History and Physical Examination
A 1-year-old male German shepherd dog is presented for failure to grow. The dog is alert and active and about the size of 4- to 5-month-old German shepherd puppy. The coat is soft and wooly and epilates easily. Some adult teeth have not yet erupted.
Following the problem-oriented format, write an initial plan for this dog.
Retarded growth is failure to attain the weight and/or height standards, characteristic of a given breed of dog or cat. The problem is more difficult to define in mongrels, since absolute standards are not available to guide evaluation. Standards for the various breeds of dogs are available from the American Kennel Club. Canine and feline growth charts have been published elsewhere (Kirk and Bistner 1985).
Dwarfism is marked under development of the body. It is one cause of retarded growth; however, not all small-sized animals are true dwarfs.
Normal growth is a critical balance of proper nutrition, oxygen, hormonal interactions, and genetic influences that control cell division and growth.
The genetic information that ultimately controls cell division and growth is primarily contained in the sex chromosomes, although the autosomes probably contribute to growth regulation. In humans, it is known that the genes that allow normal growth are contained in the X chromosome. In addition, the Y chromosome also contains growth-promoting genes. The greater size of male animals is probably explained by this mechanism. If the number of Y chromosomes is increased, as in XYY individuals, greater than normal stature is encountered, whereas retarded growth occurs in XO individuals.
Growth of the fetus is dependent on maternal health and nutrition and the ability of the placenta to transfer necessary nutrients to the developing fetus. Placental size and function may be directly related to the size and weight of newborns. So-called runts may never achieve normal size, since very little makeup growth occurs after birth.
Hormonal abnormalities during fetal life appear to exert relatively little influence on somatic growth. Fetal growth is not appreciably impaired by failure of the fetal thyroid, and animals with congenital hormone deficiencies have normal birth weights.
Normal growth is dependent on the secretion and interaction of several key hormones. In addition, adequate nutrition, including calories, protein, essential fatty acids, mineral (especially zinc and calcium), and vitamins (especially vitamin A), is necessary for maximum growth. Deficiency of growth-promoting hormones, malnutrition, and metabolic diseases are the most common causes of retarded growth.
Hormonal Regulation of Growth
The most commonly recognized hormonal regulator of growth is growth hormone (GH), or somatotropin. This polypeptide hormone of pituitary origin has both catabolic and anabolic effects. The catabolic effects (lipolysis, restricted glucose transport) are directly induced by the hormone, whereas the growth-promoting effects are mediated by insulin-like growth factors (IGF-I), or somatomedins (Eigenmann 1985).
Studies in German shepherd dwarf dogs have shown that both GH and IGF levels are extremely low compared to those in normal dogs. In addition, the IGF-I levels in these dogs appear to be subject to the control by GH (Eigenmann et al. 1984c). In dogs there is a parallel relationship between body size and plasma IGF-I levels (Eigenmann et al. 1984b). Larger dog breeds have the highest IGF-I levels, which progressively decrease in smaller breeds. There is little difference in plasma GH levels across the various breeds, regardless of size. In a study of the poodle breed, the small stature of the toy poodle was clearly associated with lower concentrations of IGF-I and the larger stature of the standard poodle with higher concentrations of IGF-I, even though GH levels were remarkably similar (Eigenmann 1984a).
Although GH deficiency results in retarded growth, a deficiency of IGF-I may also cause this problem. Since IGF-I is largely made in the liver, any serious liver problem (such as portosystemic shunts) during growth may result in small stature.
Thyroxine is a general stimulator of cellular metabolism and IGF-I activity. It has a strong positive effect on growth. Hypothyroidism that occurs in the neonatal or juvenile animal results in severe growth suppression and slow cerebral development.
Insulin enhances IGF-I production. Small stature (retarded growth) is common in dogs with congenital diabetes mellitus (keeshond, golden retriever).
One of the most common causes of retarded growth is malnutrition resulting from dietary deficiency or severe gastrointestinal parasitism. When these problems are severe or prolonged, reduced growth may never be totally made up during the catch-up growth phase that occurs once normal nutrition is established. Deficiencies of vitamin A almost always cause growth retardation. Initially, deficiency of vitamin D does not slow growth; however, the resulting abnormalities in bone metabolism and bone growth may cause severe growth suppression. The mechanism by which zinc deficiency causes growth suppression is unknown.
Animals with congenital heart defects or chronic progressive lung disease grow slowly and often fail to develop normal size. A deficiency of tissue oxygenation is the primary mechanism.
Disease of the digestive system that results in maldigestion or malabsorption of nutrients may cause severe growth retardation. Pancreatic insufficiency in dogs may occur prior to puberty and may result in severe growth retardation. The syndrome known as juvenile pancreatic atrophy occurs in large breeds such as the German shepherd and Great Dane. Congenital megaesophagus may also cause retarded growth.
The most common metabolic causes of retarded growth are liver disease and kidney failure. Severe liver disease due to portosystemic shunts, copper intoxication (Wilson’s syndrome), or infection such as feline infectious peritonitis virus is a common cause of retarded growth. Congenital renal diseases such as polycystic kidneys and progressive renal failure of Lhasa Apso and Norwegian elkhounds cause severe growth reduction. Although growth reduction occurs in these diseases, more specific signs are likely to be present.
|A. Abnormal endocrine regulation|
|1. Growth hormone deficiency—pituitary dwarfism (German shepherd)|
|2. Congenital hypothyroidism|
|3. Diabetes mellitus—Rottweiler, golden retriever, and keeshond|
|B. Genetic disorders of bone and cartilage|
|1. Chondrodysplasia—chondrodysplastic dwarfs (Alaskan malamutes)|
|2. Mucopolysaccharidiosis—Siamese cats|
|3. Achondroplasia—basset hound, collie, miniature poodle, and Scottish terrier|
|C. Nutritional deficiencies|
|1. Major nutrients—protein (essential amino acids), fats, carbohydrates|
|2. Minerals—zinc and calcium|
|. Vitamins A and D|
|4. Oxygen—congenital heart disease (developmental defects) and chronic lung disease (as in “swimming puppies”)|
|D. Congenital (inherited) disorders of cell metabolism|
|1. Lysosomal storage diseases|
|2. Glycogen storage diseases|
|E. Chronic inflammation, infection, and parasitism|
|1. Immunodeficiency diseases|
|2. Intestinal parasitism|
|F. Congenital or acquired major organ failure|
|1. Congenital heart failure due to developmental defects|
|2. Congenital pancreatic atrophy|
|3. Hepatic failure—portosystemic shunts|
|4. Renal failure|
|a. Familial progressive renal insufficiency (Lhasa Apso, shih tzu, Norwegian elkhounds)|
|b. Canine Fanconi syndrome (Basenjis)|
|c. Congenital polycystic kidneys (Persian cats)|