Cat Dilated Cardiomyopathy and Immune Mediated Hemolytic Anemia in Daschunds - Research Paper Example

FELINE DILATED CARDIOMYOPATHY INTRODUCTION Dilated cardiomyopathy (DCM) is a cardiac disease characterized by dilation of heart chambers, unusual enlargement and significantly diminished contraction. The left ventricle is typically implicated in the pathology. As the disease progresses, advanced cases present with the dilation of all heart chambers. Fluid build-up may occur in body cavities, as well as clot formation in blood vessels. (Hill's Pet Nutrition, 2011) With the increased captivity and disposal resources available to pet owners and thus their pets, there are decreased opportunities for cats to receive necessary nutrients from native food sources. An increased dependency on formulated cat foods produces the potential for deficiency; but the same formulations allow for the correction of this lack. Total Nutrient programs from the pet food industry are the response to this valid concern. Vision loss, as well as cardiomyopathy can result from such dietary deficiencies. (Hayes et al. 1982), (Hill's Pet Nutrition, 2011) PURPOSE This report outlines the pathology of feline dilated cardiomyopathy and related heart conditions, as well as contributing factors. The prognosis and treatment modalities are discussed; as well as means by which this condition can be prevented. CLINICAL REVIEW Cats do not possess the ability to synthesize the amino acid Taurine; which is necessary for muscle growth; and proper retinal development in kittens. This is presumed to be a central factor in the evolutionary development of felines. Modern processed cat food contains nutritional supplements to alleviate this problem. LITERATURE REVIEW Feline DCM's now relatively rare. In the past, feline dilated cardiomyopathy could be blamed on dietary deficiency in the amino acid taurine. (Petplace Veterinarians, 2011), (Pion, et al. 1987) Taurine is an essential component of the feline diet, whereas dogs do not require it. (Pion et al. 2007) The breeds typically affected are Abyssinian, Burmese, Siamese, and mixed/mongrel housecats. The Cat food industry responds to this risk by taking steps to ensure taurine dietary supplements are included as basic nutrition in most cat foods. The feline food industry has risen to the challenge of addressing the need of nutritional supplements in a form highly palatable to the animals. At the same time, the more sedentary lifestyles that felines and canines now share with their human owners still creates its own battery of assorted health risks to all three species. (Obesity being a noteworthy factor.) In terms of diagnosis, a complete medical history should be provided to the veterinary professional. Initially, a thorough physical examination is performed. Special emphasis is paid to auscultation of the heart for obvious reasons. Heart murmurs, irregular sounds, and irregular heart rhythms are indicative of cardiac pathologies. For treatment, it is important to delineate between related conditions; such as hypertrophic cardiomyopathies. An enlargement of all four heart chambers is diagnostic when associated with fluid buildup, thin ventricular walls, and a diminished ability to contract. (Hill's Pet Nutrition, 2011) Further Laboratory tests are still needed to confirm the diagnosis to the exclusion of similar conditions. The progression of the disease must be determined before treatment can be prescribed. Investigations of dozens of felines with dilated cardiomyopathy revealed a 25% decrease in taurine levels compared to normal cat plasma. (Pion et al. 1987) Signs of cardiac failure in the cats were rectified efficiently (within 5 weeks) with supplements of 0.5 grams taurine in conjunction with captopril and furosemide. After 5 weeks the secondary supplements could be discontinued; though the felines will require taurine on an ongoing basis. Drug treatment can prove a challenge, as the administration of calcium channel blockers, β-adrenergic blockers, or angiotensin-converting enzyme inhibitors yields insufficient effects on disease outcome/survival for other feline cardiomyopathies. The data suggests that the majority of cases of feline dilated cardiomyopathy can be clinically resolved if the underlying predilections for general heart failure can be controlled for up to four weeks with cardiotonic drugs while blood-plasma and tissue levels of taurine are augmented with the therapy. Cats need a significant taurine receptacle, for the purpose of conjugation of bile acid in the liver. (Hayes et al. 1982) Taurine is a necessity in this process in cats; whereas dogs - including Dachsunds utilize glycine rather than taurine. (Pion et al. 1987) DISCUSSION Taurine is necessary for felines due to a variety of other health reasons; as deficiencies can lead to central retinal degeneration among other conditions. (Bellhorn et al. 1974) Taurine is an essential amino acid, with a sulfonic acid moiety replacing the usual carboxylic acid structure that would be found in glycine. It originates within mammalian metabolism through the breakdown and conversion of methionine into cystine and then eventually to taurine. This occurs as a result of the normal process of sulfur amino acid digestion and metabolism. This function appears to be exclusive to the animal kingdom. (Hayes, 1982) Not all animals are capable of the production of this amino acid to the same degree. Taurine, due to its sulfur-based functional group has a diminished capacity to incorporate itself into proteins; it is rarely a part of any link of carbon-based repeating structures. While taurine originates in the animal kingdom certain animals must attain sources of free taurine in their diet. Felines in particular. Most other mammals do appear capable of this synthesis however, (Hayes & Sturman, 1982) requiring special care in the dietary considerations of the felines. For many decades it has been established from dietary studies that kittens will suffer eye lesions leading to blindness if fed a diet without this supplementation. (Scott et al. 1964) these defects were noted earlier, but were mistakenly thought to be the result of congenital illnesses. This deficiency follows the exhaustion of the taurine supply in the blood plasma. (Hayes et al. 1975) While the developmental consequences can appear early in the cat's life, some source of taurine is essential for felines throughout their lives in order to avoid other conditions, such as heart related myopathies. Feline dependency on taurine is likely a phylogenetic artifact of their carnivory. In that an interrelationship likely exists between feline inability to synthesize this amino acid, and the fact that many carnivores can receive amino acid supplementation by devouring prey animals. One might suppose that mutations leading to this condition contributed to the evolution of the feline as a strict meat eater. Other mammals have the ability to store taurine in their tissues. Where, as mentioned above it is useful for bile acid conjugation, but also for the growth of muscle mass. For many decades, it has been observed that, in the developing kitten, there exists the perfect storm of rapid growth and muscular expansion combined with low taurine synthesis as a result of high levels of amino acid secretion in cat urine. (Avizonis and Wriston, 1959), (Rabin et al. 1976) Cardiac tissue of course, is largely composed of specialized muscle – and thus it is not difficult to imagine how insufficient taurine, even in a fully developed cat could lead to cardiac myopathies. SUMMARY Cats need to eat prey animals due to an inability to generate and store the amino acid taurine in their tissues. This leads to heart-disease; (cardiomyopathies) if the substance is not regularly included in the feline diet. The rapid muscle growth of kittens compared with other mammals creates a strong demand for taurine; making it an essential supplement in the feline diet. There is little that can be done should the cat suffer this insufficiency early in life; but cat food companies supply taurine in their products to maintain the health of adult cats. IMMUNE MEDIATED HEMOLYTIC ANEMIA IN DACHSUNDS INTRODUCTION Also known as IMHA, immune mediated hemolytic anemia is a condition in which the immune system of the dog in this case, mistakenly identifies its own red blood cells as a foreign invader. Thus antibodies will attach to the surface of red blood cells, on the cellular level this will allow for the implementation of the complement cascade a process by which the antibodies serve as the framework for the assembly of a protein apparatus that functions as a molecular drill, a 26 protein microscopic construct that will perforate the surface of the cell membrane. (Fix, 2011) Usually this process occurs with bacteria, in which case the cell wall of the invader will be punctured dozens of times, causing the internal fluid (cytoplasm) to bleed out, resulting in the death of the bacterial invader. Complement has many functions, but it operates under three activation pathways when the adaptive immune system passes chemical signals that activate the cascade. (Janeway, 2001) The dog's health is seriously threatened when this process becomes activated against the animals own blood cells. (Erythrocytes) Red blood cells have a finite life span, within roughly 120 days after their emergence from the bone marrow they are recycled within the spleen. (Pierigè et al. 2008) The liver receives iron from the recycled hemoglobin in the form of the yellow pigment known as Bilirubin. In addition, surface proteins upon red blood cells can be interpreted by the immune system to determine the viability of that red blood cell. Cells reporting viral infection, or exhibiting signs of cancerous growth will be slated for destruction by white blood cells. In this manner, older or defective red cells are removed from circulation. Anemia results when it too many cells are marked as cancerous or co-opted by viral invaders, (Brooks, 2011) or in some cases the cells may be actually mis-identified as invaders themselves. PURPOSE This article describes hemolytic anemia in canines. (dachsunds) Describing the pathology of the illness, and the limited treatment options. The deviations in the proper functioning of the immune system leading to this condition are examined. CLINICAL REVIEW The causes of hemolytic anemias are not always apparent. It is auto-immune mediated destruction of red blood cells; and can be distinguished from anemia due to bleeding from a jaundiced condition, rather than a pale complexion. A complete cure is unlikely; but the symptoms can be moderated with drugs, and blood substitutes. LITERATURE REVIEW When white blood cells Mark read this for destruction and recycling, the process is known as extravascular hemolysis. When misfiring complement components attracted by antibodies trigger the perforation and destruction of red blood cells, as if they were a pathogen – it is known as intravascular hemolysis. The normal fluids within the cell, including bilirubin can increase during intravascular hemolysis, and will lead to a jaundiced appearance in the animal. Upon yellowish or yellow-tinged presentation, the veterinarian should order blood tests; anemic blood serum will appear bright orange; rather than a pale near-yellow. (Brooks, 2011) As the process continues; anemia results in that there will be insufficient cells to transport nutrients, oxygen - and to eliminate carbon dioxide byproducts of cellular respiration. The Dachsund, or any mammal will experience fatigue, and discoloration. In the case of actual bleeding, the mammal will typically appear pale, from the loss of overall blood volume. But a hemolytic anemia will result in a more yellowish tinge due to the leakage of cellular contents. (Brooks, 2011) DISCUSSION The causes of IMHA, in humans or dachsunds are less clear; an actual triggering agent for an autoimmune condition may prove elusive in many cases. Some possibilities include severe viral infection; should a pathogen be able to partially mimic the surface antigens of a host cell as a defensive mechanism, then the eventual defeat of the infection may lead to the production of antibodies with cross-reactivity with the bodies' own tissues. Genetic predisposition may be a factor; especially disorders affecting red blood cells, in the case of canine IMHA. Other diseases, such as hormonal disorders may include autoimmune diseases as a complication. (rightdiagnosis.com, 2011) But there are causes of autoimmunity that can result from toxicity. In some cases, large quantities of Onions, can lead to toxic hemolysis, zing poisoning can be a factor, or in some cases invasion from a blood-borne Parasite. (Vetinfo.com, 2011.) A Coombs test will likely be ordered by the veterinarian for diagnosis. Once confirmed, treatment modalities may include veterinary artificial blood; if the canine is in a state of immediate crisis; Artificial blood under the brand name Oxyglobin has the properties of hemoglobin, but does not contain actual cell structures; thus there are no novel antigens introduced that are likely to provoke further antagonism from active immunity. Other options include corticosteroid treatment to the purpose of immune suppression; Prednisone may be prescribed. In certain extreme cases, a splenectomy may be necessary to offset the destruction of needed red blood cells.(Vetinfo.com, 2011) Dachsunds, or other canines suffering from this condition should be tested for the ingestion of suspicious liquids or hazardous substances at dog-elevation. Although, in 60-75% of canine cases, without the possibility of vocal confirmation, the exact causative agent is not discovered. (Brooks, 2011) SUMMARY In most mammals, the causes of auto-immune disorders are less understood than the means by which they can be addressed. Prednisone can suppress certain immune responses; but many drugs and blood substitutes are stop-gap measures. Hemolytic anemia is caused by immune-mediated destruction of red blood cells outside of the normal hepatic-spleen recycling/reclamation that is common when erythrocytes surpass their normal lifespan. Causes may be an overactive immune system as a response to viral or bacterial infection that mimics host antigens. Other triggering factors may be toxic exposure; of which dogs are more at risk – being unable to read hazardous material data sheets or warning labels. Even in cases where a triggering agent can be determined, it is unlikely that a complete reversal of the condition can be achieved. REFERENCES AVIZONIS, P. and WRISTON, J.C. JR. Biosynthesis of felinine. Biochim. biophys. Acta 34: 279. 1959. 4. BELLHORN, R.W., G.D. 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