Ocular Surface Disease in Rodents (Guinea Pigs, Mice, Rats, Chinchillas).

This article discusses the clinical appearance, differential diagnoses, and treatment considerations of corneal disease in the most common domesticated species of rodent: mouse, rat, chinchilla, and guinea pig. Many corneal diseases are related to inbred strains of either research or pet rodents. Diseases are complicated by husbandry and treatment-related challenges in this small, social species. This article is broken down by species, first discussing normal anatomy, then discussing commonly encountered diseases, and concluding with treatment considerations.

Vitamin C Depletion in Prenatal Guinea Pigs as a Model of Lissencephaly Type II.

Humans and guinea pigs are unable to produce vitamin C, with deficiency resulting in a well-known disorder of collagen synthesis. Pial basement membrane structure preservation is essential in the proper migration of neurons. In our study, intrauterine deprivation of vitamin C in guinea pig fetuses led to a collagen synthesis disorder, weakness, and finally a breach of pial basement membrane. We found excessive migration of the external germinal layer cells into the subarachnoid space of the cerebellum through defects in the pial basement membrane. The changes ranged from focal rupture of pial basement membranes to their complete disintegration. The loss of proper folia formation resulted in macroscopically visible flattening of the cerebellar surface. Different grades of dysplastic changes in the folia of the cerebellar cortex were observed in 2 experimental groups assigned different limits to mark the time of commencement and duration of vitamin C deprivation. The most severe form of dysplastic changes was characterized by marked irregularity of the cerebellar cortex similar to that in lissencephaly type II. Thus, prenatal vitamin C deficiency represents a novel animal model to study the effects of collagen synthesis on development of breaches in the pial basement membrane, disordered migration of neurons, dysplasia of cerebellar cortex, and the pathogenesis of lissencephaly.

Scurvy in capybaras bred in captivity in Argentine.

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.

Transgenic expression of L-gulono-gamma-lactone oxidase in medaka (Oryzias latipes), a teleost fish that lacks this enzyme necessary for L-ascorbic acid biosynthesis.

Transfer of the gene for L-gulono-gamma-lactone oxidase, the missing enzyme in L-ascorbic acid biosynthesis in scurvy-prone animals, into medaka (Oryzias latipes) was successfully done. The expression plasmid pSVL-GLO, carrying rat liver L-gulono-gamma-lactone oxidase cDNA, was microinjected into the cytoplasm of fertilized eggs during the one-cell stage. Four male F0 fish having the transgene in their germ cells came to maturity, and F1 progeny derived from one of the F0 fish possessed L-gulono-gamma-lactone oxidase activity, indicating that the transgene was functionally expressed in the fish. Genomic Southern blot analysis demonstrated that the transgene existed in both chromosome-integrated and extrachromosomal forms.

L-ascorbyl-2-sulfate alleviates Atlantic salmon scurvy.

Duplicate lots of 150 Atlantic salmon (Salmo salar), average weight 0.5 g, were fed NRC diet H-440 base containing L-ascorbic acid (C1) or L-ascorbyl-2-sulfate (C2S); or L-ascorbyl-2-monophosphate (C2MP): at 0 or 100 mg C1; 50, 100, 300 mg C2S; or 50, 100 mg C2MP per kg dry diet in 12 degrees C freshwater tanks. After 12 weeks, negative controls (no vitamin C) exhibited reduced growth, scoliosis, lordosis, and petechial hemorrhages typical of fish scurvy. All other lots grew normally. Four 100-fish lots of scorbutic salmon, average weight 3.3 g, were placed on recovery diets of 0, 50, or 300 mg C2S, or 100 mg C2MP per kg dry diet. After 5 weeks, fish fed either level of C2S intake had recovered and resumed growth. Negative controls continued to develop acute scurvy. The 41 survivors in this no-vitamin-C group all had advanced scurvy, whereas all fish in both C2S-fed recovery groups appeared normal. Tissue assays for C vitamers disclosed normal levels of C1 and C2S in the recovery groups. All other test treatment lots containing C1, C2S, or C2MP had fish with normal appearance and no significant differences in growth response for the 17-week test period. C2S at 50 mg or more per kg diet as the sole vitamin C source promoted normal growth in young Atlantic salmon for more than 20-fold increase in weight.

Subclinical scurvy in the guinea pig.

Twenty-eight guinea pigs from nine episodes of subclinical scurvy had diarrhea, weight loss and dehydration. The classical signs of scurvy were not seen. Microscopically the epiphyses were attenutated and irregular. The amount of osteoid was less than normal. Many guinea pigs had acute enteritis. In some there were many hemosiderin-laden macrophages in the intestinal lamina propria. All episodes were associated with either autoclaving food without adequate supplementation or other inadequate feed management practices.

Diseases of guinea-pigs.

Information on diseases of guinea-pigs is generally available in research institutes and breeding establishments. When dealing with an individual patient it is tempting to extrapolate from this pool of information, without realising that a number of factors can affect the disease situation in a colony which need not apply to the individual animal kept as a pet--or vice versa. Thus diseases may appear as an explosive outbreak in a group of cavies kept under uniform conditions while a single animal may be exposed to amateur management (Townsend 1975) and suffer in consequence. The diseases generally encountered in this species are dealt with here as they appear clinically.

A survey of laboratory animal disease in Kenya.

Diseases and infections diagnosed in laboratory mice, rats, guinea-pigs, golden hamsters and rabbits at the Veterinary Research Laboratory, Kabete, Kenya, are listed and discussed. Zoonoses encountered included salmonellosis and lymphocytic choriomeningitis. A number of traditionally recognised conditions were recorded but there were some notable omissions. The changing picture in laboratory animal science in East Africa is outlined and attention is drawn to the need for work on related diseases and infections.