thinner can cause a human to bleed out, rodents who have ingested anticoagulant rodenticides bleed to death.
Rodents exposed to anticoagulant rodenticides don’t just bleed to death – they bleed to death slowly. Rodents are very intelligent. They are so intelligent, in fact, that the use of toxins that immediately harm a rodent have proven to be completely ineffective because rodents learn not to eat things that instantaneously kill their kin. Anticoagulant rodenticides are effective because they can be mixed with rodents’ favorite foods as bait and the 3-7 days it takes for exposure to kill rodents makes it very difficult for them to understand what is killing them.
Anticoagulant rodenticides have been in use since the late 1940s, and by the early 1980s, genetic resistance to what are now called “first-generation anticoagulant rodenticides” was reported in rats and mice around the world. These first-generation anticoagulant rodenticides include the chemicals diphacinone, warfarin, coumatetralyl, and chlorophacinone and they killed rodents only after prolonged or repeated exposure. Due to genetic resistance, second-generation anticoagulants developed. These chemicals – which include difenacuom, brodifacoum, bromadiolone, difethialone, and flocoumafen – are much more potent, have a longer half-life, and can kill rodents after only one feeding. This potency poses an increased risk of harm non-target species.
Inevitably, predators who eat rodents are exposed to the rodenticides ingested by their prey. In one study, 70% of mammals tested in California were found to have been exposed to anticoagulants. Anticoagulant rodenticides were detected in 49% of the raptors tested in New York City, including in 81% of the great horned owls tested. A study of three species of owls in British Columbia and the Yukon detected anticoagulant rodenticides in 62% of barn owls, 92% of barred owls, and 70% of great horned owls. In sum, the Canadian researchers detected anticoagulant rodenticides in 70% of 164 owls. They also confirmed that rodenticides killed two barn owls, three barred owls, and one great horned owl.
As described above, rodents usually do not die for several days after consuming a lethal dose. This means they may continue to move through habitat shared with predators and they may continue to feed on poisoned bait. Additionally, rodents – exposed to anticoagulant rodenticides and who may be hemorrhaging internally – spend more time in open areas, stagger as they move, and sit motionless before death. All of this makes them easier prey for predators.
Coyotes, and especially urban coyotes, rely heavily on rodents for food. And, it appears anticoagulant rodenticides are harming coyotes. Scientists in the Denver metropolitan area, for example, researching the effects of anticoagulant rodenticides on coyotes, found a dead juvenile male with no obvious external injuries or other signs of trauma. However, when they necropsied the young coyote, they “found free blood in the abdominal cavity” and “a puncture wound [that] was present on the left side of the body overlying the spleen but not penetrating the abdominal wall.” They determined that the coyote died from “acute severe hemorrhage, disproportionate to the amount of trauma observed.” The coyote’s liver tested positive for an anticoagulant rodenticide. In other words, it’s likely that the rodenticide in the coyote’s body turned a minor injury lethal.
These scientists found another young male coyote dead on a two-lane road “with minor evidence of skin tearing over the ventral neck and chest.” When they necropsied the coyote, they found that the coyote’s chest was filled with blood and they concluded that the coyoted was killed by “severe acute hemorrhage, disproportionate to the mild to moderate trauma received from being hit by a vehicle.” The scientists suspected rodenticide exposure. And, sure enough, the coyote’s liver tested positive for two types of anticoagulant rodenticides. Again, rodenticides turned a small injury into a coyote’s death.
There have been many more studies demonstrating the harmful effects anticoagulant rodenticides have on non-rodent species. Some of these studies include harmful effects on buzzards, mountain lions, otters, endangered European mink, polecats, and, even, freshwater fish. Anticoagulants, in fact, act on all vertebrates – not just the rodents they’re intended for. Scientists have also discovered anticoagulant rodenticides in raw and treated wastewater, sewage sludge, estuarine sediments, and particulate matter suspended in the air.
For brevity’s sake, I’ll stop here. But, it bears mentioning that as I sifted through study after study describing the havoc anticoagulant rodenticides wreak on natural communities and felt my stomach grow increasingly sour, I learned the literal meaning of another phrase: ad nauseum. It is also important to remember that, despite the amount of studies being conducted on the effects of anticoagulant rodenticides on non-target wildlife, scientists caution us that most of this poisoning remains undetected because the necropsy and liver analysis required is labor and cost intensive. Similarly, unless an animal is being tracked through radiotelemetry, finding dead animals in a non-decomposed state, is difficult.
***
After learning about problems with anticoagulant rodenticides, the torturous manner in which these chemicals kill, and how they are making predators of rodents more susceptible to mange, most people want to know: What can I do?
This is the wrong question. Don’t ask: What can I do? Ask: What needs to be done? What do bobcats – blue eyes unblinking despite the pain of internal hemorrhaging – need us to do? What do coyotes – scraping their inflamed skin against fence posts, the corners of concrete walls, and rough tree trunks – need us to do? What do rodents – intelligent, sociable, and bleeding to death – need us to do?
Rodents, and all those who eat them, need us to stop the manufacture and application of anticoagulant rodenticides. And, they need this to happen as quickly as possible.
This is, of course, much easier said than done.
Individual home or other property owners, as opposed to government or business entities, account for a portion of total anticoagulant rodenticide use. If these individuals could be convinced to live and let rodents live, or to employ non-lethal, non-toxic measures such as blocking holes and other openings rodents use to access buildings, practicing better sanitation, or trapping rodents and removing them to better habitat, then the total use of anticoagulant rodenticides could be reduced.
There are several barriers making it unlikely that many individual property owners will forego the use of anticoagulant rodenticides, however. First, fear of rodents is so pervasive in the dominant culture that there are multiple words to describe this fear including musophobia (fear of mice specifically), murophobia (fear of the taxonomic family Muridae, which includes mice and rats), and suriphobia (which comes from the French souris meaning “mouse). Similarly, calling someone a “rat” is a grave insult.
Second, anticoagulant rodenticides are simply more economical. Sealing up holes in a house and live-trapping rodents can be costly and can require much more labor than using poison. In fact, a member of California’s Department of Consumer Affairs, Structural Pest Control Board recently estimated that pest control services employing only sanitation, exclusion of rodents, and removal of harborage can be 2-5 times more costly than using rodenticide due to labor and material costs.
I want to be clear here: I am not saying we shouldn’t try to convince everyone we can to stop using anticoagulant rodenticides. This is, of course, one reason I wrote this piece. I am saying, however, that coyotes, bobcats, other predators of rodents, and rodents, themselves, need us to do much more than to simply refuse to stop using anticoagulant rodenticides in our own homes.
Many people assume that if homeowners stopped using these rodenticides the problem would go away. Unfortunately, this is not the case. National and global anti-rodenticide market data are protected by business privacy laws as “confidential business information.” However, it’s safe to say that while individual, residential use of anticoagulant rodenticides accounts for a portion of global rodenticide use, governments and agricultural corporations are likely the biggest users of anticoagulant rodenticides.
Statistics from California tend to support this point. In 2012, California imposed stricter regulations on second-generation anticoagulant rodenticides including restricting sales of these chemicals to the general public. Then, in 2014, they imposed a new round of restrictions that were specifically intended to restrict the access of homeowners to second-generation anticoagulant rodenticides. But, using data from the California Department of Pesticide Regulation’s Pesticide Use Reporting database, it does not appear that the amount of second-generation anticoagulant rodenticides applied between 2012-2017 was significantly reduced despite the new regulations.
So, if homeowners are only a part of the problem, and governments and corporations are the worst offenders, how do we stop governments and corporations from using anticoagulant rodenticides?
A common response is: change the law. It is highly unlikely, however, that governments will ever impose a true ban on anticoagulant rodenticides. The agricultural lobby is one of the most powerful political forces in American politics. Meanwhile, in the United States, rodents are responsible for an estimated $19 billion in economic damages annually through the consumption and contamination of stored grains. Rodents don’t just pose a threat to agricultural interests, either. A British study, which attempted to determine the cost of physical damage to the built environment caused by rodents, estimated that rodents cost the British economy £200 million per year.
An astute reader may be saying to herself: “Didn’t California recently ban anticoagulant rodenticides?” And, of course, despite the headlines, California did not ban anticoagulant rodenticides. To understand this, we must look to the actual text of the California Ecosystems Protection Act of 2020 (also known as Assembly Bill No. 1788). Courts applying law do not rely on newspaper headlines – they rely on what a piece of legislation actually says.
The pertinent section (12978.7(c)) reads: “Except as provided in subdivision (e) or (f), the use of any second generation anticoagulant rodenticide is prohibited in this state until the director makes the certification described in subdivision (g).” So, first, the prohibition only applies to second generation anticoagulant rodenticides and excludes the less potent but still deadly first generation anticoagulant rodenticides.
Second, if we scroll down to the exceptions provided in subdivisions (e) and (f), we see how hollow this “prohibition” really is. Subdivision (e) declares that the prohibition does not apply to governmental agency employees who use second generation anticoagulant rodenticides for public health activities or for protecting water supply infrastructure and facilities; to mosquito or vector control districts; to efforts to eradicate nonnative invasive species on offshore islands; to efforts to control an actual or potential rodent infestation associated with a public health need, as determined by a declaration from a public health officer; or for further research into the dangers posed by second generation anticoagulant rodenticides.
Subdivision (f) creates exceptions to the prohibition for medical waste generators and for “agricultural activities” conducted at warehouses used to store foods for human and animal consumption; slaughterhouses; canneries; factories; breweries; an agricultural production site housing water storage and conveyance facilities; and agricultural production sites housing rights-of-way and other transportation infrastructure.
The power of agricultural interests should be clear from these lists of exceptions to this so-called “prohibition” on second generation anticoagulant rodenticides. It should also be clear that the California Ecosystems Protection Act of 2020 has not banned anticoagulant rodenticides. At best, the law simply prevents individual homeowners and property owners from using a subset of anticoagulant rodenticides while exempting those who likely use second generation rodenticides the most.
To repeat, it is unlikely that governments will ever truly ban anticoagulant rodenticides. This does not mean that we have no power to stop the manufacture and application of these poisons It is true that we must raise awareness about the harms of anticoagulant rodenticides. And, anyone who reads this, please, please stop using these toxic chemicals. Similarly, pushing for legislation to limit the use of anticoagulant rodenticides can help. But, if we truly want to protect rodents, and the predators who eat them, from horrible deaths, and if we truly want to keep these poisons out of the natural communities we depend on for life, we will have to do it ourselves.
As with any truly effective tactic that impedes humans’ ability to destroy the natural world, stopping anticoagulant rodenticides will require exceptional bravery. To find that bravery, I return to the first mangy coyote I saw. If it was me, and my skin was covered in itchy sores and lesions, my organs were hemorrhaging blood, and my movements were growing ever slower, I’d likely give in, lay down, and let death take me.
But, that first mangy coyote I watched struggle to keep moving through a roadside ditch did not give up. She kept moving in an effort to fulfill her species’ ancient role as a trickster lesson-giver. She wanted us to see her. She wanted us to know what happened to her. And, she wanted us to stop those who hurt her.
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