Hypertrophied Heart (HCM)
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)
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. Each breeding pair with proper breeding rights, health screening, with showing confirmation easily starts at $10,000+, 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.
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. Article on HCM: https://www.winnfelinefoundation.org/docs/default-source/cat-health-library-educational-articles/hypertrophic-cardiomyopathy-for-breeders.pdf?sfvrsn=2&fbclid=IwAR3xafKxoQujiQXbnCiPCkNOGNAdVzcAdlgvdSMCVRM3dIiOJxOLFZ9YRFg
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.
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
Dr. Pedersen has studied FIP for the past 55 years and was at Cornell University in July 2019 for the Fred Scott Symposium. I am honored to share that Liberty Bengals was chosen by The International Feline Foundation (TIFF) to be a recipient for the Jean Mill Scholarship where we were sponsored to attend Dr. Pedersen's presentation. Below you will find an attachment PDF of our notes and report of such an informative event: Coronavirus Explained - PDF