Wombats are typically around 76 cm long, and there are two main types- hairy nosed and common. The former weighs ~19-32 kg while the latter weighs around 25-40 kg.
In terms of habitat, they are indigenous to Australia and Tasmania, wherein they live in forests, mountains, and grasslands. They are efficient diggers, and create burrows consisting of many tunnels and sleeping chambers (3-30 m long, and 3.5 m deep). Some wombats even have discrete burrosw that they live in during the duration of the year.
Some wombats are social (hairy-nosed) whilst others are loners (common). A group of wombats is called a mob or a colony.
Wombats are nocturnal, and although they do not climb trees, they are vigorous swimmers.
In terms of digestion, they typically consume things such as herbs, grasses, roots, scrubs, and bark. They have special enzymes in their stomachs to help digest fortuitous roughage! In total, it takes around 14 days for a wombat to digest a meal.
Further along, wombats pass cuboidal feces. They actually use these to mark their territory by placing them on rocks, fallen trees, and/or fresh mushrooms. The cuboidal shape ensures that they do not roll of (the feces, that is).
Wombats mate during times of food abundance, in order to wean their young in the best possible conditions. Male wombats fight for the right to mate with females, and the male wombats will chase a female until she slows down long enough that he can catch up to her to mate. While the female wombats are being chased, they make a coughing noise. The gestation period of a wombat is approximately 21-30 days. Only one joey (baby wombat) is born at a time.
The mother gives birth every two years. At birth, a joey’s weight is 2 grams, and it is the size of a jellybean. The joey stays in the mother’s pouch for about five months. A wombat’s pouch opens towards the bottom, which prevents dirt and debris from entering whilst the burrowing is occurring. The joey clamps onto its mother’s teat to ensure that it does not fall out. After these months have passed, the joey will climb in and out of the pouch for another few months. Finally, the wombat will be considered mature at 1.5-3 years old. The lifespan of a wombat is 5-15 years in the wild and over 20 years in captivity.
Only the Northern hairy-nosed wombat is considered endangered, which is due to their habitat quality declining because of invasive exotic grasses. During the Pleistocene, herds of large wombats the size of rhinoceroses traversed the plains of southern Australia. Wombats can run up to 40 km/h.
 Wombat bottoms have very thick skin and are filled with cartilage, so this withstands biting quite well. As a result, wombats will often use their rears to block their burrow entrances for safety purposes!



Hemophilia is a group of bleeding disorders. The two most common types are Hemophilia A (or classic hemophilia) and Hemophilia B (or Christmas disease).

The F8 (Factor VIII) gene produces the protein antihemophilic factor (AHF) in humans.This protein is essential for routine blood clotting functions. In individuals with hemophilia A, this protein is absent or dysfunctional. For those with the less common hemophilia B,  Factor IX is the gene responsible.

Symptoms of the disorder:

  • Severe nosebleeds
  • Easy bruising
  • Blood in urine (hematuria) /stools
  • Heavy bleeding/hemorrhage after bumps, dental work, minor cuts, or other trauma
  • Joint pain
  • Heavy menstrual bleeding in women who are carriers

Associated Complications:

  • Damage to joints (including elbows, knees, and ankles)
  • Damage to muscles, causing significant scarring and pain
  • Severe anemia as a result of blood loss
  • Bleeding in digestive system
  • Bleeding inside head (intracranial hemorrhage)
  • Compartment syndrome (develops when bleeding in muscles puts pressure on the arteries and nerves within, resulting in serious limb damage)


Hemophilia is caused by a sex-linked mutation-that is, a mutation to genes that are carried on either the X or the Y chromosomes. Both types of hemophilia discussed are X-linked recessive traits.Therefore, females are usually only carriers, as they have two X chromosomes. In order for a female to have hemophilia, both of her parents must pass on the faulty genes. Males, on the other hand, have only one X chromosome, and thus if a male inherits the faulty gene, hemophilia will develop.



It is possible for a new genetic mutation to occur-that is, the person gets hemophilia even if neither parent carries a genetic mutation.


Detection of Carriers

Carriers of hemophilia are detected by a process of carrier testing. These tests may involve:

  • Creating a family tree. A genetic counselor or physician may help a woman create a detailed family history called a pedigree chart in order to determine information for three generations. This chart would aid in identifying possible carriers within the family.
  • Factor levels can be tested. Factor level tests, accurate 70% to 90% of the time in determining carrier status, involve the testing of the blood of the woman. On average, carriers have lower levels of factors 8 or 9 than women who are not carriers.
  • DNA testing is still the most accurate method. For this test, DNA of the tested is examined for genetic changes that could cause hemophilia. The two types available are direct mutation testing, and linkage (indirect testing).
  • Prenatal testing involves testing a small amount of amniotic fluid, blood from the umbilical cord or placenta, and can be done early in the pregnancy.


Hemophilia can be treated by injecting AHF (isolated from donated blood) into the hemophiliac (the AHF is slowly injected or dripped into the veins). The donated blood must be meticulously screened and scrutinized for infectious diseases, however the AHF injections relieve the most severe effects of the disorder. With appropriate treatment, hemophiliacs can live relatively normal lives.

Even though gene therapy remains a great hope, so far there is no workable cure for hemophilia. In a small number of hemophiliacs with liver transplants, their hemophilia was completely cured, due to the clotting factor being made in the liver. Transplants, however, are much too risky to be used as a cure.

Another possible cure is fetal hepatocyte transplantation. Fetal hepatocytes are the liver cells of an aborted fetus. These cells can function as normal liver cells would and can be grown in a laboratory. As the scientists research, they hope that these cells can eventually be placed in the body of a hemophiliac and thus produce the clotting factor for the affected person.

Some precautions to take are:

  • Avoid taking nonsteriodal anti-inflammatory drugs and aspirins (these may contain blood thinners).
  • Get vaccinated with the hepatitis B vaccine.
  • Avoid circumcising male offspring of women known to be carriers until the infant has been tested for hemophilia.
  • Carry identification information identifying those with the disorder.
  • Avoid activities with a high collision risk.
  • Take extra care to protect the head from injury.
  • Be aware of the effects of activities with high impact.
  • Practice good dental care to reduce the risk of major dental work.

So far, there are no guidelines as to how to prevent hemophilia. However, talk to genetic counselors if you have a family history of the disease so that you can calculate the risk for potential offspring.

Interesting Facts:

  • Hemophilia earned the nickname “royal disease” or “disease of kings” because Queen Victoria passed on the disorder to her son Leopold who in turn passed it through many royal lineages of Europe.
  • Hemophilia B is also called Christmas disease. The name originates from the first patient reported to have it, a man named Stephen Christmas.
  • The disease was first called haemorrhaphilia.

Works Cited

Carson-DeWitt, Rosalyn, MD. “Hemophilia (Hemophilia A—Factor VIII Deficiency; Classic Hemophilia; Hemophilia B—Factor IX Deficiency; Christmas Disease).” Consumer Health Complete. EBSCOhost, June 2013. Web. 25 Oct. 2014.

“Complications of Hemophilia-Topic Overview.” WebMD. WebMD, 03 Aug. 2013. Web. 25 Oct. 2014.

“Gene Therapy as an Alternative to Conventional Treatment of Haemophilia.” Evoscience. Evoscience, n.d. Web. 26 Oct. 2014.

“Hemophilia Carrier Testing.” Steps for Living. NHF, 2014. Web. 25 Oct. 2014.

“Hemophilia.” KidsHealth. Ed. Suzanne Nielsen. The Nemours Foundation, 01 Jan. 2011. Web. 25 Oct. 2014.

“Hemophilia Tests.” Hemophilia Tests. RnCeus, n.d. Web. 26 Oct. 2014.

“Hemophilia.” University of Maryland Medical Center. University of Maryland Medical Center, 07 May 2013. Web. 25 Oct. 2014.

“Heredity of Hemophilia.” – Canadian Hemophilia Society. Canadian Hemophilia Society, 2014. Web. 26 Oct. 2014.

“History of Bleeding Disorders.” National Hemophilia Foundation. NHF, n.d. Web. 26 Oct. 2014.

“HoG Handbook.” Curing Hemophilia Hemophilia The Basics HoG Handbook Hemophilia of Georgia. Hemophilia of Georgia, n.d. Web. 25 Oct. 2014.

Levine, Joseph, Ph. D. “Sex-Linked Genetic Disorders.” Biology. By Kenneth R. Miller. Third ed. New Jersey: Prentice Hall, 1995. 238. Print.

“Living With Hemophilia – Bayer HealthCare.” Living With Hemophilia – Bayer HealthCare. Bayer Group, 18 June 2014. Web. 26 Oct. 2014.

Miller, Kenneth R., Ph. D., and Joseph Levine, Ph. D. Biology. Third ed. New Jersey: Prentice Hall, 1995. Print.

“National Hemophilia Foundation.” National Hemophilia Foundation. NHF, n.d. Web. 26 Oct. 2014.

“Patient Education: About Hemophilia.” UC San Diego Health System. UC San Diego Health System, 2014. Web. 25 Oct. 2014.

Shapiro, Amy D., MD, and Whitney Sealls, Ph. D. “Hemophilia B.” Rare-Diseases. National Organization for Rare Disorders, 2014. Web. 26 Oct. 2014.

“What Causes Hemophilia? :: DNA Learning Center.” DNALC Blogs. Cold Spring Harbor Laboratories, n.d. Web. 25 Oct. 2014.

“What Causes Hemophilia?” – NHLBI, NIH. NHLBI, NIH, 31 July 2013. Web. 25 Oct. 2014.