Nice huh? But before we get to garbage, rats, and second generation anti-coagulant poisons here is something from Diane D'arcy in the NEVER UNDERESTIMATE A RED-TAIL category.
I met up with a bird watching friend today who has a home in Haymarket, Virginia, where he built a koi pond on his one acre. He tells me that the Red-tails regularly hunt the koi pond and have "knocked-off" about a dozen over time. He says they perch in a nearby tree, watch the water, and then pounce. Sometimes they fail to go off with their catch but he finds the koi bottom up after few days later with lacerations!
What to do you make of this one"
As I said never underestimate a Red-tail! I'm wondering if maybe just maybe one day, a Red-tail was sitting in a tree watching for prey and noticed some Eagles doing some fishing over in the river and thought, "Hmmm, those fish look tasty. But that river looks deep and fast. Hey there goes a vole!"
Then later when she saw those chubby Koi fish in their still pond, the picture of fishing eagles came back to her and ta da, fishing Red-tails! Of course it may have happened nothing like that, but I figure we could use a little whimsy before we get to the heavier discussion.
So back to unwhimsical poison, the top photo is from my Rat Watching Phase: The restaurant up the street from this little neighborhood park doesn't want to put their trash in front of their restaurant. ICK! So they put it here, down the street from the eatery toward evening.
As soon as it's dark, the rats scurry out for their feast, gnawing through those black plastic bags in a nano-second. Then when the garbage truck arrives, the rats momentarily scurry out of sight and as the bags are now full of holes, well, things fall out. Don't tell me that the garbage man cares, he doesn't. Does he get paid for scraping garbage off the curb? No he does not, so it stays there. The truck leaves and the rats say, "Hurrah!" and come out for the second course which doesn't stop until dawn. Yummy!
But you know, the patrons of the restaurant sitting at the sidewalk tables, come eight o'clock or so can see big fat rats hustling back and forth across the street. Geez, that isn't good for business.
Does the restaurant get rat proof containers for their trash. No they do not! Do they clean up the trash area? No they do not.
They have the licensed exterminator come with his poison pellets. Yes, the bait is supposed to be in bait boxes but, the guy is being pressured by the restaurant to get rid of the rats NOW. So he leaves the bait all over the ground.
TRUE STORY. Now there is no way someone would get away with this in places as visible as the parks in NYC but it does happen in other areas of the city.
This is why I'm concerned about the EPA's lack of monitoring in the below scenario. Which is a step in the right direction but were some children poisoned by the bait first? As I said, how about a little sanitation?
AN UPDATE FROM THE AMERICAN BIRD CONSERVANCY COURTESY OF NYC AUDUBON
EPA ANNOUNCES DECISION ON RAT POISON
May 29th the U.S. Environmental Protection Agency (EPA) announced a landmark decision to control the sale and use of rat poisons throughout the United States. The decision is aimed at protecting children, pets, and wildlife.
The most toxic rat poisons will be removed from the consumer market and replaced with less toxic alternatives, which have been shown to be equally effective in controlling rodent populations in cities and farm settings.
All over-the-counter sales of these alternatives will be required to be in the form of bait stations to prevent accidental poisoning of children and pets. Licensed pest control operators and livestock ranchers will still be able to purchase the more toxic “second-generation” rodenticides for use only in areas where the products will not be accessible to children.
Dr. Michael Fry, Director of Conservation Advocacy at American Bird Conservancy and the Natural Resources Defense Council have been pressuring the EPA for years to address the threats to wildlife and human health posed by rat poisons.
The EPA began its evaluation of rodenticides in 1998. A lawsuit brought by NRDC over child poisonings, along with the threat of action by American Bird Conservancy and Defenders of Wildlife over the poisoning of San Joaquin Kit Foxes and birds of prey, convinced EPA to develop a mitigation plan for both ecological effects and children. The manufacturers of these chemicals fought back, pressuring EPA to accept less stringent, alternative plans, and threatening them with lawsuits.
The final decision is not as strong as the proposed mitigation plan presented by EPA in January 2007, which called for the second generation products (brodifacoum, bromodialone, difethialone and difenicoum) to be labeled “restricted use”, with sales only to licensed pest control operators. Instead, they will still be available through farm supply stores to ranchers.
American Bird Conservancy believes the final decision will be very helpful in reducing the exposure to birds and mammalian scavengers in suburban areas, where they may come into contact with poisoned rodents. Because of budget cuts and overall decreased funding for monitoring programs, the EPA will not have a monitoring program to evaluate the effectiveness of their final decision.
Manufacturers will have 90 days to agree to comply with the new regulations or to voluntarily agree to cancel the registration of their product and remove it from the market. Manufacturers will have 18 months to provide new bait station packaging and test results of package safety to the EPA, and EPA will provide an approval decision within one year.
This means registrants must agree to the above conditions by September 4, 2008, and have testing and packaging applications submitted by December 4, 2009. The final decision allows distribution and sale of current products until June 4, 2011. More information is available at http://www.epa.gov/pesticides/reregistration/rodenticides/finalriskdecision.htm To view the ABC press release, please visit http://www.abcbirds.org/newsandreports/releases.html
I'm concerned by the lack of monitoring by the EPA, as these second generation anti-coagulant products my still be bought a feed stores in ranching and rural communities and transported anywhere. The ruling may help Urban and Suburban wildlife but what about all the animals that will suffer secondary poisoning in the areas in which the poison will be sold.
As it turns out, dogs too are incredibly susceptible to these second generation poisons...
(Sorry this isn't as easy to read as it might be Folks, Blogger is acting up and won't keep the paragraphs and spacing when it publishes. D.B.)
FROM PAM GREENWOOD--GEORGE MASON UNIVERSITY IN MARYLAND
Anticoagulant Rodenticide Toxicosis in the Dog and Cat
Todd W. Harrell, DVM; Kenneth S. Latimer, DVM, PhD; Perry J. Bain, DVM, PhD; Paula M. Krimer, DVM, DVSc
Class of 2003 (Harrell) and Department of Pathology (Latimer, Bain, Krimer), College of Veterinary Medicine, The University of Georgia, Athens, GA 30602-7388
Anticoagulant rodenticides are probably the most commonly used rodenticides in the United States today (Table 1). It has been estimated that approximately 95% of all rodenticides used are anticoagulant baits.4 Not only are these baits easy to use and readily accessible over the counter, they are extremely effective in killing rodents and other pests. However, they also are lethal to non-target species, including domestic dogs and cats. The most common route of rodenticide toxicosis is by direct ingestion of the baits. Capture and ingestion of poisoned rodents also can lead to toxicosis, especially with newer second-generation anticoagulant rodenticides.1,4 Physicians commonly prescribe oral anticoagulants to human patients with various thrombotic disorders,3 but there have been no case reports of coagulopathy in companion animals due to the ingestion of these oral medications.
Table 1. Commonly used commercial anticoagulant rodenticides
Anticoagulant rodenticides exert their effect by inducing a secondary vitamin K-dependent coagulopathy leading to uncontrollable hemorrhage and death. Reports of natural anticoagulant rodenticide toxicosis are relatively common in dogs but have not been published concerning cats. One possible reason that more dogs than cats are poisoned by rodenticides is that lethal doses of many common anticoagulant rodenticides is much lower in the dog versus the cat.1
Veterinarians should consider anticoagulant rodenticide toxicosis in the differential diagnosis whenever any bleeding disorder is encountered, especially in dogs. Newer second-generation rodenticide compounds may be more lethal and have prologed effects on hemostasis after ingestion. Anticoagulant rodenticide toxicosis is a potentially fatal condition, but it may be treated successfully if the diagnosis is made quickly and appropriate therapy is instituted.
Pathophysiology of Anticoagulant Rodenticide Toxicity
Anticoagulant rodenticides exert their effect by interfering with the recycling of vitamin K1. Vitamin K is an essential cofactor in the post-ribosomal carboxylation of clotting factors II, VII, IX, and X by a vitamin K-dependent carboxylase that is synthesized in the liver (Fig. 1).1-4
Figure 1. Vitamin K is responsible for the carboxylation or activation of clotting factors II, VII, IX, and X in the liver. Vitamin K reductase enzymes keep the vitamin in an active (reduced) state.
Factors II, VII, IX, and X are proteins that serve as enzymatic factors (serine proteases) in the intrinsic, extrinsic, and common pathways of coagulation (Fig. 2).
Figure 2. Schematic diagram of the intrinsic, extrinsic, and common pathways of coagulation. The vitamin K-dependent clotting factors (II, VII, IX, and X) are shown in red. Factor IX is in the intrinsic pathway, factor VII is in the extrinsic pathway, and factors X and II are in the common pathway. These four clotting factors are not activated if the function of vitamin K1 is inhibited.
Each of these coagulation proteins is synthesized by the liver. Carboxylation of these clotting factors is necessary to bind phospholipid membrane surfaces in a Ca2+-dependent manner. The vitamin K-dependent carboxylase concomitantly converts the active vitamin K to an inactive epoxide, which is then recycled back to vitamin K by another enzyme, called vitamin K epoxide reductase. The vitamin K epoxide reductase is the enzyme that is inhibited by anticoagulant rodenticides (Fig. 3), blocking the turnover of vitamin K and rapidly depleting the liver of its active vitamin K stores.
With the depletion of liver vitamin K stores, coagulopathy occurs because factors II, VII, IX, and X are not carboxylated and remain nonfunctional. Because anticoagulant rodenticides do not block activated (functional or carboxylated) circulating clotting factors, there is a lag of approximately 12-24 hours between ingestion of the offending compound and the onset of clinical signs of bleeding.
Figure 3. Anticoagulant rodenticides inhibit the activity of vitamin K epoxide reductase (red arrow). If vitamin K1 is not maintained in a reduced state by vitamin K epoxide reductase, then clotting factors II, VII, IX, and X will not be activated via carboxylation. Clinical signs, including internal bleeding and respiratory distress, will occur if these four clotting factors are nonfunctional.
Currently, there are two families of anticoagulant rodenticides: the hydroxycoumarins and the indandiones.1 The hydroxycoumarins are further subdivided into first-generation and second-generation rodenticide compounds. The indandiones usually are grouped with the second-generation compounds because their properties are very similar to second-generation hydroxycoumarins. The most common first-generation anticoagulant rodenticides encountered in the United States are warfarin and coumafuryl. These compounds rarely are encountered today; they gradually are being phased out because of the emergence of rodents that are resistant to these first-generation compounds.
1,4 The newer second-generation compounds were developed to kill rodent populations that had become resistant to the first-generation rodenticides. Today, these second-generation compounds are largely implicated in rodenticide toxicosis. The most common second-generation compounds that will be encountered in veterinary practice are brodifacoum and bromadiolone (hydroxycoumarins), as well as diphacinone and chlorophacinone (indandiones).6
Although first- and second-generation rodenticides share the same mechanism of secondary vitamin K-dependent coagulapathy, they differ significantly in their duration of action and response to therapy. The first generation compounds are considered "short-acting" compounds and often require multiple doses to exert their toxic effects.1,4,7 Warfarin, for example has a half life of 14.5 hours in the dog. Its clinical effects last only 1 week, even at a high concentration.4 Second-generation compounds, on the other hand, have a much longer half-life (4-6 days) and their clinical effects can last anywhere from 12 to 30 days, depending on the amount of rodenticide ingested.4,7 They also differ from first-generation compounds in that only a single dose is needed to cause clinical signs of hemorrhage.1,4 Inandiones, in addition to their effects on vitamin K recycling, also interfere with pancreatic exocrine function, potentially altering the uptake of oral, lipid-soluble vitamin K.7 However, the significance of altered pancreatic exocrine function has not been determined. Secondary anticoagulant rodenticide toxicosis also can occur if poisoned rodents are captured and consumed. In such cases, a second-generation compound is most likely involved.
Certain drugs such as fluconazole, cimetidine, phenylbutazone, and sulfonamides may prolong or exacerbate the effects of anticoagulant rodenticides, as can anti-platelet drugs such as aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs).1,3,12
It is extremely important that veterinarians familiarize themselves with the common anticoagulant rodenticides, particularly the long-acting, second-generation compounds. Treating a case of second-generation rodenticide toxicosis with a treatment regimen indicated for first- generation rodenticide toxicosis often will be ineffective and may lead to fatal hemorrhage that may have been avoided.
Clinical Signs and Diagnosis of Anticoagulant Rodenticide Toxicosis
Animals poisoned with anticoagulant rodenticides often may be initially asymptomatic. Because anticoagulant rodenticides do not have a direct effect on activated vitamin K or active clotting factors II, VII, IX, and X circulating in the blood, there is often a delay of about 12-24 hours post ingestion before clinical signs develop.4 Initial clinical signs are rather nonspecific and include lethargy, weakness, and pallor.4 Signs of external hemorrhage such as melena, petechial to ecchymotic hemorrhage of mucosal surfaces, hyphema, hematamesis, epistaxis, and hematuria may or may not be apparent. With second-generation anticoagulant rodenticide toxicosis, internal hemorrhage is common and may include hemothorax, hemoperitoneum, hemomediastinum, hemorrhage into fascial planes, and ventral hematomas.4,9 Hemorrhage into the cranial vault also may occur, but is uncommon.4,12
Lethargy and respiratory distress of rapid onset are the two most common clinical signs reported in second-generation rodenticide toxicosis.5,6,9,10 Thoracic radiographs of these animals often reveal pleural effusion and pulmonary edema.4,5 Pericardial effusion with cardiac tamponade also may occur.9 Formation of large hematomas, persistent bleeding at venipuncture sites, and / or persistent bleeding during surgery strongly suggest anticoagulant rodenticide toxicosis.4,5
Because these clinical signs are not pathognomonic for anticoagulant rodenticide poisoning, a thorough medical history and appropriate laboratory testing are necessary to exclude other hemostatic abnormalities such as disseminated intravascular coagulation (DIC), autoimmune thrombocytopenia, and hereditary coagulopathy. While specific toxicologic (rodenticide analysis) and diagnostic laboratory tests (PIVKA, proteins induced by vitamin K absence) are available to diagnose anticoagulant rodenticide toxicosis, they are costly and, more importantly, too time-consuming to be of any benefit to the veterinarian, owner, or patient when faced with acute respiratory distress or hemorrhage.4,6,11 Thus, the veterinarian must rely on the clinical signs, medical history, physical examination, and response to vitamin K1 therapy to make a presumptive diagnosis of rodenticide toxicosis.
Laboratory findings in animals poisoned with anticoagulant rodenticides are rather nonspecific, but can provide critical information to guide treatment. The complete blood count will often reveal a normocytic, normochromic anemia that is either regenerative or nonregenerative, depending on the acuteness and severity of blood loss.4,5 Leukocytosis is commonly present,4 but thrombocytopenia may or may not be present.4,5 The routine biochemical profile shows no consistent pattern related to anticoagulant rodenticide toxicosis, although a hypoproteinemia commonly is observed 24 to 48 hours after acute blood loss.
Coagulation screening tests (one-stage prothrombin time [OSPT or PT], activated partial thromboplastin time [APTT or PTT], thrombin time [TT], and activated clotting time [ACT]) are necessary for the presumptive diagnosis of anticoagulant rodenticide toxicosis.4,5,7,8,12 The OSPT is the first test to be prolonged in anticoagulant rodenticide toxicosis.5,7,8 The OSPT detects deficiencies in both the extrinsic and common coagulation pathways (see Fig. 2). It is the most sensitive of the assays because factor VII, a component of the extrinsic pathway, has the shortest half-life of all the vitamin K-dependent clotting factors.4,7 The ACT and APTT assays both detect deficiencies in the intrinsic as well as the common coagulation pathways (see Fig. 2). The ACT is the least sensitive assay, as prolonged clotting times may not be evident until 3 days after rodenticide ingestion.8 The ACT is not prolonged until the activities of factors IX, X, and/or II are <5%>15 seconds), vitamin K1 therapy should be continued for two more weeks and then the OSPT should be rechecked. If the OSPT prolongation is mild, then a 1- week additional course of vitamin K1 is sufficient.4
Anticoagulant rodenticide toxicosis can present with a variety of acute and chronic clinical signs. However, with the introduction of second-generation anticoagulants, the presenting clinical signs will often be acute and severe. The most common clinical signs include lethargy, respiratory distress, and persistent bleeding post-venipuncture; external bleeding may or may not be apparent. Because the clinical signs are nonspecific and rapid diagnostic tests often are not available, the veterinarian must obtain a thorough history from the owner, including the identification of the offending anticoagulant rodenticide, if known. The best coagulation screening test to assist in clinical diagnosis and monitor treatment of anticoagulant rodenticide toxicosis is the OSPT. The treatment of choice is vitamin K1, although whole blood or plasma may have to be transfused in more severe cases of toxicosis. Oral vitamin K1 therapy should continue for up to 6 weeks (second-generation compounds) after the patient is stabilized, and a follow-up OSPT is recommended 2-3 days after cessation of therapy.
1. Petterino C, Paolo B: Toxicology of various anticoagulant rodenticides in animals. Vet Human Toxicol 43:353-360, 2001.
2. Furie B, Bouchard A, Furie B: Vitamin K-dependent biosynthesis of ?-carboxyglutamic acid. Blood 93:1798-1808, 1999.
3. Hirsh J: Oral anticoagulant drugs. New Engl J Med 324:1865-1875, 1991.
4. Mount M: Diagnosis and therapy of anticoagulant rodenticide intoxicants. Vet Clin N Am Small Anim Pract 18:115-129, 1988.
5. Schulman A, Lusk R, Lippincott C, Ettinger S: Diphacinone-induced coagulopathy in the dog. J Am Vet Med Assoc 188:402-405, 1986.
6. DuVall M, Murphy M, Ray A, Reagor J: Case studies on second-generation anticoagulant rodenticide toxicities in nontarget species. J Vet Diagn Invest 1:66-68, 1989.
7. Mount M, Feldman B: Mechanism of diphacinone rodenticide toxicosis in the dog and its therapeutic implications. Am J Vet Res 44:2009-2017, 1983.
8. Woody B, Murphy M, Ray A, Green R: Coagulopathic effects and therapy of brodifacoum toxicosis in dogs. J Vet Int Med 6:23-28, 1992.
9. Peterson J, Streeter V: Laryngeal obstruction secondary to brodifacoum toxicosis in a dog. J Am Vet Med Assoc 208:352-353, 1996.
10. Petrus D, Henik R: Pericardial effusion and cardiac tamponade secondary to brodifacoum toxicosis in a dog. J Am Vet Med Assoc 215:647-648, 1999.
11. Mount M, Kass P: Diagnostic importance of vitamin K1 and its epoxide measured in serum of dogs exposed to an anticoagulant rodenticide. Am J Vet Res 50:1704-1709, 1989.
12. Murphy MJ: Rodenticide anticoagulant poisoning. In: Tilley L, Smith F (eds.): The 5-minute Veterinary Consult. Lippincott Williams and Wilkins, Baltimore, 2000, pp. 1176-1177.
Goldfinch may be wary but he's not about to leave all those Sunflower seeds until it's an emergency.
And it did become an emergency. A male Cooper's Hawk was in a Maple tree next door, all the Grackles and Robins, around 75 of them, mobbed him until he headed out for quieter hunting grounds.
P.S. If the illustration in the NY Times Sunday Book Review is from the children's book about Pale Male, the illustrator seems never to have seen the 927 Fifth Avenue nest. Strangely the underpining of the nest in the picture looks remarkably like Junior and Charlotte's old nest corbel on the Trump Parc. Tsk.