Diseases

Chronic Interstitial Nephritis (CIN)
Chronic Interstitial Nephritis (CIN), a progressive destruction of the tiny blood filtering units of the kidneys, is encountered in cats of all species and is somewhat insidious in nature. It often remains undetected because of the tremendous capacity of the cat's kidneys to compensate for loss of tissue until deterioration is well advanced. As long as one third of the kidney is still functional, there are usually no obvious signs of sickness. Beyond this point, illness will develop with symptoms of excessive thirst, frequent urination and loss of weight becoming evident. Vomiting may also occur. Cats with this disease become dehydrated and emaciated if not treated. Chronic interstitial nephritis is not always a death sentence. With an appropriate diet, supplementation, natural medicines and regular hydration therapy, felines may choose to continue to live a relatively normal life for many years. Of course, awareness and preventative health care is always the best treatment. Testing is possible by scan.

Feline leukaemia virus (FeLV)
Feline leukaemia virus (FeLV) infection is responsible for more deaths among cats than any other infectious disease. The virus affects domestic cats and occurs in some wild felines as well. After the initial infection, the virus replicates in the tonsils and pharyngeal lymph nodes (the pharynx is the muscular tube in the neck). Then it spreads via the bloodstream to other parts of the body, especially the lymph nodes, bone marrow, and intestinal tissue, where it continues to replicate. FeLV usually spreads through infected saliva. It can also spread through infected urine, tears, faeces, and through an infected mother to her kittens during gestation and nursing. Veterinarian researchers generally agree that FeLV cannot be transmitted to humans.

Feline immunodeficiency virus (FIV)
Feline immunodeficiency virus (FIV) causes an infectious disease in domestic cats similar to human immunodeficiency virus (HIV infection) in humans. It attacks and weakens the body's immune system, making the animal susceptible to infections and diseases that don't affect healthy cats. There is neither a cure nor a vaccine for FIV. Though eventually fatal, an FIV-positive cat can live for many years without any signs of illness. FIV is a lent virus, a virus that causes slowly developing disease. FIV is transmitted primarily through deep, penetrating bite wounds. A mother cat may transmit the virus to her newborn kittens during gestation, passage through the birth canal, or nursing. FIV can also be transmitted through the transfusion of contaminated blood. FIV affects only felines.

Glycogen storage disease type IV (GSD-IV)
GSD-IV is an inherited disorder of the Norwegian Forest Cat where an essential enzyme required to produce glucose (energy) is deficient. Afflicted kittens are usually stillborn or death within a few hours of birth, probably due to insufficient glucose available to produce energy during the birth process and the first hours of life. On rare occasions, an affected kitten will survive the neonatal period and appear normal until 5 months of age before suffering terminal neuromuscular degeneration. By eight months of age, GSD-IV results in severe muscular weakness, atrophy and contractures, and inability to use the limbs. The cat may die suddenly from heart failure. The disorder is autosomal recessive; both parents must be carriers of the trait in order for offspring to be affected. Practically, this means that, though clinically-normal, both parents of an affected kitten are obligate carriers of the trait. The parents will pass their carrier status along to 50% of all their offspring, both male and female, when mated to a non-carrier cat. When two carriers are mated, 25% of the offspring will be affected and two-thirds of the clinically-normal littermates will be carriers. Because they are clinically-normal, carriers of GSD-IV may be active breeders in a cattery, passing their carrier status along to the next generation, and never suspected until an affected kitten is born. To overcome these problems they have developed a definitive, DNA-based test. The new DNA test detects directly whether the mutation that causes GSD-IV is present in a cat's DNA.

There are three genotypes:
1. Genotype N/N (clear or homozygous normal): meaning that the cat does not carry the mutation and will not develop GSD-IV. Since it also cannot pass the mutation onto its offspring, it can be mated to any other cat.
  
2. Genotype N/GSD-IV (carrier or heterozygous): meaning that the cat has one copy of the GBE1 gene with the mutation and one copy without the mutation and will not develop GSD-IV. It can pass the mutation onto its offspring and should therefore only be mated to clear cats.
  
3. Genotype GSD-IV/ GSD-IV (homozygous affected): affected kittens have two GBE1 gene copies with the mutation. They will always pass the mutated gene onto their offspring.

Hypertrophic Cardiomyopathy (HCM)
Hypertrophic Cardiomyopathy is a terminal condition where the heart muscle enlarges and thickens progressively over time. It can be a cause of sudden death, and symptoms may be mild or nonexistent. HCM in humans, in the majority of cases, is an inherited genetic disorder, with new mutations occurring frequently. The disease is caused by mutations in several genes and passed down to offspring by autosomal dominant inheritance. "Autosomal" means that the gender of the cat is of no importance, both males and females can be affected by the disorder. "Dominant" means that if a kitten has inherited the abnormal gene from one of its parents, it will develop the disease. With a recessive inherited disorder both father and mother have to pass down the abnormality to show the disease. Any cat regardless of breed can be afflicted with the disease. No cure is known at this time. If diagnosed early, medication (to both thin the blood and retard the growth of the heart wall) can slow the process down. Late diagnosis is usually post-mortem, or when the disease has reached an acute state.

Death by HCM can occur via three mechanisms: (1) sudden cardiac death with arrhythmia and ventricular fibrillation, (2) heart failure with tachycardia, increased respiration, shortness of breath, pulmonary oedema and pleural effusion or (3) thrombus formation. Thrombi can form either in the left atrium due to abnormal blood circulation or in the heart chamber itself due to severe hypertrophy and cardiac weakness. Atrial thrombi can brake free and reach the arterial blood circuit, thereby often causing blood congestion at the branching of pelvic and crural arteries with paralysis of the hind legs.

There is now HCM research going on in several countries; so far there is one DNA test available for the MyBPC3 mutation in Maine Coons. Research in the mutation(s) in Ragdolls is still going on and there is now talk about the (suspected?) recessive form of HCM occurring in Ragdolls. In most other breeds the HCM mutations seems to be more dominant, as far as known at this date (2007). Obviously the hope exists that a single mutation is present in all cats across the world. However this seems unlikely. It is more likely that there are many different mutations present within the feline population leading to the many different manifestations of the disease. The best hope for HCM, it seems at the moment, is to diagnose animals. And don't let them breed when afflicted with HCM. When not afflicted with HCM there is however no guarantee that the cat is free from HCM until the DNA tests are available and accurate.

Testing by scan is possible from an age of 10 months, only for indication. From the age of 2 years the heart of a male is full-grown and a female the heart is full-grown with 3 years. Certitude is 80%. when the test result is negative for HCM. But when the test result is positive for HCM the certitude is 100% . Equivocal means that anomalies have been observed but at the time of the testing, it is not clear what those anomalies mean or will mean. Not every cat who is assessed as equivocal, will develop HCM. On the other hand, the possibility does exist. 

* More about the HCM Screening Form, what it says and what it means.
* More about recommendations for testing and breeding.
* More about the progress of DNA testing (at moment of writing only progress in Maine  Coon and Ragdolls research).
* HCM DNA Research Project Norwegian Forest Cat: To foster awareness and encourage screening for HCM and support research directed towards finding a DNA test.
* Send in your sample for DNA research of the Norwegian Forest Cat, when scanned normal
* Send in your sample for DNA research of the Norwegian Forest Cat, when scanned positive

Patellar luxations (PL)
Patellar luxations (dislocation of the knee-cap) occur frequently in dogs and rarely in cats. Patellar luxations can be grouped into two main categories. First, and most commonly, is Medially Luxating Patellas (MLP) which are congenital (existing from birth) and commonly affect cats and smaller breed of dogs. The second type is Laterally Luxating Patellas (LLP) which are often the result of trauma and can affect any pet. Lameness occurs as the patella luxates and often resolves when it spontaneously reduces. Lameness is often intern-intermittent and animals will learn to reduce the patella themselves by extending the hip and the knee together behind them. Diagnosis is made on physical examination and may be confirmed with radiographs. Radiographs will demonstrate the patella luxation if the patella is dislocated -at the time the radiographs are taken. All animals with patellar luxation can develop some degree of arthritis.

The patella normally moves up and down in a groove in the lower femur bone called the trochlear groove. In patella luxation the groove is often shallow. This shallow groove prevents the patella from seating deeply and predisposes it to dislocation. This results in the luxation of the patella as the leg is used. The quadriceps or extensor muscles of the leg are associated with the patella. In patellar luxation, the extensor muscles are often maligned to the inside or outside of the leg, The degree of patella luxation is graded from I to IV depending on the relative ease with which the patella luxates. Grade I is the mildest and grade IV the most severe. Grade I and II patellar luxations may be completely asymptomatic and may be incidental findings is mature dogs and cats who have never been lame. Grade III and IV MLP patients are usually lame. Severe cases may develop abnormal growth of the long bones of the leg or a non-functional knee.

Patellar luxation is diagnosed based upon history, physical exam findings and radiographs.
Medially Luxating Patellas (MLP) is a heritable disease and breeding with affected cats is not recommend.
Note: Cats should not be tested under the age of 2, under this age the cat can be permanently injured during the investigation.

Polycystic kidney disease (PKD)
Polycystic kidney disease is an inherited disease where cysts are present on the kidney from birth and usually present on both kidneys. These cysts are progressively destroying the organ and causing terminal renal failure. The cysts are cavities filled with fluids that originate from normal kidney tissue. In kittens these cavities are in the majority of cases very small (1 to 2 mm). As the animal matures these cavities will become larger (even larger than 2 cm). In one kidney there can be as many as 20 to 200 cysts present. Ultrasound can detect PKD as early as 10 months of age and is 98% accurate; a DNA test has been developed for cats stemming from Persian/Exotic lines, but the disease has been seen in other breeds and non-pedigreed cats. With an adapted treatment the animals afflicted with PKD can still reach a high age. Not all cats with PKD will develop kidney failure. Animals with very little or very small cysts will probably never show any signs of PKD. PKD is inherited in an autosomal dominant way. "Autosomal" means that the gender of the cat is of no importance, both males and females can be affected by the disorder. "Dominant" means that if a kitten has inherited the abnormal gene from one of its parents, it will develop the disease. With a recessive inherited disorder both father and mother have to pass down the abnormality to show the disease. Testing is possible from the age of 10 months, certitude is 98%.