Larry

Seeing the beavers are on the neighbors property there is nothing you can do about them its is up to your neighbors to take care of them you legally can't do anything.

Anyone shooting the Rinehart 100 this weekend in Batavia.

My son leaves for the Army on Monday for a 5 year stay, he will spend the next 16 weeks at Fort Benning then off to Fort Bragg. A Georgia in the summer. He has no clue what he’s in for he thinks it’s call of duty This is no game. I am proud that he wants to serve but with the @#$ hole we have in the white house I’m scared to death for him. His MOS is 18 X-ray

I have a Rem xp-100 in 35 rem its a good shooter I have killed 3 deer with it, it works recoil can be a bit stout.

Lurking your 2nd picture I have one just like I’ll see if I can find it

There is no one best caliber for North America, so here what I think are the best in their class. Varmint I think the 223 and 22-250 are best in this class. I am partial to the 22-250. Deer size game this is a hard one I use a 444 marlin, for less than 200yds I’ll stay with my 444 out to 300 I like the 7mm-08 for long range 300 win mag. Large game and the big bears I think the 338 RUM is the best caliber in this category. The 338RUM can send a 250gr. Bullet down range at around 3000fps and with over 5000 energy foot pounds.

Just remember they don't call them GUT HOOKS for no reason!!

Just call them tell them what happen and that the bird is 50 years or older and you don’t know what to do with it. Tell them you don’t know where it came from. You can get a permit to keep it. The worst thing that will happen is you may have to turn it over to them and you were going to do that anyway.

i would of had the dec check it out to make sure it didn't have cwd or something

If you did EAB you would have to scrape the dmp system. You could end up killing to many does where you shouldn’t and not an enough where you need to

Why would you want to go to a 1 buck per-season rule its counter productive and with only 5% of hunters killing 2 bucks in a season it doesn’t have any effect on deer populations. I have not killed 2 bucks in a season since 2004. Here’s what would of happen if I didn’t have a 2nd buck tag the camp I hunt out of is in 9p I didn’t get a dmp I killed a buck during bow a nice 8pt. Without the 2nd buck tag I would not go to camp and if I don’t my 2 sons don’t go. I’m not going to go there and not hunt. I did not fill the tag even though I could of I would of if the deer was bigger than the 1 I shot during bow

the dec has the town by town break down on there web site

Try putting your camera aimed down the trail instead of across the trail. It will keep the animal in the picture longer. Also at night the PR sensor will pick up the heat and movement farther out then the flash can illuminate.

Permit Requirements for Take of Canada Geese in New York try this off the dec web site

I was just wondering if the guy knows how fast his bow was shooting or just taking a wag. Like with my bow it says the IBO seed is 320. But I know with the arrow, draw weight and head combination I shoot. My arrow seed is 286 avg. for 10 shots.

To dbHunterNY how do you know your bow shoots 345fps? Are you using the IBO stated speed or did you run your arrows over a chronograph.

It doesn’t matter what the faze the moon is in. Best time to be out is the last 5 days in October to the start of gun season.

Maybe fall but not this spring regs. are not in place

So what it’s saying is during the early bow season the last 14 days you can’t kill a buck. If so that will cut down on the guys using a crossbow in the bow season I think most guys wanted a chance at a second buck.

these are raccoon tracks

Epizootic Hemorrhagic Disease (EHD) is the most important infectious viral disease among white-tailed deer. The landmark outbreak of the virus was identified and described in New Jersey in 1955. It occurs every year in many southeastern states and has been recently reported throughout the mid-Atlantic. In states where the disease has been detected, it has not had a significant negative impact on the long-term health of the deer herd. It tends to infect only localized pockets of animals within a geographic area. In October 2007, the first case of EHD in New York was confirmed by the National Veterinary Services Laboratory in Ames, Iowa and the Southeast Cooperative Wildlife Disease Study Group. Several deer carcasses from parts of Albany and Rensselaer Counties were submitted to the DEC Wildlife Pathology Unit for examination and tissue analysis. In November, Niagara County was added to the confirmed list

check this map out its from usgs shows where cwd is along with game farms. http://www.nwhc.usgs...cwd/cwd_map.jpg

I found this on the CDC web site Fatal Degenerative Neurologic Illnesses in Men Who Participated in Wild Game Feasts --- Wisconsin, 2002 Creutzfeldt-Jakob disease (CJD) is a fatal neurologic disorder in humans. CJD is one of a group of conditions known as transmissible spongiform encephalopathies (TSEs), or prion diseases, that are believed to be caused by abnormally configured, host-encoded prion proteins that accumulate in the central nervous tissue (1). CJD has an annual incidence of approximately 1 case per million population in the United States (1) and occurs in three forms: sporadic, genetically determined, and acquired by infection. In the latter form, the incubation period is measured typically in years. Recent evidence that prion infection can cross the species barrier between humans and cattle has raised increasing public health concerns about the possible transmission to humans of a TSE among deer and elk known as chronic wasting disease (CWD) (2). During 1993--1999, three men who participated in wild game feasts in northern Wisconsin died of degenerative neurologic illnesses. This report documents the investigation of these deaths, which was initiated in August 2002 and which confirmed the death of only one person from CJD. Although no association between CWD and CJD was found, continued surveillance of both diseases remains important to assess the possible risk for CWD transmission to humans. Case Reports Case 1. In December 1992, a Wisconsin man aged 66 years with a history of seizures since 1969 sought treatment for recurring seizures, increasing forgetfulness, and worsening hand tremors. Electroencephalographic (EEG) examination demonstrated focal epileptiform activity and nonspecific diffuse abnormalities, but no specific diagnosis was made. In February 1993, he was hospitalized for increasing confusion, ataxia, and movement tremors of his extremities. A magnetic resonance image (MRI) demonstrated mild, nonspecific enhancement along the inferior parasagittal occipital lobe. A repeat EEG showed bifrontal intermittent, short-interval, periodic sharp waves, suggesting a progressive encephalopathy; a diagnosis of CJD was suspected. The man died later that month; neuropathologic examination of brain tissue during autopsy indicated subacute spongiform encephalopathy, compatible with CJD. The man was a lifelong hunter who ate venison frequently. He hunted primarily in northern Wisconsin but also at least once in Montana. He hosted wild game feasts at his cabin in northern Wisconsin from 1976 until shortly before his death. Fixed brain tissue obtained during the autopsy was sent for analysis to the National Prion Disease Pathology Surveillance Center (NPDPSC) and reexamined at the institution where the autopsy was conducted. Histopathologic examination did not substantiate the diagnosis of prion disease. In addition, 27 brain tissue sections were negative for prions by immunostaining despite positive antibody reactions against other proteins (controls), which indicated that other epitopes in the tissue samples were preserved. Case 2. In May 1999, a Minnesota man aged 55 years with no previous history of a neurologic disease sought evaluation and treatment following a 3-month history of progressive difficulty in writing and unsteadiness of gait. A computerized tomography (CT) scan and MRI examination of his head did not indicate any abnormality. In June 1999, he was hospitalized following onset of dementia, speech abnormalities, and myoclonic jerking. An EEG indicated left-hemispheric periodic sharp waves and moderate generalized background slowing; CJD was diagnosed clinically. In July 1999, following worsening symptoms and development of right upper extremity dystonia, the patient died. Neuropathologic evaluation of brain tissue during autopsy demonstrated widespread subcortical spongiform lesions, consistent with CJD. The man was not a hunter but had a history of eating venison. He made an estimated 12 visits to the cabin where the wild game feasts were held, but he participated in only one feast during the mid-1980s. Sections of fixed and frozen brain tissue obtained during autopsy were analyzed at NPDPSC, and prion disease was confirmed by immunohistochemical and Western blot testing. The Western blot characteristics and prion disease phenotype in this patient were consistent with the most common form of sporadic CJD, classified as M/M (M/V) 1 (3). Subsequent genetic typing confirmed the presence of methionine homozygosity (M/M) at codon 129 of the patient's prion protein gene. Case 3. In June 1992, a Wisconsin man aged 65 years sought treatment for progressive slowing of speech, worsening memory, and personality changes. By January 1993, his speech was reduced to one-word utterances. Neurologic examination showed a flat affect, decreased reflexes, and apraxia. A CT head scan showed mild atrophy, and an EEG was normal. Pick's disease was diagnosed. By May, he was unable to perform any daily living activities; he died in August 1993. Neuropathologic evaluation of brain tissue during autopsy showed symmetrical frontal lobe cerebral cortical atrophy and mild temporal lobe atrophy. No Pick's bodies or spongiform lesions were observed. The man had a history of eating venison and participated regularly in wild game feasts held at the cabin owned by patient 1. He was a lifelong hunter and hunted mostly in Wisconsin but also in Wyoming and British Columbia. No game was brought to the wild game feasts from his hunting trips outside of Wisconsin. Examination of fixed brain tissue sent to NPDPSC demonstrated no lesions indicative of CJD, and immunohistochemical testing with antibody to the prion protein did not demonstrate the granular deposits seen in prion diseases. Epidemiologic Investigation Wild game feasts consisting of elk, deer, antelope, and other game that occurred at a cabin in northern Wisconsin owned by patient 1 began in 1976 and continued through 2002. These feasts typically involved 10--15 participants and usually occurred on weekends before or during hunting seasons in the fall and occasionally in the spring. Wild game brought to these feasts usually were harvested in Wisconsin, but three men who attended these feasts reported hunting in the western United States and bringing game back to Wisconsin. These activities took place in Colorado (near the towns of Cortez, Trinidad, Collbran, Durango, and Meeker), Wyoming (near the towns of Gilette and Cody), and Montana (near the town of Malta). CWD was not known to be endemic in these areas at the time that these hunting activities took place. Information was obtained for 45 (85%) of 53 persons who were identified as possibly participating in the wild game feasts; all were male. Information was obtained by direct interview or from family members of decedents. Of the 45 persons, for whom information was obtained, 34 were reported to have attended wild game feasts. Seven of the 34 feast attendees were deceased, including the three patients. None of the four other decedents had a cause of death attributed to or associated with a degenerative neurologic disorder. None of the living participants had any signs or symptoms consistent with a degenerative neurologic disorder. Reported by: JP Davis, MD, J Kazmierczak, DVM, M Wegner, MD, R Wierzba, Div of Public Health, State of Wisconsin Dept of Health and Family Svcs. P Gambetti, National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, Ohio. L Schonberger, MD, R Maddox, MPH, E Belay, MD, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; V Hsu, MD, EIS Officer, CDC. Editorial Note: CWD was first described in the United States in the 1960s and classified as a TSE in 1978. Previously localized to a contiguous endemic area in northeastern Colorado and southeast Wyoming, since 2000, CWD has been found in free-ranging deer or elk in Illinois, Nebraska, New Mexico, South Dakota, Wisconsin, and outside the previously known endemic areas of Colorado and Wyoming. CWD has been identified also in captive deer or elk in Colorado, Kansas, Minnesota, Montana, Nebraska, Oklahoma, South Dakota, and Wisconsin (4). Because a variant form of CJD, with specific neuropathologic and molecular characteristics that distinguish it from sporadic CJD, has been associated with eating cattle products infected with a prion that causes bovine spongiform encephalopathy (5), concern has been raised about the possibility that the prion associated with CWD might be transmitted to humans in a similar way. In this investigation, because only one of the three cases in Wisconsin had neuropathologic confirmation of a prion disease, no association could be made between case participation in the wild game feasts and the development of CJD. Although patient 2 had confirmed CJD, he was unlikely to have eaten CWD-infected venison at these feasts because venison and other game from outside Wisconsin that was served at these feasts did not originate from known CWD-endemic areas, and the man participated in the feasts only once. In addition, the prion disease in this case was consistent with the most common form of sporadic CJD, without apparent unusual neuropathologic or molecular characteristics that might occur if the prion related to CWD had been responsible for the disease. The findings in this report are subject to at least two limitations. First, not all members participating in wild game feasts could be identified, and not all persons listed as participating could be contacted for interviews. Second, interviews that were conducted required recall of events that occurred up to 25 years ago, limiting the detail or accuracy of events. However, the similar responses obtained from different sources support the accuracy of the investigation findings. A previous investigation of unusually young CJD patients in whom the transmission of CWD was suspected also did not provide convincing evidence for a causal relationship between CWD and CJD (2). However, limited epidemiologic investigations cannot rule out the possibility that CWD might play a role in causing human illness. Ongoing surveillance of CJD, particularly in states with CWD, is important to assess the risk, if any, for CWD transmission to humans. Because the confirmation of CJD and the detection of a new prion disease require neuropathologic study of brain tissue, physicians are encouraged to contact NPDPSC (http://www.cjdsurveillance.com; telephone, 216-368-0587) to confirm diagnoses of CJD and to distinguish its various subtypes. Because of the known severity of TSEs in humans and the possibility that the CWD prion can affect humans, animals with evidence of CWD should be excluded from the human food or animal feed chains. Hunters and wild venison consumers should follow precautionary guidelines available from the Wisconsin Department of Agriculture, Trade, and Consumer Protection (http://datcp.state.wi.us/core/consumerinfo) to prevent potential exposures to the CWD agent.

you might want to check this out Wisconsin : Mysterious Marathon County case underscores lack of knowledge of CWD Date: March 10, 2014 Source: Marshfield News Herald Contacts: Marshfield News Herald ELAND — It’s been almost five months since a prize buck on a game farm in eastern Marathon County tested positive for chronic wasting disease, and investigators are as befuddled about the case today as they were in November. The game farm, Wilderness Whitetails, and its affiliated breeding farm in Portage County have followed all of the protocols set forth by the Wisconsin Department of Agriculture, Trade and Consumer Protection intended to prevent the spread of the deadly disease. Wilderness Whitetails is a 351-acre, family-run hunting ranch that started business 37 years ago, owner Greg Flees said in December. The disease was found in a routine test after a hunter killed the animal. The herd had been “closed” for more than a decade, Flees said, meaning that no deer had been brought into the operations from the outside. The breeding farm is double-fenced, which keeps wild deer from getting close to the captive animals to prevent the spread of chronic wasting disease, but the hunting preserve is not, in accordance with state regulations. No deer had tested positive on the preserve before; it was the first new CWD-infected deer tested on any Wisconsin farm since October 2008, and the farthest north a captive deer had been found to have the disease. The infected buck was one of the preserve’s 270 deer, game for people who pay for the right to hunt them. Flees cooperated fully with the investigation of how the buck got sick, said Paul McGraw, state veterinarian. But even with Flees’ help and subsequent investigative efforts, McGraw said he doesn’t think there ever will be an answer as to how that buck got sick — which leaves hunters in eastern Marathon County nervous. “This guy has got a real good record,” McGraw said. “This particular farm has done a lot (to prevent CWD exposure). There’s a low risk that CWD is in the breeding herd.” The case underscores just how little is known about CWD, and the knowledge gap makes it difficult to manage the disease. “There’s not been a lot of research done on it,” McGraw said. “And there are not a lot of good answers.” CWD upswing The Wilderness Whitetails case comes at a time when the disease continues to run rampant among wild deer in Iowa County and western Dane County, where the state Department of Natural Resources says that one in four adult male deer has the fatal disease. The prevalence rate of 25 percent is based on 2013 test results from that deer management zone. The rate has more than doubled since 2002, when 8 percent to 10 percent of bucks had the disease. The CWD stakes are high in a state that places a premium on hunting socially, culturally and economically. In 2010, deer hunting licenses and permits generated $22.7 million for the DNR, according to PolitiFact Wisconsin. Estimates of the overall economic impact to the state as a whole exceed $1 billion. CWD affects elk and moose as well as deer, according to the U.S. Department of Agriculture. It was first recognized in 1967 and belongs to a family of diseases called transmissible spongiform encephalopathies. Other TSEs include bovine spongiform encephalopathy in cattle, scrapie in sheep and goats and Creutzfeldt-Jacob disease in humans. CWD, though, is distinct from those other diseases, the USDA said. The growth of CWD in southern Wisconsin, coupled with the Wilderness Whitetails case, is troubling, said Marcell Wieloch, 71, of Mosinee, a longtime deer hunter with gun and bow. “The elephant in the room, the fear that some people have, is if they shoot that deer, and eat that deer, sooner or later it’s going to transfer to Creutzfeldt-Jacob disease,” Wieloch said. “You start bringing those threads together.” No one understands specific causes of CWD. Most scientists believe, however, that TSE diseases are caused by proteins called prions. And scientists agree that CWD often is transmitted directly from one animal to another through saliva, feces and urine containing abnormal prions, according to the USDA. Records show the buck killed at Wilderness Whitetails never came in contact with another infected deer, so it’s a mystery as to how it contracted CWD. Three possibilities include that the buck got the disease spontaneously; that it came from exposure in the herd of the hunting preserve or breeding farm; or that it picked up the disease in the environment, McGraw said. “We don’t know if there are prions in the soil, whether it can survive a while in the environment,” McGraw said. “We don’t see any scientific way of naming any one of these possibilities as the reason (the Wilderness Whitetails buck had the disease.)” Unknown future The state DNR, which oversees CWD policy among wild deer, uses one main tool to quash the disease. It prohibits deer baiting and feeding in areas where CWD has been found in deer. Marathon County already was under the restriction because farm deer in Portage County had been tested as CWD positive. The Wilderness Whitetail case extended the region to Shawano and Waupaca counties, said Tami Ryan, chief of the DNR’s wildlife health program. The DNR also will step up its surveillance for CWD in the area to get a better idea how prevalent the disease is. “There is no CWD in the wild deer in Marathon County, as far as we know,” Ryan said. Did finding CWD in a captive herd increase the potential for the disease to spread to wild deer? It’s a concern, Ryan said, but there is no way to know. Wieloch would like to see the DNR take a more aggressive stance against CWD. Other states, such as Colorado, he said, have helped limit its spread by using sharpshooters to kill deer in CWD zones. Ryan said one reason the DNR hasn’t taken more drastic steps is because of the public and hunters as a whole, have opposed those measures. “We respond by social influence and outlook, attitude and opinion,” Ryan said. “The tide is shifting a little bit. Based on our past experience, we’re seeing more public sentiment that wishes we were doing more, taking a stronger stance.” © Chronic Wasting Disease Alliance http://www.nwhc.usgs.gov/images/cwd/cwd_map.jpg

Look all kidding aside the DEC has never said there are no cougars in NY. They have said no breeding population of cougars in NY it doesn’t mean one hasn’t passed though the state. If you think anyone in this state could keep something like a secret stocking program in this state a secret. I have some UFO crash debris to sell you.