This article is from the WSSF 2004 AFRMA Rat & Mouse Tales news-magazine.
By Carmen Jane Booth, D.V.M.
Chase as a baby.
A normal rat on the left, Chase on the right.
Charlene M. Crain, River Ridge, LA
Q I got a complimentary issue today of Rat & Mouse Tales. I was very surprised. I was even more surprised and elated when I saw my sweet Fancy on page 17 in her reindeer ears. Anyway, I have the most special rat ever. His name is Chase. He is a Seal Point Siamese Dumbo. These pictures were taken when he was a baby. He is 8 months old now. He is a hydrocephalic rat. He is mentally retarded and physically runted. I think I am one of the few people who have a healthy living hydrocephalic mentally retarded rat. Most of them die before two months. He was born in March and predicted not to live past 6 weeks. He is very loving. He is beautiful. I am very proud of this little courageous rat.
Question by Karen Robbins: Is this condition inherited from one or both parents or is it one of those congenital birth defects. Is this something to be concerned about when breeding if it shows up in a litter? What are the percentages of getting one of these rats in a person’s breedings?
A Hydrocephaly is a dynamic process. Its natural progression is not completely understood, but it is almost always associated with other intracranial and extracranial anomalies that interfere with drainage of the cerebral spinal fluid. It might begin as mild enlargement of the ventricles in the brain and progress to a more serious state. Mild ventricular enlargement without an increase in head size might be a normal variant. When I did a PubMed search on hydrocephaly and genetics, there were many different papers describing genetic defects that can result in hydrocephaly in rodents. In reality, everything that happens to a living being is likely the result of differences in genetics. The affected rat probably carries a mutation in one or more genes that resulted in his developing hydrocephaly. As to the parents, one just does not know. I have seen mild to severe cases of this over the years and it is considered an incidental finding unless significant number of animals are affected.
Elisabeth Brooks, Kansas City, MO
Q I had gotten one of the Variegated rats (KK Imagine My Surprise) from the “2 Fathers Sire One Litter” (Fall 2002 issue) and “Variegated X Self = Berkshire, not Variegated” (Fall 2003 issue). I bred her to one of my rats (totally unrelated) and kept a son which I then bred back to mom. In that litter there were six pups—one with anencephaly, two fully-formed dead pups, and three live, normal, healthy-looking pups. I was not there to witness the birth, and therefore, I don’t know if the baby with anencephaly was born alive. I have to assume that the two fully-formed pups might have been lost due to the doe having trouble delivering the anencephaly pup (larger than normal amniotic sac?). When I did find Ginnie (Imagine My Surprise) with her new babies, they were all clean and in the nest—all six of them. She was acting normal—ready for treats and scritches but happy to be back with her pups when play/treat time was over. The live pups had milk bands and were pink and wiggly. I did not think to weigh the pups.
The dead anencephaly rat. Photo from Elisabeth Brooks.
The sire of this litter with the anencephaly pup came from a litter that consisted of 11. All of them lived (thrived) and are doing well in pet homes and in breeder homes.
There have been no incidences of health problems with any related rats to the mom, KK Imagine My Surprise. Her aunt was pregnant and delivered about the same time her mother, “KK1837 Yuma,” did. There has been a brother-sister breeding from those litters, and none have had any health issues.
My pregnant does do get higher protein foods and extra veggies. The base of the diet is Harlan Teklad 2018 for females (2014 for adult males), and when I can’t get it, they get Purina’s LabDiet 5001 (adults) or 5008 (babies and pregnant or nursing does). They do not receive any special supplements (i.e. Nutri-Cal, Ensure, etc.) until after their pups are born because we have concerns that the pups might be too big for mom to deliver. Their water comes from the tap, aged for a day or so, and then poured into clean bottles with stainless steel tubes.
The bedding used for pregnant does and their pups is aspen shavings. They are housed in Sterilite bins with ventilation on one side and on the top and are given “out time” each day.
The only objects I put into mommy bins before pups reach two weeks are toilet paper rolls, and sometimes, paper napkins. They do not get any other toys or bowls as I have lost pups due to bowls being turned over on top of them. I haven’t been weird about checking how much folic acid they are getting until this litter; however, I have been breeding for 4½ years, and this is the first time I’ve had such a problem come up. In relation to other breeders that isn’t much experience, but I do have more than 10 litters per year. I have also checked on a few forums and e-mail groups, and no one has run into this problem with their rats . . . ever . . . that I can find.
The three living siblings to the anencephaly pup are doing well. Two of them, SRR Hubba Hubba, a male, and SRR Oh Baby, a female, live here at Spoiled Ratten. The other from the litter, a male named SRR Wowza, is at Kim Richardson’s rattery “Landmark.” My girl, Ginnie, is as healthy and happy as ever. I love that rat!
UPDATE: SRR Wowza was not bred. SRR Hubba Hubba was bred to his sister SRR Oh Baby, and she died in labor. The vet found nothing unusual about the pups (and no anencephaly) and nothing abnormal about the amniotic sacs. There was a large (but not abnormally large) pup in the birth canal. SRR Hubba Hubba died at 14 months of age.
A Anencephaly is one of a variety of defects during the development of the neural tube which becomes the brain. It is one of the end results of different neurological developmental defects. Neural tube defects have a well-established genetic basis, although no single genetic factor has been identified as a major risk factor in NTD susceptibility in people. A large number of association studies have been conducted to investigate the possibility that NTD susceptibility is linked to variation in genes involved in early embryonic development or in the absorption or metabolism of folate, a nutrient that has been clearly associated in humans with a reduction in the risk of NTD. (Except from Clin Genet. 2003 Nov;64(5):424-8.) If the mother of the anencephalic rat was on a good diet and only one of the neonates was affected, than I would surmise that the cause is some error in development that occurred solely in the affected rat. These things happen and often it is from a genetic mutation that occurred after fertilization and is not present in either parent.