White Locket Example
Liberty Bengals routinely tests for:
PRA-b (Bengal Blindness)
PK Deficiency (Hemolytic Anemia)
PKD1 (Polycystic Kidney Disease)
HCM (Hypertrophic Cardiomyopathy - Heart Disease)
FIV (Feline Immunodeficiency)
FeLV (Feline Leukemia Virus)
Current Random Fecal PCR Test: CLICK HERE
The old saying you get what you pay for holds true especially in the realm of Bengals. Breeding is expensive and when done properly there truly isn't much profit, in fact we have yet to profit which we're proud to admit. The very first set of health tests and screening for each breeding pair easily starts at $1000 and up, but the reassurance is priceless when it prevents future heart ache in their offspring. We hope as you visit our website you see the passion and commitment we have to every life within our home that we consider a serious hobby and deeply enjoy. As you visit other breeders write down a check list and questions you may have. Your breeder should be like a funnel, filtering out diseases in the parents before they get passed onto offspring and able to assist you with providing proof and feedback. The last thing you want is to invest yourself into a kitten that will fail to even reach adulthood due to a lack of preventive measures that is considered a standard among all ethical breeders.
PRA-b - Bengal Progressive Retinal Atrophy
PRA-b causes an autosomal recessive blindness in Bengal cats. The disease causes the destruction of the cells that register light (photoreceptors) in the back of the eye (the retina). The loss of the cells begins around 7 weeks of age and slowly progresses until the cat has very compromised vision by approximately 2 years of age. The mutant DNA variant appears to be novel to the Bengal breed and occurred early in a popular lineage of the Bengals. Two copies of the mutant DNA variant are required for the cats to be blind, if only one parent is a carrier the offspring will not be effected. The blindness can be detected either by the DNA test or by an eye exam prior breeding age. Carriers, cats with one copy of the mutation, can only be detected by the DNA test.
PK Deficiency - Erythrocyte Pyruvate Kinase Deficiency
Erythrocyte Pyruvate Kinase Deficiency (PK Deficiency) is an inherited hemolytic anemia caused by insufficient activity of this regulatory enzyme which results in instability and loss of red blood cells. The anemia is intermittent, the age of onset is variable and clinical signs are also variable. Symptoms of this anemia can include: severe lethargy, weakness, weight loss, jaundice, and abdominal enlargement. This condition is inherited as an autosomal recessive. Two copies of the mutant DNA variant are required for the cats to develop this disease, if only one parent is a carrier the offspring will not be effected.
PKD1 - Polycstic Kidney Disease
Polycystic Kidney Disease (PKD1) is a well documented abnormality in domestic cats. Cystic kidneys can sporadically occur in any population of cats. PKD1 is not a new disease and has been reported in the literature for over 30 years. The heritable form of PKD1 may not have initially occurred in Persians as a new mutation, but perhaps in random bred cats. Unfortunately, PKD1 does not have a strong clinical presentation. The presentation of PKD1 is similar to one of the most common causes of death for any cat, renal failure. Thus, PKD1 has gone unnoticed for many years and has spread throughout the Persian breed. Any breed that has used Persians in their foundation or propagation should have concerns for PKD1.
In Persians, the condition has been shown to be inherited as a single autosomal dominant gene. It is estimated over 37% of Persians have PKD1, a breed that accounts for nearly 80% of the cat fancy. Many lines and catteries have been able to greatly reduce this frequency by using ultrasound screening methods and improved breeding practices. Early onset, bilateral presentation (both kidneys), and multiple cysts are all traits of the heritable form of the disease. The kidney cysts for PKD1 present early, often before 12 months of age. Renal failure, however, usually occurs at a later age. Thus, PKD1 is considered a late onset renal disease. In the fancy cat breeds, PKD1 is inherited as an autosomal dominant condition. This implies that one copy of the gene is required to produce PKD1. Generally, 50% of PKD1 positive cats' offspring will inherit PKD1.
HCM - Hypertrophic Cardiomyopathy
Hypertrophic Cardiomyopathy is the most common cardiac disease in cats. HCM is thickening of the wall of the left ventricle. Severe thickening results in scar tissue formation. The thickening and scar tissue make it difficult for the left ventricle to relax. If severe, this can result in heart failure, the accumulation of fluid in or around the lungs. This fluid accumulation, when severe, results in rapid and difficult breathing. The left atrium (*the chamber behind the left ventricle) enlarges also in cats whose left ventricle cannot relax properly. This enlargement causes blood flow through this chamber to slow and so blood to sludge, predisposing to clot formation. When a clot breaks loose from its attachment in the left atrium, it travels down the aorta to the rear legs, blocking blood flow and causing the sudden onset of paralysis and severe pain (so-called saddle thromboembolus). The scar tissue can also predispose to abnormal electrical activity in the left ventricle which is manifested as an arrhythmia. The arrhythmia that is seen is thought to predispose cats with HCM to sudden death. So cats with severe HCM can develop heart failure, die suddenly or experience the pain of a saddle thromboembolus. There is no genetic test available to detect it in Bengals, as breeders our only option is to have a board certified cardiologist perform an echocardiogram on each breeder every 1-2 years screen for it's current function and measurements.
FIV - Feline Immunodeficiency Virus
Cats infected with feline immunodeficiency virus (FIV) may not show symptoms until years after the initial infection occurred. Although the virus is slow-acting, a cat’s immune system is severely weakened once the disease takes hold. This makes the cat susceptible to various secondary infections. Infected cats receiving supportive medical care and kept in a stress-free, indoor environment can live relatively comfortable lives for months to years before the disease reaches its chronic stages.
FeLV - Feline Leukemia Virus
First discovered in the 1960s, feline leukemia virus is a transmittable RNA retrovirus that can severely inhibit a cat’s immune system. It is one of the most commonly diagnosed causes of disease and death in domestic cats. FeLV weakens an animal’s immune system and predisposes cats to a variety of infections and diseases, including anemia, kidney disease and lymphosarcoma, a highly malignant and fatal cancer of the lymph system. Sadly there is no cure for FeLV, and it is estimated that less than 20% of clinically infected cats survive more than three years of active infection. In the case of those cats who develop cancer, chemotherapy can help prolong life, but treatment often focuses on providing the best quality of life.
FIP - Feline Infectious Peritonitis
Feline infectious peritonitis (FIP) is a viral disease of cats caused by certain strains of a virus called the feline coronavirus. Most strains of feline coronavirus are avirulent, which means that they do not cause disease, and are referred to as feline enteric coronavirus. Cats infected with a feline coronavirus generally do not show any symptoms during the initial viral infection, and an immune response occurs with the development of antiviral antibodies. In a small percent of infected cats (5 to 10 percent), either by a mutation of the virus or by an aberration of the immune response, the infection progresses into clinical FIP. The virus is then referred to as feline infectious peritonitis virus (FIPV). With the assistance of the antibodies that are supposed to protect the cat, white blood cells are infected with the virus, and these cells then transport the virus throughout the cat's body. An intense inflammatory reaction occurs around vessels in the tissues where these infected cells locate, often in the abdomen, kidney, or brain. It is this interaction between the body's own immune system and the virus that is responsible for the disease. Once a cat develops clinical FIP involving one or many systems of the cat's body, the disease is progressive and is almost always fatal. The way clinical FIP develops as an immune-mediated disease is unique, unlike any other viral disease of animals or humans.
One of the most difficult aspects of FIP is that there is no simple diagnostic test. The ELISA, IFA, and virus-neutralization tests detect the presence of coronavirus antibodies in a cat, but these tests cannot differentiate between the various strains of feline coronavirus. A positive result means only that the cat has had a prior exposure to coronavirus, but not necessarily one that causes FIP. To date, there is no way to screen healthy cats for the risk of developing FIP, and the only way to definitively diagnose FIP is by biopsy, or examination of tissues at autopsy. Generally, veterinarians may rely on a presumptive diagnosis, which can be made with a relatively high degree of confidence by evaluation of the cat's history, presenting symptoms, examination of fluid if it is present, and the results of supporting laboratory tests including a positive coronavirus antibody titer.
There is no known cure or effective treatment for FIP at this time. Some treatments may induce short-term remissions in a small percentage of cats; however, FIP is a fatal disease. Treatment is generally aimed at supportive care, such as good nursing care and nutrition, and alleviating the inflammatory response of the disease. Cats with FIP are often treated with corticosteroids, cytotoxic drugs, and antibiotics. Supportive care may also include fluid therapy, draining accumulated fluids, and blood transfusions.
Research is ongoing to find other immunosuppressive drugs that may slow down the progress of the disease. Attempts are also being made to find antiviral drugs that will prevent or slow down the replication of the virus. One promising approach currently being studied combines both an antiviral agent and an immune response modifier.
Valuable Vaccine Information: http://traditionalcats.com/education/medical/currentvaxrecs081706.pdf