A few weeks ago a young, black, eastern chipmunk Tamias striatus appeared on a stonewall in front of my home. Tamias means “collector and keeper of provisions”, and striatus refers to the animal’s prominent body stripes. Several years ago I spotted another, also here in my front yard, so I’m inclined to believe the gene is in the local pool. A bit of research quickly revealed that they are actually seen with some frequency, but not enough to be called “common”. They are called melanistic. Melanism refers to an increase in the average amount of the dark pigmentation that is present in an organism. The elevated pigment levels give rise to a dark individual that has, for example, dark skin, feathers, scales, or fur. The phenomenon has been observed in a variety of animals including leopards, squirrels, and wolves, and is often the result of a genetic mutation.
Normally chipmunks are not a potential threat for rabies. However, according to the October 1999 issue of the Probe, the newsletter of the National Animal Damage Control Association, a 12-year-old girl in Ohio was bitten by a chipmunk that tested positive for the raccoon strain of rabies in April of 1999. Each year a few cases of rabies in rodents are confirmed by the CDC.
(The following is excerpted from “Information on Arboviral Encephalitides”, produced by the CDC’s Division of Vector-Borne Infectious Diseases.)
Chipmunks are also known hosts of La Crosse (LAC) encephalitis, which was first identified in La Crosse, Wisconsin, in 1963 and is known to be present in several Midwestern and Mid-Atlantic states. During an average year, about 75 cases of LAC encephalitis are reported to the CDC. The virus is classified as a Bunyavirus and is a zoonotic pathogen cycled between the daytime-biting treehole mosquito, Aedes triseriatus, and vertebrate amplifier hosts such as chipmunks and tree squirrels. Most cases of LAC encephalitis occur in Minnesota, Wisconsin, Iowa, Illinois, Indiana, and Ohio. However, recently more cases are being reported from states in the mid-Atlantic (West Virginia, Virginia, and North Carolina) and southeastern (Alabama and Mississippi) regions of the country. It has long been suspected that the virus has a broader distribution and a higher incidence in the eastern United States, but is under-reported because the etiologic agent is often not specifically identified.
LAC encephalitis initially presents as a nonspecific summertime illness with fever, headache, nausea, vomiting, and lethargy. Severe disease occurs most commonly in children under the age of 16 and is characterized by seizures, coma, paralysis, and a variety of neurological sequelae after recovery. Death occurs in less than 1% of clinical cases. As there is no specific treatment for LAC encephalitis, physicians often do not request the tests required to identify the virus, and the cases are often reported as aseptic meningitis or viral encephalitis of unknown etiology.