Clubfoot (Clubfeet) in Infants

Parents know immediately if their newborn has a clubfoot. Some will even know before the child is born, if an ultrasound was done during the pregnancy. A clubfoot occurs in approximately one in every 1,000 births, with boys slightly outnumbering girls. One or both feet may be affected.

Cause

Doctors still aren't certain why it happens, though it can occur in some families with previous clubfeet. In fact, your baby's chance of having a clubfoot is twice as likely if you, your spouse or your other children also have it. Less severe infant foot problems are common and are often incorrectly called clubfoot.

Symptoms

The appearance is unmistakable: the foot is turned to the side and it may even appear that the top of the foot is where the bottom should be. The involved foot, calf, and leg are smaller and shorter than the normal side.
It is not a painful condition. But if it is not treated, clubfoot will lead to significant discomfort and disability by the teenage years.

Treatment

Nonsurgical Treatment

Treatment should begin right away to have the best chance for a successful outcome without the need for surgery. Over the past 10 to 15 years, more and more success has been achieved in correcting clubfeet without the need for surgery. A particular method of stretching and casting, known as the Ponseti method, has been responsible for this. With this method, the doctor changes the cast every week for several weeks, always stretching the foot toward the correct position. The heel cord is then released followed by one more cast for three weeks.

Once the foot has been corrected, the infant must wear a brace at night for two years to maintain the correction. This has been extremely effective but requires the parents to actively participate in the daily care by applying the braces. Without the parents' participation, the clubfoot will almost certainly recur. That's because the muscles around the foot can pull it back into the abnormal position.

The goal of this, and any treatment program, is to make your newborn's clubfoot (or feet) functional, painless and stable by the time he or she is ready to walk. (Note: Anytime your baby wears a cast, watch for changes in skin color or temperature that may indicate problems with circulation.)

Surgical Treatment

On occasion, stretching, casting and bracing are not enough to correct your baby's clubfoot. Surgery may be needed to adjust the tendons, ligaments and joints in the foot/ankle. Usually done at 9 to12 months of age, surgery corrects all of your baby's clubfoot deformities at the same time. After surgery, a cast holds the clubfoot still while it heals. It's still possible for the muscles in your child's foot to try to return to the clubfoot position, and special shoes or braces will likely be used for up to a year or more after surgery. Surgery will likely result in a stiffer foot than nonsurgical treatment, particularly as the years pass by.

Without any treatment, your child's clubfoot will result in severe functional disability. With treatment, your child should have a nearly normal foot. He or she can run and play without pain and wear normal shoes. The corrected clubfoot will still not be perfect, however. You should expect it to stay 1 to 1 1/2 sizes smaller and somewhat less mobile than the normal foot. The calf muscles in your child's clubfoot leg will also stay smaller.

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Image Before and After     

Caring for Infants & Children with OI "Osteogenesis Imperfecta"

What is Osteogenesis Imperfecta?

 
Osteogenesis imperfecta (OI) can literally be translated as imperfectly formed bones. Most forms of OI are caused by imperfectly formed bone collagen that results from a genetic defect.

Collagen is the major protein of the body's connective tissue and is the framework upon which bone and tissue are built. It can be likened to the framework around which a building is constructed. If the collagen framework is defective, the bones fracture easily, the skin is loose and transparent, and the muscles lack tone. People with OI either have less collagen than normal, or a poorer quality of collagen.

There are at least four types of OI, called types I, II, III and IV.  It is believed that there are between 20,000 and 50,000 people with OI in the United States. The disorder also affects people in other countries throughout the world.

Characteristic Features
OI varies significantly according to type, and it is very difficult to predict what symptoms or complications your child will have. Please keep in mind that very few people with OI exhibit all of the following symptoms, and that the severity of each symptom can vary tremendously between individuals. Common features include:

·    Bones that fracture easily
·    Short stature
·    Hearing loss
·    Discolored, brittle teeth
·    Blue sclera (blue color in the whites of the eyes)
·    Skeletal deformities of limbs, chest, and skull
·    Scoliosis (curvature of the spine)
·    Respiratory difficulties
·    Weak muscles
·    Excessive sweating
·    Constipation
·    Tendency to bruise easily
·    Loose joints and ligaments
·    High-pitched voice

Genetics
It is important for you to understand that nothing you or your spouse did during conception or pregnancy caused this condition in your child. OI has been prevalent for thousands of years. Genetic counseling, which is available at most hospitals, may help you understand the type of OI your child has. If you are thinking about having more children, you should consider contacting a geneticist, who can help determine the probability of recurrence of OI in your family.



Learning That Your Child Has OI
If there was a previous history of OI in either the mother's or the father's family, you probably have some idea what to expect and how to manage the disease. You should be aware, however, that a child's symptoms and severity may differ from those of the parent with OI; that is, the child may not necessarily be affected in the same way that the father or mother was.

 When you are not expecting your child to be born with a disability, it can be a terrible shock and may be very upsetting. Having a child with a disability such as OI can be very trying, and is not something that you had ever thought could happen. Don't be ashamed to cry and express your disappointment to friends and loved ones. As with any grieving process, you will most likely find yourself repeatedly going through stages such as refusal to believe there is a problem, anger and/or looking for someone to blame, depression and, finally, acceptance. There are many excellent books available that deal with the birth of a child with a disability that you may find helpful.

Most psychiatrists agree that parents of children with disabilities will benefit from joining with other parents whose children have similar problems. Our hope at the Osteogenesis Imperfecta Foundation is to provide you not only with information, but with a support network of others who are grappling with, or have solved, some of the same issues that you will be facing.

If you have not already done so, you will need to contact a pediatrician and an orthopedic surgeon. It will be worthwhile to find doctors whom you trust and with whom you will be able to work closely, preferably those with experience treating patients with OI. The OI Foundation's physician referral list is available to assist you in locating a doctor. Many OI families find that their doctors become like members of the family. Eventually, you may find it necessary to take your child to a physiatrist (a habilitation and rehabilitation specialist). Physical and occupational therapists can help your child develop muscle tone, strength, and cognitive skills. Social workers who work with children with disabilities may also be helpful with family and marital difficulties should they arise.

It would be wise to evaluate your health insurance coverage. OI can become very expensive, and the financial strain can often become as burdensome to a family as the health problems. There are many organizations and clinics that help with some of the costs associated with birth defects. One organization is the Shriners Hospitals for Children, which provides free medical services to those who qualify. Medical services vary greatly from state to state; check with your local and state governments to determine what is available in your area.

One note of caution: Because awareness about child abuse is rising, it is not uncommon for parents of children with OI to be mistakenly suspected of this crime. When you find it necessary to seek medical help away from your regular doctor, be prepared to answer questions about your child's condition calmly and with understanding. A physician's primary concern is usually the overall welfare of the child, and knowledge of OI is not as widespread as we all would like it to be. It is a good idea to carry a letter from your doctor with you at all times, stating that your child has a diagnosis of OI and explaining what that means. Many parents also carry a copy of this letter in the glove compartment of the car. When you travel, carrying copies of your child's medical records can alleviate many potential problems.

Taking Care of a Child with OI
In most ways, caring for the child with OI is just like caring for any child. There are, however, a few precautions and tips unique to handling babies with OI that we would like to share with you.

Car Seats and Strollers
You will need a car seat to take your baby home from the hospital. Look for an infant seat that reclines as much as possible, with careful consideration of how easily the child can be placed into or removed from the seat. You may want to pad the seat with egg crate foam, available from medical supply stores, or one-inch foam, available from fabric stores. In addition to lining the bottom of the seat, place a layer of foam between the harnesses and the child for extra protection.

As with any child, it is important that the child with OI be safely confined in an approved car seat placed in the back seat. For maximum safety, never place an infant or child car seat in the front passenger seat--airbags can be dangerous, especially for children with OI.

For when the child is able to sit up, Snug Seat manufactures an excellent car seat for toddlers with OI. The seat is adjustable to accommodate the child when he or she is in a spica cast (a cast that goes up over the child's hip).

As with your car seat, you will need a stroller that reclines considerably and is wide enough to accommodate casts. Fisher Price manufactures a three-wheeled stroller that many parents have used very successfully. Sling or umbrella-type strollers are unsuitable because they lack leg support and provide poor positioning of the spine and head.

Handling
Common sense is the best guide when handling a child with OI. Remember that the bones are very fragile and can break with little or no pressure. Be especially careful of the long bones in the body, i.e., the arms, legs, and ribs. You should not lift your baby under the armpits or pull on his/her arms or legs. When you change diapers, lift the baby by the buttocks and not by the ankles, as is customarily done. Spread your fingers apart as far as possible, and put your hand under the buttocks, with your forearm under the baby's legs to prevent them from dangling. To lift the baby onto your shoulder, or carry the baby, use the same technique, but with one hand behind the head and the other behind the buttocks, again with fingers spread as far as possible. When lifting or moving your child, be careful that little fingers and toes do not get caught on clothing you are wearing, such as shirts or blouses that button down the front. Many parents find it helpful to insert a piece of egg crate foam rubber or a thick piece of foam rubber into a pillowcase and use this to transport the baby. Some parents use a pillow. This type of support can also be used as a base when holding the baby.

 It is usually best to avoid lifting or moving a child with a painful fracture as much as possible. After some degree of healing occurs, the fracture will be less painful and moving your child will be easier. Unfortunately, leaving your child in one position for a long time can cause skin rashes and sores. Putting a child in different positions not only prevents these problems, but helps the child develop different sets of muscles, which is important for later mobility. Some parents have found the following method for shifting a baby from their stomach to their back, or vice versa, to be very useful when conventional methods cause discomfort:

 This procedure is best accomplished by two people. Position the baby on his/her back on a pillow or a covered piece of foam rubber. Turn the baby's head to one side. Then place a second pillow or piece of foam on top of the baby, sandwiching the child. With one person at the baby's head and the other person at the feet, each person places one hand under the bottom pillow and the other hand on top of the upper pillow and, at the count of three, the child is flipped onto his/her tummy. Be sure both participants agree beforehand on the direction that the baby will be turned. This method, although a little awkward, provides you with a way to change the baby's position without causing unnecessary discomfort.

When lifting your child, remember to use good body mechanics to prevent back injury to yourself. Always have the child as close to you as possible before beginning to lift. Flex your knees slightly and lift with the legs instead of the back.

Do not be afraid to show affection to your child by cuddling, rocking, touching, and talking to him or her. Frequent stimulation is necessary for sound emotional and social development.

Clothing
Children with OI are frequently affected by warm temperatures and are often bothered by excessive sweating. Lightweight, cotton clothing seems to be the most comfortable. Look for clothes with buttons or snaps down the front and at the crotch. Many parents fashion cast underwear by placing snaps or Velcro at the crotch of their child's underwear to simplify toileting. 

Since children with OI generally do not outgrow their clothes as quickly as other children, many parents feel that it helps to increase the child's self esteem to invest in current styles and fashions. A positive self-image for a child with OI is sufficiently difficult without having the child feeling self-conscious about his or her clothes.

Pancreatic Carcinoma

Symptoms
Treatment
Causes
Tests & diagnosis
Prognosis
Prevention
Complications
When to contact a doctor

U.S. National Library of Medicine Find this content and more from trusted sources.

Pancreatic carcinoma

Overview

Pancreatic carcinoma is cancer of the pancreas.

Symptoms

• Abdominal pain
• Back pain
• Clay-colored stools
• Depression
• Diarrhea
• Fatigue
• Indigestion
• Jaundice
• Loss of appetite
• Nausea and vomiting
• Paleness
• Weakness
• Weight loss

Treatment

At the time of diagnosis, only about 20% of pancreatic tumors can be removed by surgery. The standard procedure is called a pancreaticoduodenectomy (Whipple procedure).
This surgery should be done at centers that perform the procedure frequently. Some studies suggest that surgery is best performed at hospitals that do at least nine of these surgeries per year.
When the tumor is confined to the pancreas but cannot be removed, a combination of radiation therapy and chemotherapy may be recommended.
When the tumor has spread (metastasized) to other organs such as the liver, chemotherapy alone is usually used. The standard chemotherapy drug is gemcitabine, but other drugs may be used. Gemcitabine can help approximately 25% of patients.
For patients who have a blockage of the tubes that transport bile (biliary obstruction) and the tumor cannot be totally removed, the blockage must be relieved. There are generally two approaches to this:

• Surgery
• Placement of a tiny metal tube (biliary stent) that is similar to stents placed in the arteries of the heart, to relieve blockages during ERCP

Management of pain and other symptoms is an important part of treating advanced pancreatic cancer. Hospice can help with pain and symptom management, and provide psychological support for patients and their families during the illness.

Causes

Pancreatic cancer is slightly more common in men than in women. The risk increases with age.
The cause is unknown, but it is more common in smokers and in people who are obese. Almost a third of cases of pancreatic cancer are due to cigarette smoking.
There is controversy as to whether type 2 diabetes is a risk factor for pancreatic cancer. A small number of cases are known to be related to syndromes that are passed down through families.

Tests & diagnosis

• Abdominal CT scan
• Abdominal MRI
• Abdominal ultrasound
• Endoscopic retrograde cholangiopancreatography (ERCP)
• Endoscopic ultrasound
• Pancreatic biopsy

This disease may also affect the results of the following tests:

• Liver function tests
• Serum bilirubin

Prognosis

Some patients with pancreatic cancer that can be surgically removed are cured. However, in more than 80% of patients the tumor has already spread and cannot be completely removed at the time of diagnosis.
Chemotherapy and radiation are often given after surgery to increase the cure rate. For pancreatic cancer that cannot be removed completely with surgery, or cancer that has spread beyond the pancreas, a cure is not possible and the average survival is usually less than 1 year. Such patients might consider enrolling in a clinical trial (a medical research study to determine the best treatment).
This cancer has a 5-year survival rate of less than 5%, meaning 95% of the people diagnosed with it will not be alive 5 years later.

Prevention

• If you smoke, stop smoking.
• Eat a diet high in fruits, vegetables, and whole grains.
• Exercise regularly.

Complications

• Blood clots
• Depression
• Infections
• Liver problems
• Pain
• Weight loss

When to contact a doctor

Call for an appointment with your health care provider if you have:

• Back pain
• Fatigue
• Loss of appetite
• Persistent abdominal pain
• Other symptoms of this disorder

Dr. Murray Feingold: 'Yea' vs. 'yes'

Retrieved From Wickedlocal.com: Saugus

By Dr. Murray Feingold

Tue Nov 03, 2009, 01:04 PM EST

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- I have done a non-scientific study concerning a specific aspect of child development that has interested me since I was raising my own children.

The subject is: How do you stop children and adolescents from saying "yea" and start using the word "yes"?

This malady appears to be a chronic condition that thus far has defied effective treatment.

I have queried many parents of my pediatric patients concerning this linguistic misuse and have received varied responses.

Some say it doesn't bother them that their children continually say "yea." They were not included in the study.

Others responded to the question by saying, "Yea, it bothers me." They were also not included in the study.

Also excluded from the study were those who said it bothered them but not enough to do anything about it.

I then asked those who were concerned enough to do something about the issue, what did they did, and its effective rate.

Some parents said their initial approach was to explain to their children that the use of "yea" was not proper English, was a slang expression and they preferred that the child would not use it.

The success rate of this approach was zero.

The next approach was to correct the child each time he or she said "yea." This resulted in continuous corrections but little evidence that it was helpful.

The third approach was bribery. Whenever the child said "yes," he or she would be given a nickel or some other reward.

They also tried the opposite approach, charging the child a nickel each time "yea" was uttered. This resulted in receiving no nickels, many IOUs and meager success.

What is the etiology of this malady that is so resistant to treatment?

The "yea" syndrome affects both males and females, children of all economic levels, and has no regional limits. Yea can be heard in Boston, Omaha or San Francisco.

But why is treatment so elusive? Should the National Institutes of Health provide funding to find a cure for this chronic linguistic syndrome? Or, should we just accept that "yea" has become part of today's vocabulary? Is it really worth the effort to convince children they should no longer use it?

And, aren't there many more important childhood issues that need to be addressed?

The answer is yes.

However, like a stubborn warrior, I will continue to wage the battle against the pervasive use of "yea."

All helpful suggestions will be greatly appreciated.

Massachusetts-based Dr. Murray Feingold is the physician in chief of the National Birth Defects Center, medical editor of WBZ-TV and WBZ radio, and president of the Genesis Fund. The Genesis Fund is a nonprofit organization that funds the care of children born with birth defects, mental retardation and genetic diseases.

It Will Again! True or False? The Influenza Epidemic of 1918 killed more people than died in World War One.

Retrieved from the National Achieves

The Deadly Virus

The Influenza Epidemic of 1918

 

View the Documents and Photos

 



Hard as it is to believe, the answer is true. 

World War I claimed an estimated 16 million lives. The influenza epidemic that swept the world in 1918 killed an estimated 50 million people. One fifth of the world's population was attacked by this deadly virus. Within months, it had killed more people than any other illness in recorded history.

The plague emerged in two phases. In late spring of 1918, the first phase, known as the "three-day fever," appeared without warning. Few deaths were reported. Victims recovered after a few days. When the disease surfaced again that fall, it was far more severe. Scientists, doctors, and health officials could not identify this disease which was striking so fast and so viciously, eluding treatment and defying control. Some victims died within hours of their first symptoms. Others succumbed after a few days; their lungs filled with fluid and they suffocated to death.


The plague did not discriminate. It was rampant in urban and rural areas, from the densely populated East coast to the remotest parts of Alaska. Young adults, usually unaffected by these types of infectious diseases, were among the hardest hit groups along with the elderly and young children. The flu afflicted over 25 percent of the U.S. population. In one year, the average life expectancy in the United States dropped by 12 years.


It is an oddity of history that the influenza epidemic of 1918 has been overlooked in the teaching of American history. Documentation of the disease is ample, as shown in the records selected from the holdings of the National Archives regional archives. Exhibiting these documents helps the epidemic take its rightful place as a major disaster in world history.

Whomever Reads My Blog Receives a Hug Certificate

A Hug Certificate For You!
 

If I could catch a rainbow
I would do it just for you
And share with you its beauty
On the days you're feeling blue.


If I could build a mountain
You could call your very own;
A place to find serenity,
A place to be alone..

If I could take your troubles
I would toss them in the sea,
But all these things I'm finding
Are impossible for me.

I cannot build a mountain
Or catch a rainbow fair,
But let me be what I know best,
A friend who's always there.

This is a Hug Certificate!!

Send One to All Your Friends  

Who You Think Deserve A Hug (

Life  is a coin, you can spend it anyway you wish, but  you can only spend it once.

Inspired by Pauline

Polydactyl Cats - My Ping-Ping Who Is All Black - Her Sister Precious Is Black and White (Not Polydactyl)

*Ping-Ping died a couples of years ago.

Their names are Ping-Ping and Precious. In June 2004, I had two surgeries in one day. As you know, your body and your mind have to repair themselves after surgery. Since I had two surgeries in one day, my body and mind took more time to recuperate even though I do not have a full functioning body. One evening in early November, I called up a friend to see if he could do anything for me such as shopping or any errands due to a lack of caregivers at that moment in time. During the conversation with him on the phone, I was pushed into a flashback and I cannot remember November and December of 2004. He does not believe that I have flashbacks and that is the reason for the tragic misunderstanding. Due to the tragic miscommunication, they do not live with me anymore since November 2004.

For the persons that they are living with now; I would like to bring attention that Ping-Ping gets depressed, and Precious was very frightened and lived in my closet for a couple of months. They brought great joy in my life as well as the persons who lived with me.

Animals do have emotions. For the persons that they are living with now; I hope that you are paying attention to their emotions. Hopefully, you are taking great care of Ping-Ping and Precious as we took great care of them.


Ping-Ping and Precious, I send all my love to you each day. I do hope that the persons who Ping-Ping and Precious are living with now know the depth of emotional pain I am in not to be able to see them.

The reason that I put my picture of Ping-Ping and Precious on this post is that Ping-Ping's front paws were double paws. She had not pain when she walk. I knew that she was a "Polydactyl Cat". It was very sweet to look at Ping-Ping's front paws, due to they looked like "Mittens".

An article from Cornell University, Cat Watch (1998), cited studies into polydactyl cats from the 1940´s through to the 1970´s. The study indicated that the trait may have occurred in cats taken to Boston by English Puritans during the 1600s and speculated that the mutation developed in cats already in the Boston area rather than in cats in England. The progeny of these cats may have travelled on trading ships from Boston to Yarmouth, Massachusetts and Halifax, Nova Scotia, two areas which also have a high incidence of polydactyly. Charles Darwin wrote of polydactyl cats in his book "The Variation of Animals and Plants Under Domestication" published in the 1850's "I have heard of several families of six-toed cats, in one of which the peculiarity had been transmitted for at least three generations" pre-dating claims elsewhere that the first scientific recording of feline polydactyly was in 1868.

Polydactyl cats are said to be virtually non-existent in Europe, because "unusual looking cats" were destroyed due to witchcraft superstitions, practically eliminating the trait (Kelly, Larson,1993). I do not know whether Britain was included in the generic term "Europe" or whether it meant mainland (continental) Europe only. In Norway, polydactyl cats are known as "ship's cats" as the extra toes supposedly gave them better balance on ships in stormy weather; they are not uncommon and polydactyl kittens are sought after pets. Polydactyl random-bred cats have been reported in Sweden though other European cat lovers (locations not reported) had apparently never seen a polydactyl. They are common enough in Britain to be considered unremarkable.

Polydactyl cats were considered "lucky" by sailors. Sailors also believed polydactyl cats to be superior mousers and ratters. Employed as ships' ratters and lucky mascots, they would have reached America with early British settlers hence their greater frequency in Eastern states. A disproportionately high number of "lucky" polydactyl cats, compared to normal-toed cats, would have found their way there. This would lead to a greater proportion of polydactyls than usual for a random-breeding cat population. Back in Britain, with its large cat population of which the polydactyl formed only a small part, the trait remained less common (though there have been localised pockets of higher than average incidence). There is a higher incidence of polydactyly in South-West England, possibly associated with ports from which ships set sail for the New World.

Bjørn B Svingen, owner of a polydactyl cat, provided the following information on polydactyl cats in Norway and their associaiton with ships: "I have heard people say that these genes came to Norway long ago. The story was that the genes were inherited from Spanish or Portuguese ship cats with this "'disorder'. These cats were supposedly common on ships trading on the Norwegian coastline. They have again become popular, at least in our area, and are plentiful in Trøndelag in mid Norway." As a result, they are also known there as "Skipskatt" (ship-cat).

In a survey and detailed account of cats he found in Singapore in 1959, Searle had not noted any polydactyls. The only polydactyls I noted in the Malaysia/Singapore region were the Lake Chini cats.

THE GENE(S) FOR POLYDACTYLY

There are two forms of polydactyly described by embryologists. Pre-axial polydactyly refers to extra digits on the inside edge (thumb-side) of the paw. Post-axial polydactyly refers to extra digits on the outer side (little finger side) of the paw and is uncommon.

One of the earliest inheritance studies was by Poulton (probably 1880s/90s) which is mentioned by Thomas Hunt Morgan (Professor of Experimental Zoology, Columbia University) in Experimental Zoology (Publ. Macmillan & Co, London, 1910): Poulton has given some records of polydactyl cats that appear to be exphcable, so far as they go, along Mendelian Hnes. Three young were produced from a polydactyl female by an unknown father. They were all polydactyl. If polydactylism dominates over the normal condition, this result is simple dominance. One of these individuals (F1) produced three litters (by unknown fathers), in which four normal and six abnormal kittens appeared. If the father was normal, five normal and five polydactyl young would be expected. Thus:- (P + N) + (N + N) = (2NP + 2NN) [P being poly foot and N being normal foot]

Sis & Getty (1968) describe polydactyly as an monogenic autosomal dominant trait affecting the pre-axial part of the limb. This is the typical and harmless form of polydactyly though other forms may exist. Both Danforth and Chapman & Zeiner proved in their research that normal feline polydactyly is a simple incomplete dominant gene with variable expression. According to geneticist and TICA Genetics Committee Chair Dr Solveig Pflueger "most polydactyl cats... have a form of pre-axial polydactyly with the extra digits(s) on the thumb side of the foot... " The Pd gene causes the entirely harmless form of polydactyl.

The main studies on feline polydactyly are Danforth's studies Heredity of Polydactylism (1947) and Morphology of the Feet in Polydactyl Cats (1947) plus Chapman & Zeiner's study The Anatomy of Polydactylism in cats with Observations on Genetic Control (1961). The Danforth and Chapman & Zeiner studies observed examples of both mitten-foot and patty-foot polydactyly in their studies (some refer to the patty foot as "snowshoes" but I avoid that term as there is a cat breed called the Snowshoe). Danforth, and Chapman & Zeiner, stated that polydactyly was never observed in the hind feet except when it was also present in the front feet. A hind-foot polydactyl must have extra digits on the front feet, though sometimes these are not readily discernible and can only be found by x-ray.

The gene(s) for polydactyly specifically affects the tissue formed at the very end of the limb (apical cap) of a developing embryo. This is the area where the toes will form. Danforth studied the way normal pre-axial polydactyly developed in embryos based on data from 150 cats. He discerned evidence of polydactyly in the 20th day of gestation in the form of excess development on the edges of the limb buds that would form the forelimbs. If the apical cap is larger than normal, extra toes will develop from it. It is worth noting that physical damage to the apical cap might also trigger the development of extra toes. Branching of the apical cap will lead to complete double paws or, if it branches early enough, to doubled limbs.

The first major study into classical polydactyly (thumb cats) was conducted in 1947. For his study "Heredity of polydactly in the cat" (Journal of Heredity 38, 107, 1947) Danforth studied two female polydactyl cats that he housed at his laboratory, The cats came from locations 85 km from each other in California, but the possibility of them being related could not be ruled out. He mated these females with different males and recorded the dates of mating and the physical traits of the kittens. He collated additional information from friends with polydactyl cats.

He noted that the effects of polydactyly could always be seen on the front paws and sometimes also on the hind paws. On the front paws, the first digit was at least enlarged in one front paw and might be doubled or tripled. If the hind paws were also affected, there was at least a rudimentary dew-claw and sometimes additional claws. Where there was a doubled first digit, it was sometimes incompletely formed with the additional digit between the first digit and the other claws. The position of the first digit was also changed a little from normal to resemble a thumb. The four images show different footprints: a normal-footed front paw and 3 expressions of polydactyly:

Danforth mated all possible combinations of his cats: Poly x Poly, Poly x Non-Poly, Non-Poly x Non-Poly. This confirmed that polydactyly was a dominant gene, because in every mating where at least one parent was polydactyly there were polydactyl offspring. In matings between two normal-footed cats there were never any polydactyl offspring. In 3 matings, all offspring were polydactyl and therefore one or both parents were probably homozygous for polydactyly.

In guinea pigs, one form of polydactyly is lethal when homozygous. Danforth's studies indicated that this was not the case in cats. In a mating Pp x Pp (heterozygous parents) on average 25 % of the young will be homozygous for polydactyly, 50 % heterozygous for polydactyly and 25 % normal-footed. If the gene was lethal, the 25% of homozygous offspring would die before birth and the litters therefore would be smaller than expected. Danforth found the average litters to be almost the same size (4.12 with offspring homozygous for polydactyly compared to 4.35 for litters where no offspring could be homozygous). This also affected the ratio of polydactyl and normal-footed offspring in a litter. If the gene was lethal when homozygous, there would be (on average) 2 poly kittens for every normal-footed kitten. Danforth's cats produced a ratio of 77 poly kittens to 22 normal-footed kittens.

	Offspring polydactyl		Offspring normal
Probable Mating	Observed	Expected	Observed	Expected	Total
PP x Pp	8	8	0	0	8
PP x pp	11	11	0	0	11
Pp x Pp	69	68.25	22	22.75	91
Pp x pp	33	31.5	30	31.5	63
pp x pp	0	0	61	61	61

From these studies, Danforth concluded that polydactyly was a variable expressed dominant gene with no reason to suspect it was lethal when homozygous: "these data lend no support to the assumption that polydactyly in the cat is lethal when homozygous" nor was it associated with the cat's gender "The trait is not related to sex, and no evidence is found that its gene is lethal" He did not find evidence of split foot or radial hypoplasia (also called radial hemimelia) in his studies though his second study into feline polydactyly ("Morphology of the Feet in Polydactyl Cats", 1947) found that cats with 6 metatarsals (toes) tended to have fusion at the ulna which caused varying degrees of rotation of the joint of the radius.

Useful Formula For Describing Polydactyl Front Paws
Normal front foot	4
Foot with extra toes that do not form a thumb (patty foot)	5; 6 (etc)
Mitten foot with thumb (single digit)	4+1
Mitten foot with 2 or more extra toes	4+2; 4+3 etc
Mitten foot where extra claws are tucked between the normal foot and "thumb": (the numbers in brackets mean extra claws that aren't on a fully developed toe)	4+(1)+1; 4+(2)+1; 4+(1)+2 (etc)

In 1955, Albert C Jude, author of "Cat Genetics" (a book that had as much about mice and rabbits than cats!) documented two forms of polydactyly. He wrote that polydactylism (extra digits), and oligodactylism (reduction of toe number) were sometimes reported by the fancy, but were the exception (not selected for) rather than the rule within cat breeding. This meant little data was available on feline polydactyly to permit proper scientific study. He noted that polydactyly involving only the preaxial side of the limb had been documented in cats by Danforth in 1947 and was dominant over the normal form. Most cases of polydactylism in cats observed by Jude had affected the front feet only.

Jude also described another form of polydactyly, the type we now call "mitten cats" but which he called "posterior reduplication", in his 1955 book: Another interesting deformity - only very occasionally seen in cats, but more frequently seen in some other animals - is known as "posterior reduplication." The condition was found in a stock of mice by Danforth in 1923, and a description was published by him in 1930. This deformity is mentioned here mainly to show how information of a helpful nature can be given by fanciers. In this instance it came from Mrs. A. Winsor of Hull, a well-known English Abyssinian breeder. Before the war, says Mrs. Winsor, "I had two little black she-cats. One came into season, and a strange gray tom came to investigate. His feet were really amazing. His front legs were very thick and stout, big feet, with normal number of toes. On the inner side of each foot was another smaller foot. A sort of stalk grew from the ankle, as if the ankle bone had been split, and this ended in a complete foot which rested on the ground alongside the normal foot, and turned slightly inward, When sitting he had to advance one leg, as he could not possibly put all his four feet side by side, and when walking he sort of lifted one foot over the other. He mated my queen who was calling at the time and there were two black kittens whom we put to sleep, and two gray-striped, both females. One had just thumbs; the other had seven toes - four ordinary, and three extra where the thumb would be. There was no stalk, but these three toes had a separate pad; they were about the same length as the others, and her feet spread out like paws. She also had a sort of "thumb" half-way up each hind foot, with a claw on the end. The other gray-striped female - the one that had just thumbs - we kept for eight years and then she died. I managed to get a granddaughter who is now seven years old. She has had countless kittens, and about half of every lifter have the ‘Family Feet.’"

It is interesting that Jude differentiated between the 2 types of polydactyly in 1955; differentiating between the two forms has recently become a concern for cat breeders due to the occurrence of Twisty Cats.

According to the late Roy Robinson in his book "Genetics for Cat Breeders", polydactyly has been officially (scientifically) recorded as early as 1868, though it had been observed earlier and seen frequently since. The distinguishing feature is the presence of extra toes, most noticeably on the front feet. Robinson explains that there is considerable variation in the number of extra toes and in how well-formed they are. The trait ranges from an enlargement of the inside digit into a "thumb" to the formation of three apparently well formed extra toes (i.e. 7 toes on the affected foot). A cat may even have different numbers of toes on each of its front feet.

The hind feet are rarely affected and are only ever affected if the front feet are also affected. I have received a report of a Maine Coon with hind foot polydactyly and apparently normal fore paws; it seems likely that it was genetically polydactyl for all four paws, but that the extra toes had not been visibly expressed in the fore paws for some reason. I also received the following report about a random-bred hind-foot polydactyl with normal front paws.

Support the Great Ape Protection Act

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On March 5, the Great Ape Protection Act was reintroduced in the House of Representatives. This landmark bill would ban invasive experiments on chimpanzees as well as breeding. IDA has been working for this since 1993.

For the past 16 years, IDA has documented and battled against abuse, fraud, waste and cruelty in chimpanzee experiments, both federally- and privately-funded. During this time, IDA shut down the world's biggest chimpanzee laboratory - the notorious Coulston Foundation - which resulted in the single largest effort ever accomplished on behalf of chimpanzees in labs: the permanent retirement of 266 chimpanzees and 61 monkeys by the state-of-the-art sanctuary SaveTheChimps. IDA also secured criminal cruelty charges against NIH-contractor Charles River Laboratories and got an entire laboratory disqualified by the Food and Drug Administration. These actions were unprecedented in the history of U.S. medical research, and helped lay the groundwork for this landmark legislation.

H.R. 1326 was introduced shortly after ABC’s Nightline aired an expose of the University of Louisiana at Lafayette’s New Iberia Research Center (ULL-NIRC) a lab that IDA has termed the “New Coulston” because it is the largest chimpanzee lab in the world, and in a published experiment tested various chemicals on chimpanzees. That study positively cited Dr. Frederick Coulston's 1982 toxicology tests of industrial solvents in chimpanzees, as well as Coulston's 1985 paper extolling chimpanzees as the "best possible model to test the fate and effects of foreign chemicals in man."

The Nightline expose prominently featured courageous whistleblower Narriman Fakier, a former ULL-NIRC employee who blew the whistle on outrageous cruelty and abuse at the lab. Her whistleblower lawsuit documents a litany of cruelty and abuse to chimpanzees and monkeys that was corroborated by the Nightline expose and the laudatory undercover video investigation by the Humane Society of the United States.

For years, IDA Research Director Eric Kleiman has provided legal assistance to Ms. Fakier as an official part of her legal team. ULL-NIRC has repeatedly tried to have the case dismissed, using one technicality after another in a vain attempt to prevent a jury and the public from seeing the evidence of cruelty and abuse that Ms. Fakier witnessed. The lab failed, and Ms. Fakier’s case continues. ULL-NIRC has complained in legal pleadings about the extensive media coverage of their cruelty and being, in their words, “bombarded” with letters from outraged citizens.

H.R. 1326 would end these horrors for the over 1,000 chimpanzees currently imprisoned in labs such as ULL-NIRC and the NIH-owned, Charles River-operated Alamogordo Primate Facility in New Mexico. Since 1993, IDA has repeatedly called for an end to chimpanzee experiments, documenting the pervasive cruelty that is not limited to ULL-NIRC but inherent in experiments on chimpanzees and other non-human animals. We urge you to support this historic legislation.

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Please Support The Great Ape Protection Act - HR 1326

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On March 5, the Great Ape Protection Act was reintroduced in the House of Representatives. This landmark bill would ban invasive experiments on chimpanzees. I urge you to support this bill and the introduction of a companion bill in the Senate.

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H.R. 1326 was introduced shortly after ABC's Nightline aired an expose of the University of Louisiana at Lafayette's New Iberia Research Center (ULL-NIRC). The Nightline expose prominently featured courageous whistleblower Narriman Fakier, a former ULL-NIRC employee who blew the whistle on outrageous cruelty and abuse at the lab. Her whistleblower lawsuit documents a litany of cruelty and abuse to chimpanzees and monkeys that was corroborated by the Nightline expose.

H.R. 1326 would end these horrors for the over 1,000 chimpanzees currently imprisoned in labs such as ULL-NIRC and the NIH-owned, Charles River-operated Alamogordo Primate Facility in New Mexico. Since 1993, In Defense of Animals (IDA) has repeatedly called for an end to chimpanzee experiments, documenting the pervasive cruelty that is not limited to ULL-NIRC but inherent in experiments on chimpanzees. I urge you to support this historic legislation.

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Chimp Behavior Mimics That of Abused Human Kids

By Keith Herrell
Published April 2009

When Linda Chernus heard about a chimpanzee attack in Connecticut that left a woman fighting for her life in a hospital, her thoughts went back almost four years and thousands of miles away to a chimp sanctuary near Girona, Spain.

Chernus, a clinical social worker and professor of clinical psychiatry at UC, worked for four days at MONA, a sanctuary for abandoned and abused chimpanzees, in July 2005.

Drawing on her experiences there, she wrote two manuscripts that were published in December 2008 in the Journal of Emotional Abuse.

The papers drew parallels between the chimps, many of whom had experienced maternal loss and social isolation after being taken from their native habitats, and human children who had been emotionally abused and neglected.

“We can learn from nonhuman primates about creating therapeutic environments for children who have been emotionally abused,” Chernus says.

MONA created an enriched family unit, Chernus says, by grouping a mother chimpanzee with five children—three of whom were not biologically her own—and adding a male chimp who had lost his mate.

The male and female—both of whom had been in captivity before coming to MONA—bonded well and nurtured each other, and the female emotionally abused and neglected. nurtured all five of the children as if they were her own, Chernus says.

“The important thing is to have an environment that’s enriched, ideally with siblings and peers,” Chernus says of the chimps. “It felt like home, so they were able to develop.”

Abuse of chimpanzees isn’t confined to physical abuse or being locked in cages, Chernus says.

“Humanization”—being dressed in clothing, or made to perform like children—is also a form of abuse, she says.

“People think it’s cute to dress little chimpanzees,” she says. “It may be cute for the people, but it’s really abusive. It’s a disruption of their normal lifestyle—what they need to grow and prosper. They’ve been traumatized by being humanized.”

The chimpanzee in the attack, known as Travis, starred in television commercials when he was younger, according to news reports about the incident. He had been born in an Arkansas compound in 1995 and was raised in the Stamford, Conn., household of Sandra Herold after his mother was shot and killed following an escape and rampage when he was three days old.

He attacked Charla Nash, a friend and employee of Herold’s, on Feb. 16, 2009, as she was trying to help lure him back into Herold’s house.

Herold has speculated that Travis attacked Nash because she Girona, Spain. Chernus, a clinical social worker and professor of clinical psychiatry at UC, worked for four days at had changed her hairstyle and was driving a different car.

Nash lost her hands, nose, lips and eyelids in the attack and suffered significant traumatic brain injury, according to the Cleveland Clinic, where she was transferred from Stamford Hospital. Doctors at the Cleveland Clinic performed the nation’s first face transplant in December 2008, but a statement from the hospital said it was too early to consider reconstructive surgery for Nash.

Travis was shot and killed by police following the attack. Chernus has been following news of the attack and is highly critical of Herold and a legal system that allows chimpanzees to be kept as pets.

“What she did is extremely bizarre; it’s very unfair to the animal, unfair to anybody,” Chernus says. “I was also surprised that the legal system had allowed that to go on for so long.”

Connecticut officials say they were aware that Travis lived in the Herold home but existing law did not give them the authority to remove him.

Since the attack, legislation has been proposed by the state attorney general that would ban primates, alligators and other types of wild and potentially dangerous animals from private homes.