NUTRITION to have a genetic defect in zinc absorption from the intestines . Therefore , this disease will often occur in dogs fed normal , balanced diets . Diagnosis is based on breed , physical examination and histopathology , which shows marked follicular and epidermal parakeratotic hyperkeratosis . Treatment is the addition of zinc supplement to the diet indefinitely . Zinc sulfate , zinc methionine , or zinc gluconate may all be used ; a dosage of 2-3 mg of elemental zinc / kg is recommended . Rarely , these dogs seemed to respond better if an essential fatty acid supplement is also given . A parenteral zinc preparation is available in Europe . Clinical signs usually are greatly improved within four to six weeks . Intact females may respond to lower dosages of zinc after being spayed .
Syndrome II occurs in rapidly growing puppies that are often fed poor-quality dog food or over-supplemented ( especially with calcium ) diets . These dogs are thought to have a relative zinc deficiency , possibly caused by a combination of low zinc intake and calcium or phytate ( plant protein ) binding of the zinc . Clinical signs are generalised crusting plaques with extensive crusting and fissuring of the foot pads . Diagnosis is by history , clinical signs and histopathology ( which resembles that of Syndrome I ). Response to zinc therapy is dramatic , though changing to a balanced diet may be all that is necessary . Supplementation with zinc is usually not needed after maturity .
Interestingly , zinc-responsive dermatosis has also been reported in the dingo ( Canis dingo ) and the red wolf ( Canis rufus ) .
Superficial necrolytic dermatitis
Also known as SND , hepatocutaneous syndrome , epidermal metabolic necrosis , or diabetic dermatosis , this disease is being seen with increased frequency in dogs , and has also been reported in the cat 20 and a red fox ( Vulpes vulpes ) 21 . The cutaneous lesions include crusting , erythema , exudation , and alopecia periorally and periocularly , around the genitals , and the distal extremities , as well as hyperkeratosis and ulceration of the footpads . The skin disease may precede the onset of the signs of the internal disease . Histopathologic findings include superficial perivascular-to-lichenoid dermatitis , with marked diffuse parakeratotic hyperkeratosis and striking inter-and intracellular edema limited to the upper half of the epidermis (‘ red , white and blue sign ’). 22 Diagnosis is usually made by clinical signs , confirmatory histopathology , and an ultra-sound finding of both hyper- and hypo-echoic areas in the liver (‘ Swiss-cheese ’ or ‘ honey comb ’ pattern ).
Superficial necrolytic dermatitis resembles the glucagonoma syndrome ( necrolytic migratory erythema ) of humans , which is usually associated with hyperglucagonemia and a glucagon-secreting alpha-cell neoplasm of the pancreas . Hyperglucagonemia has also been documented in dogs with this syndrome ; however , dogs tend to have hepatic parenchymal damage much more commonly than gluconomas . Dogs with SND have profoundly low levels of plasma amino acids .
Therapy is best effected with the infusion of amino acids ( Amnosyn ®) given intravenously in a central vein , at an approximate rate of 60-80 mg / kg / 24 hr . Osmalality and / or neurologic signs should be monitored ( although problems are relatively uncommon ). This is often performed on a daily basis for 2-3 days , and may need to be repeated on a 3-6 week basis . An alternative is the use of oral medications : ProCel ® Powder ( 1 scoop / 5kg q12h ; Global Health Products www . globalhp . com 1-800-638-2879 ), scrambled eggs , elemental Zn ( 2 mg / kg / day ), and sAME ( or similar liver protectants ).
When the underlying disease can be treated ( drug-induced hepatopathy , removal of glucagonoma ) and secondary skin infections ( bacterial and / or yeast ) are treated , these dogs have usually responded well for variable lengths of time , sometimes for more than one year .
FELINE PANSTEATITIS
Pansteatitis is caused by the consumption of high levels of unsaturated fatty acids and / or the insufficient intake of vitamin E , leading to inflammation of adipose tissue . This disease usually has been related to fishbased diets . However , non-conventional diets such as pig brains have also been implicated . The disease has also been reported in a lion ( Felis leo ).
Clinical signs include painful , nodular-to-irregular subcutaneous masses and draining tracts , pain on abdominal palpation ( due to involvement of the abdominal fat ), inappetence , depression and fever , though not all signs will be present in all cats . Less commonly ascites , pleural effusion , subcutaneous oedema may be present . Neutrophilia and leukocytosis are common findings . Grossly , adipose tissue may be yellow or discolored , and firm to hard ( dependent on the presence of mineraliSation ).
Histological examination shows necrosis of fat cells , severe inflammation of the interstitial tissue with neutrophils , giant cells and macrophages containing acid-fast droplets of ceroid pigment . Treatment has been reported as vitamin E ( alpha-tocopherol 50 mg / kg q24 h ), prednisolone ( 1 mg / kg q12 h ), and changing the diet to a fish-free , balanced cat food . Pain management is very important ! Even with these treatments , 25 % or more of these cats will die or be euthanased due to poor response .
References available online : www . vet360 . vetlink . co . za
Issue 03 | JUNE 2017 | 27