The confirming diagnosis remains culturing the fungus from the skin, sputum, synovial fluid, and cerebrospinal fluid. Smears should be taken from the draining tracts and ulcers. Cats with sporotrichosis are unique in that the exudate from their lesions may contain numerous organisms. This makes cytological evaluation of exudate a valuable diagnostic tool in this species. Exudate is pyogranulomatous and phagocytic cells may be packed with yeast forms. These are variable in size, but many are cigar-shaped. Differential diagnosis
Differential diagnosis includes: leishmaniasis, nocardiosis, mycobacterium marinum, cat-scratch disease, leprosy, syphilis, sarcoidosis and tuberculosis. Prevention
The majority of sporotrichosis cases occur when the fungus is introduced through a cut or puncture in the skin while handling vegetation containing the fungal spores. Prevention of this disease includes wearing long sleeves and gloves while working with soil, hay bales, rose bushes, pine seedlings, and sphagnum moss. The risk of sporotrichosis in cats is increased in male cats that roam outdoors. Accordingly, the risk may be reduced by keeping cats indoors or neutering them. Isolating infected animals can also be a preventive measure. The risk of spread from infected cats to humans can be reduced by appropriate biosafety measures, including wearing protective equipment when handling a cat with suspected sporotrichosis and by washing hands, arms and clothing after handling the cat. Treatment
Treatment of sporotrichosis depends on the severity and location of the disease. The following are treatment options for this condition:
Oral potassium iodidePotassium iodide is an anti-fungal drug that is widely used as a treatment for cutaneous sporotrichosis.
Carnitine palmitoyltransferase I deficiency is a rare metabolic disorder that prevents the body from converting certain fats called long-chain fatty acids into energy, particularly during periods without food. It is caused by a mutation in CPT1A on chromosome 11.Carnitine, a natural substance acquired mostly through the diet, is used by cells to process fats and produce energy. People with this disorder have a faulty enzyme, carnitine palmitoyltransferase I, that prevents these long-chain fatty acids from being transported into the mitochondria to be broken down. Symptoms and signs
Signs and symptoms of this disorder include low levels of ketones (hypoketosis) and low blood sugar (hypoglycemia). Together these signs are called hypoketotic hypoglycemia. People with this disorder typically also have an enlarged liver (hepatomegaly), muscle weakness, and elevated levels of carnitine in the blood. Genetics
Mutations in the CPT1A gene cause carnitine palmitoyltransferase I deficiency by producing a defective version of an enzyme called carnitine palmitoyltransferase I. Without this enzyme, long-chain fatty acids from food and fats stored in the body cannot be transported into mitochondria to be broken down and processed. As a result, excessive levels of long-chain fatty acids may more rapidly build up in tissues, damaging the liver, heart and/or brain. This condition has an autosomal recessive inheritance pattern, which means the defective gene must be inherited from both parents.