Lillies: Asian Lily (liliaceae), Easter Lily, Glory Lily, Japanese Show Lily, Red Lily, Rubrum Lily, Stargazer Lily, Tiger Lily, Wood Lily
Shrubs: Cycads, Heavenly Bamboo, Holly, Jerusalem Cherry, Mistletoe "American", Oleander, Precatory Bean, Rhododendron, Saddle Leaf Philodendron, Sago Palm, Tree Philodendron, Yucca
Succulents: Aloe (Aloe Vera)
Trees: Avocado, Buddist Pine, Chinaberry Tree, Japanese Yew (aka Yew), Lacy Tree, Macadamia Nut, Madagascar Dragon Tree, Queensland Nut, Schefflera, Yew (aka Japanese Yew)
Vines: Branching Ivy, English Ivy, European Bittersweet, Glacier Ivy, Hahn's self branching English Ivy, Needlepoint Ivy
Misc/Uncategorized: American Bittersweet, Andromeda Japonica, Azalea, Bird of Paradise, Buckeye, Caladium hortulanum, Calla Lily, Castor Bean, Clematis, Fiddle-Leaf Philodendron, Florida Beauty, Fruit Salad Plant, Golden Dieffenbachia, Gold Dust Dracaena, Heartleaf Philodendron, Horsehead Philodendron, Hurricane Plant, Mexican Breadfruit, Mother-in-law, Panda, Philodendron Pertusum, Red Emerald, Red Princess, Ribbon Plant, Satin Pothos, Spotted Dumb Cane, Sweetheart Ivy, Swiss Cheese Plant, Variable Dieffenbachia, Variegated Philodendron, Yesterday/Today/Tomorrow

Many things around your home can be toxic to you & animals. Only parts of some are, others only at certain times of year, & others only in large quantities. Sprays or fertilizers may hurt & confuse symptoms. Check with your veterinarian or poison center. Common signs: Drooling, trembling, abdominal pain, vomiting, diarrhea, convulsions, coma & disorientation.

Acorns; Alcohol-ethanol, methanol, isopropyl; Almonds; Alocasia; Amaryllis, Daffodil, Iris & Tulip bulbs; Anemone; Angel's Trumpet (Datura candida); Anthurium; Apple seeds; Apple Leaf Croton; Apricot & Peach pits; Arrowgrass; Arrowhead; Asparagus Fern; Autumn Crocus; Avocado; Azaleas.

Balsam Pear; Baneberry; Bayonet; Beargrass; Begonia; Belladonna; Bird Of Paradise berries; Bittersweet; Black Cherry; Black-Eyed Susan; Black Locust; Bleeding Heart; Bloodberry; Bloodroot; Bluebonnets; Boston Ivy; Bottlebrush; Boxwood; Bracken fern; Branching Ivy; Buckeye; Buddist Pine; Buckthorn; Burning Bush; Buttercup.

Cactus; Caffeine; Candelabra; Caladiums; Calamondin Orange; Calla Lily; Candlenut; Cardinal Flower; Castor beans; Ceriman; Chalice Vine; Charming Diefenbachia; Cherries, Seeds & Laural; China & Christmas Berry; Chinese Gooseberry; Chinese Sacred Bamboo; Choke Cherry; Christmas Candle; Christmas tree water; Christmas Rose; Chrysanthemum; Cigars, Cigarettes & butts - all nicotine; Cineraria; Clematis; Cordatum; Clematis; Clusia; Common Box; Common Privet; Coral Plant; Coriaria; Corn, Cornflower & Cornstalk Plant; Corydalis; Crocus; Croton; Crown of Thorns; Cuban Laurel; Cutleaf Philodendron; Cycads; Cyclamen.

Daffodil; Daphne; Datura; Deadly Nightshade; Death Camas; Delphinium; Destroying Angel; Devil's Ivy; Dicentrea; Dieffenbachia; Dogwood; Dracaena Palm; Dragon Tree; Dumbcane.

Easter Lily; Eggplant; Elaine Codiaeum; Elderberry; Elephant Ears; Emerald Feather; English Holly, Ivy & Yew; Eucalyptus; Eunymus; Euphorbia; Evergreen; Exotica Perfection Dieffenbachia.

Ferns; Fiddle-leaf Fig; Flax; Florida Beauty; Four o'Clock; Foxglove; Fruit pits; Fruit Salad plant.

Garden Glow; Garden Sorrel; German Ivy; Giant Dumb Cane; Glacier Ivy; Glory Lily; Gold Dieffenbachia; Gold Dust Dracaena; Golden Chain, Glow & Pothos; Gopher Purge; Green Dragon; Green Gold Nephthysis; Ground Cherry.

Hanh's Self-Branching English Ivy; Heartleaf Philodendron; Hellebore; Hemlock; Henbane; Holly; Honeysuckle; Horsebeans; Horsebrush; Horse Chestnut; Horsehead Philodendron; Horsetail Reed; Hurricane Plant; Hyacinth; Hydrangea.

Impatiens; Indian Laurel; Indian Rubber Plant; Indian Splurge Tree; Iris; Ivy.

Jack-In-The-Pulpit; Janet Craig Dracaena; Japanese Plum & Yew; Java Beans; Jerusalem Cherry (Solanum pseudocapsicum); Jessamine; Jimson Weed; Jonquil; Jungle Trumpets.

Kalanchoe; Kentucky Coffee Tree.

Lacy Tree Philodendron; Lantana; Lantana Camara; Larkspur (Delphinum); Laurels; Lily; Lily-Of-The-Valley; Lily Spider; Lima Beans; Locoweed; Lobelia; Lords & Ladies; Lupine.

Madagasgar Dragon Tree; Malanga; Marble Queen; Marigold; Marijuana; Matrimony Vine; Medicine Plant; Mescal; Mexican Breadfruit; Milkweed; Miniature Croton; Mistletoe; Moccasin Flower; Mock Orange; Monkeypod; Monkshood (Wolf bane); Monsteras; Moonseed; Morning Glory; Mother-in-Law; Mountain Laurel; Mushrooms.

Nandina (Heavenly Bamboo); Narcissus; Needlepoint Ivy; Nephthytis; Nicotiana (Ornamental tobacco); Night Blooming Jasmine; Nightshade; Nutmeg; Nux Vomica.

Oaks; Oleander; Onion; Oxalis.

Panda; Peace Lily; Peach, Pear & Plum seeds; Pencil Cactus & Tree; Peony; Periwinkle; Peyote; Philodendron; Philodendron Pertusum; Pigweed; Pimpernel; Plumosa Fern; Poinciana; Poinsettia; Poison Hemlock, Ivy, Oak & Sumac; Pokeweed; Pongam; Poppy; Potato leaves & stem; Pothos; Precatory Bean; Primula; Privet; Purple Foxglove; Pyracantha.

Red Angel's Trumpet; Red Emerald; Red Princess; Red-Margined Dracaena; Redwood; Rhododendron; Rhubarb leaves; Ribbon Plant; Rosary Pea; Rosemary; Rubber Plant.

Saddle Leaf Philodendron; Sage; Sago Palm; Sandbox Tree; Satin Pothos; Schefflera; Scotch Broom; Shamrock; Silver Pothos; Skunk Cabbage; Snapdragon; Snowdrops; Snow on the Mountain; Soapberry; Solandra; Split Leaf Philodendron; Spotted Dumb Cane; Spurges; Squirrel Corn; Staggerweed; Star Of Bethlehem; String of Pearls/Beads; Striped Dracaena; Sweetheart Ivy; Sweetpea; Swiss Cheese plant.

Tansy Mustard; Taro Vine; Thornapple; Tiger Lily; Toadstool; Tobacco; Tomato; Tree Philodendron; Tree Tobacco; Tropic Snow Dumbcane; True Aloe; Tulip Bulbs; Tung Tree.

Variable Dieffenbachia; Variegated Philodendron; Variegated Rubber Plant; Venus Flytrap; Virginia Creeper.

Warneckei Dracaena; Water Hemlock; Weeping Fig; Western Yew; Wild Call; Wisteria.

Yellow Allamanda & Jasmine; Yew.

ALSO Chocolate (dogs); aspirin & aspirin substitutes (cats), Lysol, Pinesol, Phisoderm, hexachlorophene, Phenol-group Coal & Wood Tar derivatives (cats); all anti-freezes; pesticides; some flea products; some fertilizers & vegetables; tinsel, ornaments, ribbons, wrappings & Christmas tree water.

Hops – May cause panting, elevated temperature, increased heart rate, seizures and possibly death

Mustard Seeds - Can have varied effects on pets

Onions and Onion Powder – Can cause gastrointestinal problems such as vomiting and diarrhea

Potato Leaves and Stems – Can cause problems with the digestive, nervous and urinary systems

Tea – Can have varied effects in pets.

Tomato Leaves and Stems - Can cause problems with the digestive, nervous and urinary systems.

Avocados (fruit, pit, and plant) are toxic to dogs. Avocados contain a toxic component called persin, which can damage heart, lung and other tissue in many animals. They are high in fat and can trigger stomach upset, vomiting and even pancreatitis. Symptoms of toxicity include difficulty breathing, abdominal enlargement, abnormal fluid accumulations in the chest, abdomen and sac around the heart. The amount that needs to be ingested to cause signs is unknown. The effects on dogs and cats are not completely understood. GI signs are commonly seen and should be treated symptomatically. In addition, the animal should be monitored closely for other clinical signs related to the cardiovascular system. (This information comes from veterinarians, the American Veterinary Medicine Association, and the ASPCA Animal Poison Control Center.)

Six ounces of semi-sweet chocolate can be toxic to the nervous system of a 20-pound dog. Section: Chocolate is Toxic to Dogs

The worst a Hershey bar can do to you is add an inch to your hips. But that same candy – even in relatively small amounts – can make a dog or cat very sick. Make no mistake: For them, chocolate is poison.

In addition to a high fat content, chocolate contains caffeine and theobromine, two different types of stimulants that affect the central nervous system and the heart muscle, as well as increasing the frequency of urination.

Symptoms of Poisoning

If your 50-pound dog gets his paws on a single chocolate-chip cookie, it probably won’t cause him serious problems. However, if he gobbles up more – a pan of brownies, say – he may develop vomiting or diarrhea.

Once toxic levels are reached, the stimulants kick in, and this is when you really have to worry. Symptoms include: restlessness, hyperactivity, muscle twitching, increased urination and/or excessive panting. If your pet isn’t treated, he could go into a seizure – possibly even die.



How Much Is Toxic?

The amount of chocolate that it takes to poison your pet depends on the type of chocolate he’s eaten and his weight. White chocolate has the least amount of stimulants and baking chocolate or cocoa beans have the highest. Here is a list of the most common sources of chocolate and the amount that leads to toxicity:


White Chocolate. Mild signs of toxicity can occur when 45 ounces per pound of body weight is ingested. Severe toxicity occurs when 90 ounces per pound of body weight in ingested. This means that a 20-pound dog would need to ingest at least 55 pounds of white chocolate to cause nervous system signs. A 10-pound cat would need to ingest 27 pounds. Yes, that is twenty seven pounds! White chocolate has very little real chocolate in it. Therefore, the levels of caffeine and theobromine are very low. Tremendous amounts of white chocolate need to be ingested in order to cause toxic signs from chocolate. It is highly unlikely that white chocolate ingestion will result in the toxic neurologic signs but, the severe gastrointestinal effects from a high fat food develop with much less white chocolate ingestion.


Milk Chocolate. Mild signs of toxicity can occur when 0.7 ounces per pound of body weight is ingested. Severe signs occur when 2 ounces per pound of body weight is ingested. This means that a little less than one pound of milk chocolate can be toxic to the nervous system of a 20-pound dog. A 10-pound cat would need to ingest 1/2 pound.


Semi-Sweet Chocolate. Mild signs of toxicity can occur when 1/3 ounce per pound of body weight is ingested. Severe signs occur when 1 ounce per pound of body weight is ingested. This means that as little as 6 ounces of semi-sweet chocolate can be toxic to the nervous system of a 20-pound dog. A 10-pound cat would need to ingest 3 ounces.


Instant Cocoa. Mild signs of toxicity can occur when 1/3 ounce per pound of body weight is ingested. Severe signs occur when 1 ounce per pound of body weight is ingested. This means that as little as 6 ounces of semi-sweet chocolate can be toxic to the nervous system of a 20-pound dog. A 10-pound cat would need to ingest 3 ounces.


Baking Chocolate. Mild signs of toxicity can occur when 0.1 ounce per pound of body weight is ingested. Severe signs occur when 0.3 ounce per pound of body weight is ingested. Two small one-ounce squares of baking chocolate can be toxic to a 20-pound dog. A 10-pound cat would need to ingest 1 ounce of baking chocolate. This type of chocolate has the highest concentration of caffeine and theobromine and very little needs to be ingested before signs of illness become apparent.

Even if your pet doesn’t eat enough chocolate to induce toxicity, the candy’s high fat content may cause him to vomit or have diarrhea at much smaller amounts than those shown. If that happens, watch him carefully. If his symptoms don’t clear up within eight hours, call your veterinarian (if your pet is very small or young, call within four hours); aside from toxicity issues, you don’t want the animal to dehydrate. Try to be as precise as you can about the type of chocolate the animal ate, how much he took and approximately when he ate it.

The sooner you get help, the better off your pet will be. If the animal is showing signs of toxicity, he has a good prognosis if he’s treated within four to six hours of ingestion. The effects of the chocolate can linger for 12 to 36 hours, though, so your pet may require hospitalization.

Turkey Skin:
Turkey skin is currently thought to cause acute pancreatis in dogs.

Walnuts are poisonous to dogs and should be avoided. In particular, there is a type of fungus common to walnuts (especially wet deadfall walnuts) that will cause severe episodes of seizuring. Many nuts are not good for dogs in general, their high phosphorous content is said to possibly lead to bladder stones.

Plants that give a rash after contact with the skin or mouth:

chrysanthemum
poinsettia
creeping fig
weeping fig
spider mum
pot mum

Plants that cause irritation (toxic oxalates), especially the mouth gets swollen; tongue pain; sore lips; some swell so quickly a tracheotomy is needed before asphyxiation:

arrowhead vine
majesty
boston ivy
neththytis ivy
colodium
pathos
emerald duke
red princess
heart leaf (philodendron)
split leaf (phil.)
saddle leaf (phil.)
marble queen

Achillea African Violet Alyssum Aster Basil Bean sprouts
Begonia Buddleia Calendula Catmint Catnip Celosia
Cleome Camomille Chervil Chives Columbine Coriander
Cosmos Cress Dahlia Dill Dorotheantus Forget-me-not
Hollyhock Hyssop Japanese Matatabi Lavender Lettuce Marum
Mint Nasturtium Orchid Oregano Pansy Parsley
Pea (garden) Peppermint Petunia Phlox Rose Rosemary
Sage Shasta Daisy Spearmint Snapdragon Spider plant Spinach
Sunflower Tarragon Thyme Vernascum Wheat sprouts Zinnia

I'm placing this here, as it's still unknown if it can be spread to domestic pets, or how to stop it.

Janet

Chronic wasting disease (CWD) is an infectious, neurologic disease of cervids, which includes North American deer, elk, and moose. A member of the family of diseases known as transmissible spongiform encephalopathies (TSEs), CWD has been diagnosed in free-ranging and captive cervids. Other TSEs include bovine spongiform encephalopathy (BSE, sometimes called "mad cow disease"), scrapie in sheep, and Creutzfeldt-Jakob disease (CJD) in humans.

Causative agent
Chronic wasting belongs to the family of diseases known as the transmissible spongiform encephalopathies. The causative agent of CWD has not been fully characterized, but three possibilities have been proposed: an unconventional virus, a prion (a self-replicating protein), or a virino (incomplete virus) comprising naked nucleic acid protected by host proteins. The CWD agent does not invoke a detectable immune response or inflammatory reaction in its host. On the basis of what is known about other TSEs such as bovine spongiform encephalopathy and scrapie, it is assumed the causative agent of CWD is extremely resistant to sterilization processes.

Natural distribution
An infectious, neurologic disease, CWD develops naturally in North American deer and elk. Species found to be affected include Rocky Mountain elk, mule deer, white-tailed deer, and black-tailed deer. Chronic wasting disease was first diagnosed in a Colorado captive elk research facility in 1967, and was identified as a TSE in 1978. It was found in the mid 1980s in free-ranging deer and elk in adjoining areas of Colorado and Wyoming. As of January 2009, CWD has been identified in free-ranging cervids in Nebraska, Illinois, Kansas, New Mexico, New York, South Dakota, Utah, West Virginia, Wisconsin, and the Canadian provinces of Saskatchewan and Alberta. The first infected farmed herd was discovered in South Dakota in 1996. CWD has also been diagnosed in captive cervids in Colorado, Kansas, Minnesota, Montana, Nebraska, New York, Oklahoma, Wisconsin and the Canadian provinces of Alberta and Saskatchewan. According to the United States Department of Agriculture (USDA), the species known to be susceptible to CWD are Rocky Mountain elk (Cervus elaphus), Mule deer (Odocoileus hemionus) and Black-Tailed deer (Odocoileus hemionus) and White-Tailed deer (Odocoileus virginianus). Because Red deer (Cervus elaphus) are genetically very similar to Rocky Mountain elk, it is likely that they are also susceptible to CWD.

Transmission
Although many years of research have been conducted, the exact mechanism of transmission of CWD is still unknown. Currently transmission is believed to be lateral (animal to animal) and to take place through contact with or exchange of bodily fluids such as saliva, urine, feces, or placental tissue. Evidence exists suggesting that vertical (mother to offspring) and environmental transmission is possible. According to the Centers for Disease Control and Prevention (CDC), evidence also supports the possibility that the disease is spread as a result of indirect exposure to prions in the environment (e.g., in contaminated feed and water sources). CWD can be highly transmissible within deer and elk populations. Several epidemiologic studies provide evidence that, to date, CWD has not been transmitted to humans.

Clinical signs of CWD in cervids
Most cases of CWD develop in adult animals. Chronic wasting disease causes progressive degeneration of the central nervous system. The most obvious and consistent clinical sign is progressive weight loss and dehydration. Other clinical signs include changes in temperament (e.g., loss of fear of humans, nervousness, or hyperexcitability), changes in behavior (teeth grinding, walking in repetitive patterns in pens), incoordination, polydipsia (increased drinking), polyuria (increased urination), drooping of the head and ears, and excessive salivation. Incubation period is typically 18 to 24 months, but can range up to 36 months. The health of affected animals typically deteriorates over a period of 12 months after infection. Chronic wasting disease is uniformly fatal.

Diagnosis
At the present time, CWD is diagnosed by postmortem microscopic examination of brain stem (particularly the obex portion) and lymphoid (lymph nodes and tonsils) tissues. Lesions of CWD resemble those of other spongiform encephalopathies. Immunohistochemistry (IHC) is very sensitive and specific to CWD and is used to confirm diagnosis by measuring accumulations of proteinase-resistant prion protein (PRPres) in brain tissues of infected deer and elk. Accumulations of proteinase-resistant prior protein have not been found in uninfected cervids. Positive test results are not detected until at least 3 months after infection so negative results cannot confirm the absence of disease (it is possible that the animal is infected, but the stage of the disease is so early that the prion is not detectable).

Colorado researchers have developed an antemortem (live animal) tonsillar biopsy test for CWD, which appears to work well for mule deer, but not for elk.

Prevention
Because transmission mechanisms are still not well understood, it is difficult to recommend measures to prevent spread of the disease. Surveillance, culling, and testing are performed in areas where cases of CWD have been identified in an attempt to contain the disease within that endemic area. Unfortunately, no vaccine or preventatives exist and there is no evidence that immunity to CWD develops.

Treatment
No treatment currently exists for cervids with CWD. The disease is uniformly fatal.

Infection control
The United States Department of Agriculture's (USDA) Animal and Plant Health Inspection Service (APHIS) provides assistance to state officials in diagnosing CWD and in monitoring international and interstate movements of captive animals to help prevent its spread. Several state and national appropriations bills have been passed to provide funding for much needed research on CWD. In an effort to contain and eventually eradicate CWD, state and federal agricultural and wildlife agencies are taking action including regulating and/or banning interstate movement of captive cervids, enforcing more stringent hunting policies, creating joint task forces, and developing state-specific guidelines.

Members of the general public, hunters, and owners of cervid game farms must be informed of the dangers CWD poses to deer and elk populations, and take precautions necessary to reduce transmission. Animals appearing to be ill should be reported to wildlife officials. Deer feeding and baiting should be limited as this is an activity that brings deer into close contact with one another. Double fencing of captive herds will lessen contact with wild animals, and vigilant surveillance and testing of these herds is recommended. Hunters should avoid harvesting deer or elk that appear sick; should wear rubber gloves while field dressing animals; should remove all bone and fatty tissue from the meat of the animals; should minimize handling of the brain, spinal cord, spleen, tonsils, lymph nodes, or eyes; should avoid consuming any animal with positive test results for CWD; and should not remove anything but pure meat (muscle) from endemic sites.

Transmissible spongiform encephalopathies in other animals
The family of transmissible spongiform encephalopathies (TSE) in animals includes scrapie, affecting sheep and goats; transmissible mink encephalopathy; bovine spongiform encephalopathy (BSE), commonly referred to as "mad cow disease," affecting cattle; and, in humans, kuru, classic and variant Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler syndrome, and fatal familial insomnia.

At the present time there is no evidence that CWD is easily transmittable to livestock or other ruminants such as sheep, cattle, or goats under natural conditions. Livestock housed with infected deer or elk, or those having ingested brain tissue of infected animals, have not developed the disease. Chronic wasting disease has been experimentally transmitted to mice, ferrets, mink, goats, squirrel monkeys, and calves.

Implications of CWD for humans
There is currently no evidence that CWD is naturally transmitted to humans, either through contact with affected animals or by eating meat from infected animals. The CDC, however, has issued the following statement:

It is generally prudent to avoid consuming food derived from any animal with evidence of a TSE. To date, there is no evidence that CWD has been transmitted or can be transmitted to humans under natural conditions. However, there is not yet strong evidence that such transmissions could not occur. To further assess the possibility that the CWD agent might occasionally cause disease in humans, additional epidemiologic and laboratory studies could be helpful. Such studies include molecular characterization and strain typing of the agents causing CWD in deer and elk and CJD in potentially exposed patients. Ongoing national surveillance for CJD and other neurologic cases will remain important for continuing to assess the risk, if any, of CWD transmission to humans.

Routine precautions should be taken when handling carcasses of animals that may be infected.