on line desde enero 2002

agosto 2003

       En la clínica veterinaria de felinos domésticos, existen grandes diferencias entre gatos que viven totalmente adentro y los que hacen vida semilibre o callejera (Fig. nº1). Obviamente me refiero a gatos domésticos urbanos, con propietarios reales que los mantienen bajo una protección relativa de "techo y comida", pero que tienen por costumbre salir  pasear  (principalmente por las noches). Esta práctica "natural" en el gato y muchas veces hasta bien vista por sus dueños, lleva implícita una serie de riesgos y peligros potenciales para el mismo gato, para sus propietarios  (zoonosis o enfermedades transmisibles al hombre), para otros gatos de la zona y para la salud pública en general.

* Fig. nº1: Los gatos callejeros tienen alto riesgo de sufrir enfermedades infecciosas y medioambientales

                           RIESGOS DEL GATO CALLEJERO

Estas incursiones callejeras comienzan alrededor de los 6 a 8 meses de vida, que es el momento en que se produce la pubertad del gato, y obedece principalmente a su mandato genético reproductor y predatorio. Es de hacer notar que aunque el gato tenga cubierta su cuota alimenticia en la casa que comparte con los humanos, no se inhibe totalmente la conducta predatoria, ya que sus mecanismos son independientes, en otras palabras, la saciedad no inhibe la conducta de cazador.

El gato va realizando inicialmente pequeñas incursiones a fin de ir delimitando un  territorio, al cual finalmente considerará como  propio y será el lugar de encuentros sexuales y eventualmente de obtención de presas. Un gato puede considerar que su territorio se extiende varios cientos de metros desde su residencia central y por lo tanto para recorrerlo deberá pasar por muchos techos, patios, jardines, calles, etc. y en todos esos lugares habrá otros gatos, perros y personas que se pueden interponer en su camino, además  en las calles encontrará todo tipo de vehículos que podrán atropellarlo tanto accidental como intencionalmente. Las incursiones se hacen más frecuentes en primavera y verano  debido al aumento de la actividad sexual de la especie en esta época.

Gato adentro vs. gato fuera:

Los gatos que viven toda su vida dentro de las viviendas humanas (casas, departamentos. etc.), tienen un tiempo de vida que llega a duplicar la vida media de un gato callejero. En estos momentos se considera,  que  un gato que vive adentro  tiene un promedio de vida de  alrededor de 15 años, llegando en muchos casos a sobrepasar los 20 años de vida. En los gatos que hacen vida semilibre o callejera, la posibilidad de contraer enfermedades infecto-contagiosas y de soportar alteraciones ambientales y traumatismos violentos, hace que se acorte ostensiblemente su término de vida, la cual generalmente no sobrepasa los 8 a 10 años, también hay que tener en cuenta  una disminución  de su calidad de vida debido a las sucesivas enfermedades adquiridas en la calle.

Enfermedades infecciosas de adquisición callejera:

Enfermedades infecto-contagiosas: el gato callejero está expuesto a diversos grados de contacto directo con otros gatos de vida libre o semilibre, ya sea por las peleas territoriales (Fig. nº 2) o por los contactos sexuales. Es muy factible que se encuentre con gatos de colonias totalmente libres, los cuales sufren una amplia variedad de enfermedades  que se podrían contagiar en estos contactos. A  continuación y a modo de ejemplo se indican  las más importantes y su forma de contagio:

VIRUS:

Rabia: el virus de la Rabia se transmite principalmente por la saliva que penetra  la piel, generalmente por mordeduras. Muchos animales pueden contraer y transmitir la Rabia, además del perro y el gato es importante tener en cuenta que varias especies de murciélagos pueden también transmitir la enfermedad. Esta enfermedad es una zoonosis.

Virus de la Inmunodeficiencia Felina: El virus del Sida Felino se transmite principalmente por mordedura entre gatos (Fig. nº2). Si bien es una enfermedad de evolución lenta, es irremediablemente mortal por la creciente falla inmunológica que produce.  Es importante destacar que este virus no afecta al ser humano,  no es zoonótica.

Virus de la Leucemia Felina:  este virus se transmite por contacto directo también a través de la saliva, puede ocurrir por mordeduras o por  el lamido reiterado entre gatos. Otras secreciones (respiratorias, orina, heces etc.) también  pueden ser infectantes  aunque en menor medida. Este virus produce una gran cantidad de trastornos inmunológicos y cancerosos, que desencadenan  la muerte del gatito en términos que van de pocos meses a 2 o 3 años. Esta enfermedad no es zoonótica.

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* Fig. nº2: En las peleas entre gatos callejeros se puede transmitir la Inmunodeficiencia Felina, la Leucemia Felina y la Anemia Infecciosa Felina entre otras enfermedades

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BACTERIAS Y RICKETTSIAS:

         Anemia Infecciosa Felina: esta enfermedad está producida por la Hemobartonella felis, que es una rickettsia que se adhiere a los glóbulos rojos del gato y los destruye rápidamente, aunque no está confirmado totalmente, se sospecha que la transmisión es por artrópodos (pulgas y mosquitos) y por inoculación directa en heridas por peleas entre gatos. Suele asociarse con el virus de la Leucemia Felina y con el virus de la Inmunodeficiencia Felina.

         Enfermedad por Arañazo de gato: esta enfermedad es producida por la bacteria Bartonella henselae.  No esta claro la forma de transmisión entre gatos, se sabe que vive dentro de sus glóbulos rojos, y se cree que las pulgas, garrapatas o heridas por mordeduras pueden favorecer el pasaje. La transmisión al humano se produce por arañazo o mordedura y la infección puede ser leve a grave de acuerdo al estado inmunológico de la persona.

PARASITOSIS EXTERNAS:

Pulgas: Las pulgas por todos conocidas, se adquieren desde  el medio ambiente contaminado con huevos y larvas . La pulga adulta vive la mayor parte del tiempo sobre los perros y gatos infectados y  elimina huevos que caen al suelo, de éstos saldrán larvas que subirán a  nuevos  huéspedes. También las pulgas adultas pueden pasar de huésped  a huésped.  Además del trastorno producido por las picaduras (la pulga se alimenta de la sangre de su huésped) hay una gran  variedad de  enfermedades que pueden transmitir entre los animales que pican.

Sarna: varios ácaros pueden producir sarna en el gato, el Notoedres cati es el agente de la sarna notoédrica, que puede ser altamente peligrosa por su  rápida diseminación en la piel del paciente comenzando por la cabeza (Fig. nº3). Se contagia por contacto directo y sin tratamiento casi siempre es mortal.

* Fig. nº3: La sarna notoédrica se contagia por contacto directo y por el ambiente, comenzando por la cabeza

PARASITOSIS INTERNAS:

Parásitos intestinales: la mayoría de los parásitos intestinales se contagian por la ingestión de huevos que han quedado en el medio ambiente (piso, tierra, areneros etc.) depositados  con la materia fecal de animales infectados. De esta forma se contagian por ejemplo el Toxocara canis y cati, los cuales tienen además, importancia zoonótica, otro tipo como la tenia Dipilidium caninun se transmite por las pulgas, y otros como el Toxoplasma gondii y los coccidios en general, además de la forma directa por los huevos en el piso, lo hacen  a través de huéspedes intermediarios como roedores, pájaros, etc.

Parásitos cardiopulmonares: la filariosis producida por la Dirofilaria immitis se transmite por la picadura de mosquitos en las  zonas endémicas  de esta enfermedad. En éstas del 5% al 15 % de los gatos puede infectarse y presentar desde la  muerte súbita a una forma crónica con signología respiratoria y gastrointestinal.

MICOSIS:

Micosis externas: la Tiña o Dermatofitosis, está producida principalmente por el hongo Microsporum canis  que  se contagia por contacto directo con material contaminado como pelos y costras tanto en el sujeto enfermo como en el medio ambiente. Es una zoonosis.

         Micosis internas: la Criptococosis es la micosis interna más frecuente del gato, está producida por el hongo Cryptococcus neoformans que es inhalado desde el suelo contaminado o de deyecciones pulverizadas  de palomas. En muchos gatos se superpone con los virus inmunosupresores (Leucemia e Inmunodeficiencia Felina) lo cual agrava el pronóstico.

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Enfermedades no infecciosas de adquisición callejera:

TRAUMATISMOS:

Es reconocida la alta incidencia de traumatismos violentos que sufren los gatos callejeros, éstos se producen por accidentes automovilísticos, peleas con perros u otros gatos, golpes con piedras, palos, heridas con armas de fuego, quemaduras, caídas de techos,  etc. Los gatos viejos disminuidos físicamente y los jóvenes inexpertos son los más expuestos. Estos gatos sufren heridas  y fracturas de todo tipo. Hay que tener en cuenta que en muchos casos estos accidentes son intencionales.

TÓXICOS:

La cantidad de tóxicos que un gato puede adquirir en la calle es muy variada. Aunque el gato no suele comer alimentos extraños, podría encontrar cebos puestos intencionalmente para roedores o para ellos mismos. Muchas veces recibimos consultas de personas que quieren  ahuyentar o eliminar gatos molestos de sus jardines o techos. Se pueden producir intoxicaciones con insecticidas, anticongelantes, anticoagulantes, etc. El agua también puede estar contaminada con desechos químicos o con residuos cloacales, y un gato sediento puede llegar a tomarla. Por último en algunas regiones se pueden producir picaduras de animales venenosos como arañas, serpientes o escorpiones.

 INCLEMENCIAS CLIMÁTICAS:

Los extremos climáticos pueden producir diversas alteraciones que van desde la hipotermia y congelamiento en climas extremadamente fríos a golpes de calor en climas muy calurosos. Si el gato callejero es sorprendido por una tormenta de nieve o queda atrapado en algún lugar como jaulas o trampas en cualquiera de estos climas  puede sufrir las consecuencias de las temperaturas extremas.

CONCLUSIONES:

Como hemos visto hasta aquí,  el gato callejero está expuesto a una gran cantidad  de enfermedades de todo tipo por el solo hecho de estar en un medio contaminado y muchas veces hostil. Algún lector podrá decir que  las recorridas de su territorio forman parte  del comportamiento natural del gato, y que los riesgos están calculados para la especie, después de todo la desaparición de algunos individuos no es más que la selección natural de la propia especie. Esto estaría bien desde el punto de vista naturista o ecológico sino intervinieran dos factores que a mi forma de ver  invalidan este razonamiento. En primer lugar el gato del que hablamos no es un gato totalmente libre, sino que tiene relación como mascota doméstica con un propietario y un grupo humano familiar,  esto pone en peligro a este grupo de personas por la posibilidad de transmisión  de enfermedades zoonóticas,  además de producir angustias y pérdidas económicas por la atención de su mascota enferma. En segundo lugar el medio urbano no es un medio natural donde pueda vivir un gato en libertad, está lleno de peligros que el gato no tiene codificado genéticamente, el gato no sabe de automóviles ni de semáforos ni de cables eléctricos ni de ninguna otra invención humana.

Otro inconveniente del gato callejero, debido a su escaso contacto con el propietario, es que se hace difícil detectar nuevas enfermedades e inclusive controlar las ya existentes; por ejemplo la Diabetes y  la Insuficiencia Renal  son  algunas de estas enfermedades que  requieren un control permanente de  dieta y medicación. Por otro lado la aparición repentina de una Obstrucción uretral  puede pasar desapercibida  si el gato está fuera de casa y puede evolucionar hasta la muerte si no es tratada en forma urgente.

Es imprescindible que nuestro querido gato no haga vida callejera,  siendo  esto  responsabilidad  de su propietario. Una vez más debemos tener conciencia que si el gato adquiere alguna enfermedad zoonótica (de transmisión al humano) no es culpa de él sino que, es responsabilidad exclusiva de su propietario.

RECOMENDACIONES:

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CONCEPTOS IMPORTANTES

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El Dr. Rubén Gatti es veterinario, vicepresidente de AAMeFe (Asociación Argentina de Medicina Felina), asesor del Pet Food Institute, CPMV Bs.As.

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The International Cat Association (TICA) tiene listo su programa para celebrar su reunión anual (Annual Meeting), una exposición con 12 rings (Annual Show), y una cena que incluye la entrega de los premios 2002 (Annual Awards Banquet):

* Annual Meeting: los dias 27, 28 y 29 de agosto, organizado por Great Lakes Region, CMC y Midwest NF Cat Club. La agenda todavía no está disponible.

* Annual Cat Show:  30 y 31 de agosto. 12 rings: Pat Harding (AB); Joe Edwards (AB); Nancy Parkinson (SP); Steven Savant (AB); Dewane Barnes (AB); Barbara Ray (AB); Fate Mays (AB); Richard Bailey (AB); Judy Chappetta (AB); Vicki Jo Harrison (AB); Robby Whyte (AB); Alexey Shchukin (SP).

* Annual Awards Banquet: 30 de agosto, a las 19:00h. en el hotel Regency Suites, Ballroom A (Green Bay, Wisconsin, USA).

	2003 Annual Awards Show & Banquet
	August 30-31, 2003 Green Bay, Wisconsin

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Las exposiciones de Andorra y Mónaco, organizadas respectivamente por CCoC y CCCAPC (clubs franceses FIFe), corren el riesgo de perder su consideración de certificados extranjeros.

Hasta la fecha, dichas exposiciones otorgan certificados válidos como tercer país aún cuando las organizan clubs franceses. La FFF (socio FIFe en Francia y responsable de los dos clubs organizadores) estima que, al celebrarse en un país independiente, los certificados son también independientes. 

La petición italiana de celebrar una exposición en la república de San Marino bajo estas mismas condiciones (certificados válidos como tercer país), fue rechazada por FIFe argumentando que los organizadores son italianos. Esta decisión conlleva la revisión de la consideración de las dos exposiciones mencionadas anteriormente, como ya se anunció en la Asamblea General FIFe de mayo 2003. 

Ahora, en la última reunión del Board FIFe (Valtice, 22-23 junio 2003), se ha acordado llevar la cuestión a la Comisión de Exposiciones para que emita una recomendación al respecto. A efectos prácticos, la exposición de Andorra (05-06/07/2003) fue anulada, mientras que se mantiene la convocatoria de Mónaco (13-14/09/2003) como certificado extranjero.

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SPECIAL GENES, SPECIAL CATS: MUTATIONS AND THE CAT FANCY

The complete blueprints to create a cat are contained in every cell of a cat’s body. The DNA code allows for accurate copying of these instructions time after time, cell replication after cell replication. But occasionally a “mistake” happens: a mutation. These mistakes are constantly happening in every vat’s body (and in the body of its owner as well). Beacuse of the nature of this code, most of the time there is no effect on the cat. Abnormal cells die or get removed from the cat’s body by the immune system. When an embryo is growing, rapid cell division can result in a higher incidence of mutations. Often, mutations that occur at this point are lethal and the fertilized egg never develops into a kitten. Sometimes the error has an adverse effect on the heslth of the cat. If a mutation occurs in the cells responsible for the reproduction of eggs or sperm, a kitten significantly different from its parents can be produced. Very rately, this can result in the appearance of an intersting new type of cat.

The cat fancy is often presented with these new cats and asked to accept them into their registries as new breeds. Should every interesting mutation be perpetuated? Each cat federation must decide for themselves the extent to wich they want to accept these special cats. Today I would like to discuss some strategies for analyzing these mutation based breeds when considering them for acceptance.

Genetics is typically presented as a series of big and small letters and lots of boxes. Today I would like to challenge you to think about genetics in a different way. We’re going to talk about subjects such as embryology and biochemistry that many discussions of genetics have avoided in the past.

Although mutations can be thought of as nature’s mistakes, they are also nature’s tools for creating the potential for individuals who can better adapt to a changing world. For example, if a plant-eating animal lives in area where 90% of the plants are poisonous, the “mutant” animal who is resistant to the poison will be at an advantage. Of course, the plants will also be mutating to protect themselves from being eaten.

NEOTENY

When it comes to domestic animals, like cats, survival takes on a different form. In the book, ·The Covenant of the Wild” by Sthephen Budiansky, a case was made that gene mutations for “cuteness” (juvenile qualities) can create a better bond between humans and domesticated animals, ensuring their survival by increasing their chances for protection by humans. The retention of juvenile characteristics in adult animals is called neoteny.

“Finally, all domestic animals, in both behavior and appearance, retain juvenile traits in adulthood. One of the very fisrst hints in the archaeological record of an animal’s domestication is the jawbone of a wolf from southwest Asia, dated twelve thousands years ago, in which the face and muzzle have begun to shortne ... an adult with the face of a puppy ... It is a process that has been repeated in every domestic animal” (Budiansky 1992: 17, The Covenant of the Wild).

One researcher designed an aexperiment that tested this theory of neoteny and its link to domestication. He rigorously selected a group of foxes based on a single trait: tameness. Only the foxes that were the most tame in each generation were kept to continue the breeding program. Within five generations, these tame-selected foxes developed many of the behaviors dogs. They licked the hands and faces of their owners; they barked like dogs; they whined they were lonely and they wagged their tails when they were happy. Their annual molting cycle was disrupted, and the females began to como into heat onli twice a year, like dogs, and unlike both foxes and wolves. They developed somo physical characteristics of juvenile foxes, such as drooping ears and shortened muzzles, and some of the variations in traits seen in other domesticated animals, such as piebald coat coloration.

EVALUATING NEW MUTATIONS AND BREEDS

When a new group of cats appears with a unique appearance due to a mutation, the cat fancy traditionally approaches the question of whether these cats should become a breed by considering a variety of factors. These often include criteria such as whether the cat is visually appealing, how popular the cat is, the opinions of judges who have handled the cats, anecdotal reports from those breeding the cats, the results of small seale breeding studies to establish the genetic mechanism of inheritance, and finally, of course, there is the political process of getting the breed accepted by a certain registry.

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INVESTIGATING FURTHER

But there is further exploration that can be done. With recent advances in sciencie, we can mechanisms that may be at work, and/or the biochemical processes behind the trait. Mutations are changes in genes and these genes make proteins. When a mutation occurs in a gene responsible for making a particular protein, the production of that protein is reduced or the function of that protein may be changed. If you can determine the normal function of that protein, it can give you clues as to what may happen in the body if that protein is affected by a mutation. This can give you insight the potential implications of the mutation.

In order to understand the affects of mutations, we need to learn about how a normal embryo develops. In a recently fertilized egg, all cells are exactly the same. Shortly thereafter, the cells of the developing embryo start to become differentiated, dedicating themselves to different functions within the developing animal. As the embryo grows, three different tissue types become evident. The endoderm is responsible for developing into the gastroinstestinal tract and the internal organs of the body. The mesoderm develops into the bones, muscles, cartilage, and connective tissues of the body. And finally, the endoderm develops into the skin and nervous system.

When a mutation becomes evident that the affects one of these embryological layers, there is a potential for changes in other tissues derived from the same layer. For example, when a mutation occurs that affects the skin, you need to make sure that there is no adverse effect on the nervous system. When a mutation occurs that affects the skeletal system, you need to make sure that there are no bad affects on the muscular system.

CARTILAGE MUTATIONS

Cartilage changes associated with certain breeds occur as a result of a mutation in mesodermally derived tissue. The American Curl, the Munchkin, and the Scottish Fold are breeds that involve mutations of cartilage. When a mutation affects the cartilage of the ears, you need to examine the affect on cartilage throuhout the body. There are multiple types of cartilage present in a cat’s body and a mutation could affect only one of these types or all of them. The normal growth of bone and development of normal joins involves a complex series of cartilage activity and a delicate balance of dididing, growing, and dyng cells. Cartilage in the growth plates provides the mechanism for the deposition of calcium and formation of bone. When cartilage is mutated into an abnormal form, the result can be abnormal joints and disrupted bone growth.

American Curl

In the American Curl, the cartilage in the ears is abnormally stiff and the cells are well organized. Sometimes excessive deposits of calcium in the ears can occur, creating a horizontal crease or crimp in the ear which is selected against by the breeders working with these cats. Despite these abnormalities, the mutation appears to be benign, with no other radiologically evident changes present in the cat’s body. These cats do not appear to suffer from any joint problems. Support of the innocuos nature of this mutation is found in the fact that homozygous cats do not appear to have any health problems, despite multiple generations of Curl to Curl breeding.

When we are analyzing a mutation, another usefull tool is to try and determine if this mutation occurs in any other species of mammal, especially in mice or humans, where the largest amount of research into genes and their affects has occurred. Ehen we look for similar traits in other speces, no analogy of thr Curl is found, except possibly in the case of “Dumbo” rats or humans born with exceptionally protruding ears. In both of these cases, the traits appears to affect only the ears and, in humans, the only medical intervention necessary to treat the condition is cosmetic surgery to pin back the ears.

Scottish Fold

In the case of the Scottish Fold, the cartilage is abnormally weak and disorganized. The normal life cycle of cartilage cells is affected, with inadequate maturation of these cells apparent. Homozygous cat suffer from severe, crippling skeletal problems due to osteochondrodysplasia. But these skeletal defects are not limited to homozygous cats. Even those with only one copy of this gene can suffer from arthritis and lameness. Because of the fact that the folder-ear mutation has incomplete penetrance, meaning that some cats have the gene mutation but appear to have upright ears, initial reports of these problems were attribted to unintentional Fold x Fold breedings. But when the problems appeared in cats where  there was absolute certainty of heterozygosity (for example, an accidental breeding between a Fold and a Devon Rex), it was established that these skeletal problems can occur despite the effors of the most careful of breeding programs. In a study perfomed in Australia by Dr. Richard Malik, 100% of all cats with folders ears had bone and joint abnormalities, especially in the hind legs and feet.

Attention to similar traits occurring in other species warn us about the potential for these problems. Similar cartilage mutations occurring in mince result in severe skeletal problems. Human dwarfism is another model for this disease, ehwrw cartilage cell maturation disruption can result in arthritis ant other health problems. When we see how similar cartilage mutations affect other animals, it gives us a warning that this type of gene mutation may be too dangerous to work in the cat fancy.

How did the Socttish Fold become such a popular and widespread breed? Initial breeding studies demonstrated that only cats from Fold x Fold breedings were afflicted with these problems. By avoiding these breedings, it was believed that the health problems could be avoided. So why has this disease progressed to the point where heterozygous cats are affected? The answer may lie in the nature of the mutation itself. Some mutations involve small sets of DNA repeating themselves inappropriately within the gene , disrupting the ability of that gene to create its associated protein correctly. These triplets of DNA can increase in number in subsequent generations, resulting in the potential for more severe effects each time the mutation is perpetuated. This is a phenomenon seen in other dominant mutations that cause disease, including the gene responsibile for polycystic kidney disease. This many also be the reason that the dominant mutation for white spotting can result in cats with more and more white fur in subsequent generations.

When we perpetuate mutations, we have an ethical obligation as breeders to do our best to investigate the mechanism at work behind the desired trait. Every time we place a pet into a home, we give a message to the general public about the nature of our hobby. What kind of impression do we make when a pet owner is faced with dealing with a beloved pet that requires constant veterinary attention and can not lead a full, healthy life?

TAIL MUTATIONS

Let’s use the same trhought process to evaluate another trait related to the skeletal system: tail abnormalities. Formation of the tail in mammals requires a specialized form of cell migration and organization inthe early embryo. The tail bud forms in the stage of embryo development called “gastrulation”, the point at wich the gastrointestinal tracts is formed. Both mesoderm and endoderm are involved in creating the tail. In mice, tail defects associated with gene mutations can result in severe internal organ defects, such as missing kidneys and cleft palates. So based on his information, we know that we should proceed with caution ehwn considering perpetuating tail trait mutations.

What evidence is there tail mutations in the cat are associated with similar health problems that are seen in these mice? Kinked and bobbed tailed cats have spontaneously apparead all over the world quite frequently. In some parts of the world, particularly in Asia, abnormal tails appear in almost 100% of the population of feral cats. When breeders encounter tail abnormalities, they rogorously select against them. Despite this selection, this trait tends to recur. Homozygous cats (bobtails) have no adverse health consequences from this trait, despite many generations of affected x affected breedings. Therefore, the long history the cat fancy has with this trait increases our level of confidence that these abnormal tail mutations are strictly cosmetic.

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COLOR MUTATIONS

I mentioned before that mutations change proteins. Some of the most important ones in the body are enzymes, proteins responsible for facilitating chemical reactions. Enzymes are involved in building cells, organizing them, and allow them to perform their normal functions. Mutations can disable these proteins or change the way they function. Mutations can affect entire groups of cells, or only specific cell types.

An example of a specific cell type with lots of chemical reactions of interest to the cat fancy is the melanocycle. These cells are located in the hair follicles of the skin and are responsible for giving our cat’s fur and skin their color. These chemical reactions involve a series of enzymes, many of which we have identified through the changes in color produced when mutations occur.

The colorless amino acid tyrosine is converted into dopaquinone by the actions of the enzyme tyrosinase. Mutations in the gene for tyrosinase result in the albinism series of cat colors, due to a reduction in color production within the melanocyte. Other mutations that have an affect on color are the tyrosinase related protein-1 mutation responsible for chocolate color and the dopachrome tautomerase mutation which is theorized as the mutation responsible for the dilute colors.

The production of black or red pigment is controlled by a recptor protein on the surface of these melanocyte cells and two proteins which bind loosely to this receptor: the agouti protein and melanocyte stimulating hormone (MSH). If MSH is created by the melanocyte, it will bind to the receptor and result in the production of black pigment. As a hair grows, the production of agouti protein in the melanocyte increases. When this reaches a suffcicient level to displace the MSH, red pigment will be produced. This results in the typical agouti coloration of a tabby cat: black at the tips of the hairs and red at the base. When the agouti protein is disrupted by a mutation, black pigment only is produced.

Color associated mutations can affect the growth and spread of melanocytes as well as their chemical processes. Melanocytes are ectodermally derived cells, so their relationship to the nervous system needs to be considered when examining mutations involving melanocytes.

An example is the albinism mutation responsible for Siamese coloration. Melanocyte cells are found in the brain as well as in the skin, particularly in the corpus collossum, the area responsible for communication between the two sides of the brain. In the Siamese form of albinism, the visual pathway is disrupted. Siamese cats do not have true binocular vision for this reason. Despite this, Siamese cats do not seem to suffer from this visual defect, and compensate so well that no reduction in their ability to inter act with their environment is see.

Even something that seems as innocuous as a change in color can have health consequences that are not always readily apparent. In some mammals, disruption of the tyrosinase related protein can lead to serious health problems. Color mutations can be associated with personality, intelligence, and obesity in mice. It has been recently hypothesized by Dr. Stephen O’Brien of the National Cancer Institute that the nonágouti mutation may have developed as a defense against bacterial or viral infection by blocking the MC1-R transmembrane receptor.

Another interesting series of color mutations are the ones responsible for creating areas of white fur on cats. These areas formed by a lack of melanocyte cells in the skin’s hair follicles. These cells migrate from an area of the embryo called the neural crest at an early stage of embryonic development. If there is not a suffciciently large population of these cells to completely cover the skin area of the cat, white spots will occur. The white spotting mutation (and to an even greater degree, the epistatic white gene) reduces the population of these cells and impairs their viability. Other cells are derived from these neural crest cells, including a type of cell, the stria vascularis, found in the cochlea of the inner ear that is essential for sound hearing.

Migration of these cells is aldo responsible for creating the tapetum lucidum, a layer of cells found in the eye. An eye without this structure is blue. The pattern of migration can be asymmetrical, causing odd-eyed cats. Sometimes migration is incomplete, and only part of one eye is affected by the lack of these neural crest derived cells. Cats homozygous for the white spotting pattern often have “van” coloration, there melanocytes are present in only the skin nearest the embryological neural crest.

Because the initial population of neural cells is reduced in white spotted cats,  a tortoishell without white has a distinctly differenr color than a tortoishell with white. In the normal tortoishell cat, many cells share the responsability of giving color to the skin, some of them creating black fur, some red fur. This results in a brindled appearance of highly intermigled red and black hairs. In the white spotted version of the tortoishell, one precursor cell is responsible for multiplyng itself many times to cover a large area of skin. This results in large clonal patches of a single color. The stronger the effect of white spotting, the less intermingled the colors will be in a tortoishell. A cat with only white feet will have a much more brindled coat than a cat with color only on the head and tail.

Completely white cats can, very rarely, be created using only the white spotting gene. Blue eyes can be created with this gene as well. However, this gene appears to be fas less likely to cause deafness than the epistatic white gene, resulting in an extremely low (approaching zero) incidence of deafness in even extreme examples of van coloration.

One interesting groups of cats have been names Ojos Azules by their breeders. Distinguishing characteristics include a white tail tip and blue eyes in otherwise fully colored cats. This is a dominant gene, like the normal white spotting gene. In human beings, over 50 different genes for white spotting (piebaldism) have been identified.

When examining any dominat trait, the question should always be posed: “What occurs in a homozygous cat?” In the Ojos Azules, what appears to be a harmless color mutation causes severe problems in homozygoud kittens including cleft palates, cranial defomities, other midline defects, and a severely kinked tail. This is consistent with a mutation that disturbs noemal cell migration at an earlier point in development than the normal white spotting gene, disrupting a variety of mesodermally derived tissue.

CONCLUSION

When the cat fancy is faced with a new breed based on a mutation, even one in which only the color is affected, questions should de asked in a systematic manner, since mutations can have effects outside of their primary identifiable trait. Knowing the normal function of tissues and proteins that cause simialr problems in other mammals can help us make logical conclusions on th viability of these new breeds. The most you know about the chemistry and developmental processes that occur to create our cats, the more educated of a decision you can make regarding the health implications of a new mutation.

As cat fanciers, our primary goal must be the breeding of healthy cats. new mutations are very tempting to perpetuate, but these tyoes of breeding programs should never be undertaken without serious consideration of the health of the cats involved.

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To date, over 250 genetic diseases have been identified in the cat and more are added every year; about half of these diseases have counterparts in humans

A feline genome project is now in its third decade and has made significant progress; researchers are lobbying to have the feline genome added to a high priority funding list for whole genome sequencing by the National Human Genome Research Institute in the United States

Two Feline Genetic Diseases conferences have been held in the United States: the first in 1998 at the University of Pennsylvania, the second in 2000 at the University of California; in May 2002, the first Canine and Feline Genomics conference was held in St. Louis; more conferences are planned for 2003

 

          POLYCYSTIC KIDNEY DISEASE (PKD):

Autosomal dominant PKD is the most common genetic disorder of humans, with an incidence of from 1 in 200 to 1 in 1000 people, 3 known genes are associated with the adult onset form of the disease

PKD has been described in Persian-type cats since the 1960s; now found world-wide

Most of the important feline research was done in the 1990s

Feline PKD is now established as a model for the disease in humans

Some affected cats develop chronic kidney failure, usually in the middle years of their lives

In the late 1980s, Dr. David Biller of the Ohio State University in the United States established a colony of PKD research cats after he acquired the offspring from a 6 year old Persian female with PKD

Ultrasounds of the sire and 5 kittens from 2 litters found the sire was not affected, 2 male offspring had PKD, 1 female offspring had PKD, 1 female offspring was not affected

Dr. Biller then developed a pedigree database of 115 cats by crossing some of the offspring with unrelated, normal DSH cats

Of the 115 cats in database, 102 were positive for PKD; analysis of the data proved autosomal dominant inheritance of PKD in cats

Starting in the late 1990s, breeders in the United States and around the world have been testing their cats for PKD

Breeds most at risk are: Persian and its related breeds, Himalayan and Exotic

Data from some recently published studies on PKD:

* In 2000, in the United States: 745 Persian/Himalayan cats ultrasounded for PKD at specially arranged clinics, over 42% of cats were positive for PKD

* In 2001, in Australia: 45% of a group of 250 Persians were positive for PKD

* In 2001, United Kingdom: almost 50% of a group of 132 Persian cats examined at the University of Bristol were positive for PKD

In all these studies, the majority of cats did not have signs of kidney failure at the time of their diagnosis

Age at which kidney failure develops in PKD patients ranges from 3 to 10 years of age, average is 7 years of age

But the high prevalence of PKD in Persians, Himalayans and Exotic Shorthairs makes this an important cause of kidney failure in cats, especially when we consider that over 40,000 Persians are produced by breeders every year in the United States alone and Persians represent about 80% of the pedigreed cat population in that country

So far, only very low rates of PKD have been reported in other breeds at risk, which include: Scottish Folds, British Shorthairs, and Birmans. In the past, Persians were allowable outcrosses for these breeds and so the PKD gene may have been introduced into some bloodlines.

Criteria for diagnosis of PKD:

* Experienced ultrasonographer with good quality machine, transducers of 7.5 to 10 MHz (7.5 MHz for adults, 10 MHz for kittens)

* Minimum 9-10 months of age; each kidney scanned carefully in two planes

* Multiple cysts in both kidneys; presence of cysts in one kidney only, especially in a high risk breed, is strongly suspicious for PKD and the cat should be re-scanned when older

On an x-ray, it may be possible able to see the enlarged kidneys in some patients

At post mortem, the kidney can be markedly misshapen, variable in size, and contains multiple cysts; the cysts may not be visible on the surface of the kidney, so examination must be done carefully, the pathologist must make several slices through the kidney to identify milder cases

Advice for breeders:

Scan all breeding stock by 10 months of age; may be wise to re-scan at 2 years of age or older because a few cats with mild PKD will not be detected at 10 months

To eliminate PKD from bloodlines, it is best to breed only normal cats

Since PKD affects such a large proportion of the breed, it may not be practical or wise to immediately eliminate all PKD positive cats (this would restrict the gene pool); you can breed normal cats to heterozygotes and keep only the normal kittens as replacement breeders. Heterozygotes are identified as affected cats that have one normal parent.

Ultimately, we need a genetic test to properly identify affected and normal cats; at least 3 different genes are known in humans and researchers will be checking these genes first to see of one of them causes feline PKD; if it is not one of these 3 genes, the search for the feline PKD gene will become much harder

A good website for PKD information: http://www.felinepkd.com/

 

        HYPERTROPHIC CARDIOMYOPATHY (HCM):

In humans, HCM often runs in families, with 50% of cases inherited in autosomal dominant fashion.

Several different gene mutations identified in humans.

HCM is the most common heart disease of cats today.

No specific gene mutations have been identified yet in cats.

Male cats are more often affected than females.

The typical HCM patient is male and middle-aged.

Many affected cats have no symptoms of heart disease when they are diagnosed.

Cats in heart failure at diagnosis may have difficulty breathing, lethargy, and a poor appetite.

Cats with blood clots blocking critical arteries may have difficulty walking or paralysis of the hind legs and may be in great pain.

The first breed identified with inherited HCM was the Maine Coon about 10 years ago (Dr. Mark Kittleson, University of California); mode of inheritance identified as autosomal dominant.

Since then, HCM known or strongly suspected to be inherited in several other breeds: American Shorthair, Persian, Rex breeds, Ragdoll, British Shorthair.

Several breeds appear to be at low risk, such as the Siamese and Abyssinian.

Characteristics of HCM vary among breeds:

Maine Coons are best studied: usually no disease before 1 year of age; disease present by 2 years old, becomes severe by age 4.

American Shorthairs appear to have a milder form of HCM.

Persians appear to have a form involving asymmetrical septal hypertrophy.

Ragdolls appear to have a severe form with early onset.

HCM is a progressive disease that may progress slowly or quickly.

Characteristics of HCM:

Hypertrophy or increase in size of heart muscle, especially of the left ventricle.

May be associated with enlargement of the left atrium.

An irregular heart rhythm may be present.

Heart murmurs are usually, but not always present – murmur can be variably present or absent in the same patient. A heart murmur that persists beyond 4-6 months of age in a kitten should be investigated.

HCM is a common cause of heart failure.

Risk of blood clots that block blood flow to critical arteries.

Sometimes the first and only sign is sudden death.

Diagnosis is most reliable by echocardiogram (ultrasound of the heart).

Treatment:

Some patients are in heart failure and must have their immediate condition stabilized (oxygen, diuretics, treatment of clots if present).

Diltiazem (Cardizem): first line drug therapy.

Beta blockers (i.e. atenolol): may be best for cats with obstructive form of HCM.

ACE inhibitors (enalapril – Enacard, Vasotec; benazepril – Lotensin, Fortekor): may be useful in cats that do not respond to other medications.

Aspirin: commonly prescribed to prevent blood clots but does not work as well as expected; recent study showed that low dose works as well as higher doses.

Treatment of asymptomatic cats is controversial: some drugs such as diltiazem or ACE inhibitors may be able to reduce the muscle hypertrophy, so it might make sense to treat these cats if they are diagnosed at a young age while the hypertrophy is still developing; some cardiologists do not treat asymptomatic cats unless the left atrium is enlarged.

Prognosis: 

Highly variable; generally worse for cats that are in heart failure or for those with severe enlargement of the left atrium; poorest prognosis is for cats with thromboembolism (blood clots in critical arteries).

Some cat family lines have more malignant forms of HCM than others.

A study published in 2002 on 260 cats with HCM:

Well cats: survived up to 10 years.

Cats with heart failure: survived an average of 18 months.

Cats with blood clots: survived an average of 6 months, high risk of clot happening again.

Advice for breeders of Maine Coons:

Screen breeding stock with ultrasound.

We can fully assess males by age 2, females by 3-4 years of age.

Advice for breeders of other breeds:

Ragdolls: often have disease before 1 year of age, so can screen earlier with ultrasound.

Other breeds: ?? Similar to Maine Coon.

Presents difficulties for breeders because cats have often produced offspring before they can be fully assessed.

A genetic test is needed to identify affected cats earlier, but no gene responsible for feline HCM has yet been identified.

Good website for HCM information: http://members.aol.com/jchinitz/hcm/index.htm

 

          Feline Hip Dysplasia (HD) & Patellar Luxation (PL)

Although little information is known about feline HD compared to canine HD, reports of HD in cats date back to at least the 1960s.

Recent research shows feline HD is more common than once thought.

Feline HD is similar to canine HD in some ways:

It is a developmental malformation of the hip joint.

It is not congenital (not apparent at birth).

Most cats with HD are asymptomatic, and are often diagnosed incidentally when x-rays are taken for other reasons.

One study showed a potential link between HD and patellar luxation (dislocating kneecaps) in cats.

Males and females are equally affected

Studies done in the United States show some breed predispositions:

Devon Rex (about 40% affected).

Persian/Himalayan (about 20% affected).

Maine Coon (about 23%).

Non-pedigreed cats (about 5.8% affected).

HD is assumed to be an inherited trait in cats, likely polygenic; the role of environmental factors (ie. breed, size, diet, growth rate, etc) is unknown.

Maine Coon breed most studied: 

Concerns about HD in this breed date to the 1980s

Orthopedic Foundation for Animals (http://www.offa.org/) in United States has data on 617 Maine Coon cats from 1974-2000:

23.3% were dysplastic; only 4.5% scored excellent.

OFA will give a preliminary report on cats as young as 4 months of age, but will not give a final score until at least 24 months of age.

May be necessary to x-ray breeding cats yearly since cats rated normal at 2-3 years of age may have HD in later life.

Clinical Signs of hip dysplasia:

Decreased activity.

Abnormal gait (bunny hopping, crouched, wobbly).

Reluctance to jump or play.

Limping after vigorous exercise.

Pain on urination/defecation or on touching hindquarters.

Some cats develop constipation due to reluctance to defecate.

Most cats have no signs at all!

Physical findings and x-ray findings do not necessarily correlate: cats with severe HD on x-ray may not have any clinical abnormalities or pain.

Genetic predisposition for patellar luxation (PL) noted historically in Devon Rex, Abyssinian. HD is also prevalent in Devon Rex.

University of Pennsylvania study (1999), 78 cats (25 cats with HD and 53 cats without HD):

64% of Devon Rex had PL; 32% had HD and PL.

80% of Abyssinians had PL; 30% had HD and PL.

45% of Maine Coons had PL; 18% had HD and PL.

17% of non-pedigreed cats had PL; 29% had HD and PL.

Overall 58% of cats had PL, most were Grade 1 (mild) and most were affected in both knees; 24% had HD and PL.

Only 22% of cats had clinical signs referable to either PL or HD.

The authors concluded that cats were 3 times more likely to have HD and PL together than either condition alone.

Conservative therapy for HD and degenerative joint disease (DJD):

Weight reduction if obese.

Avoidance of activities that worsen pain and lameness.

NSAIDs: aspirin, ketoprofen, meloxicam; used with caution in cats and only under veterinary supervision.

Neutraceuticals: (Adequan, Cosequin, Glycoflex) have become popular with pet owners, perceived to have low risk of adverse effects, no controlled trials have evaluated their use for treatment of chronic DJD.

Corticosteroids: such as prednisone are controversial for treatment of DJD since they have negative effects on cartilage metabolism; may be best to leave to last resort.

Surgical therapy for HD and degenerative joint disease (DJD): considered when conservative management fails, or when owner perceives quality of life is unacceptable.

Goal is to relieve pain and restore mobility.

Best surgical technique is femoral head and neck ostectomy (FHO); also called excision arthroplasty.

Cats do very well post-operatively; experience pain relief and return to normal function.

Good website for feline HD information: http://www.fhda.com

          Amyloidosis

Amyloidosis is a diverse group of diseases of human and animals, first identified 150 years ago; cause of familial Mediterranean fever in humans.

Familial amyloidosis found in Shar-Pei dogs and in Abyssinian and Oriental/Siamese cats.

Serum amyloid A (SAA) is a protein produced in the liver as part of the immune response.

Amyloidosis occurs when deposits of amyloid protein AA (which is closely related to SAA) are found in body organs such as the liver and kidneys.

Amyloidosis can be due to chronic inflammatory disease, genetic predisposition.

Abyssinian form:

First reported in 1982; research funded by Winn Feline Foundation and Aby breeders since 1983; discovered much about the disease and the nature of the amyloid protein

Familial, inherited disease but mode of inheritance not yet known; appears to be at least 3 genes involved, each with multiple forms; disease probably due to genetics, stressors, and immune system dysfunction

Primarily attacks the kidneys of cats between 2 and 5 years of age; causes kidney failure

Diagnosed with kidney biopsy and special stain (Congo red)

Treatment as for any cause of kidney failure

Need to identify the gene or genes involved to develop a simple test

Oriental/Siamese form:

The liver is main target organ; sometimes kidney involved too

Liver becomes enlarged and swollen, fragile and bleeds easily

First reported in 1992; affects non-pedigreed cats as well as Siamese and Oriental type cats; also reported in one Devon Rex and one Burmese

Affected cats are usually under 5 years old

Signs: life-threatening hemorrhage from the liver; queens may be affected at the time of delivery of a litter; sudden death from hemorrhage may occur

Genetic sequencing has shown that the amyloid proteins in the Aby form and the Siamese form are not the same, so they are caused by different genes

Appears to be a familial predisposition in some Siamese and related breeds

The mode of inheritance is not yet known; some cases appear to be spontaneous

Diagnosis: suggestive clinical signs, susceptible breed; biopsy of liver

Treatment:

Supportive: vitamin K for blood clotting, cage rest, antibiotics

Drugs used in human forms: colchicine (used to treat Mediterranean fever), cyclophosphamide and chlorambucil (used to treat some forms of kidney amyloidosis in humans), other drugs targeting amyloid formation only used in research settings with mice

Prognosis is grave for affected cats. We need a genetic test.

What breeders can do:

Request full necropsies on cats that die with symptoms suspicious of amyloidosis

Request full necropsies on cats that die unexpectedly

Track amyloidosis on your pedigrees, keep good records

Be willing to share information with other breeders and with researchers

 

For more information on many feline diseases and feline research, see the website of the Winn Feline Foundation: http://www.winnfelinehealth.org

Normal Growth and Development

w        Typical birth weight 90 to 110 grams (roughly 3-4 ounces).

w        Influenced by many factors such as breed, number of kittens in litter.

w        Weigh kittens at birth on a gram scale, again 12 hrs later, and daily for first 2 weeks of life.

w        Identify each kitten accurately and keep a growth chart; first sign of illness may be failure  to grow.

w        Normal kittens gain 50-100 grams per week (10-15 g/day); should double birth weight by 2 weeks old.

w        Well fed kittens have plump abdomens and appear content; hungry kittens cry excessively,appear restless, have lean abdomens.

w        Eyes open about 10 days of age (range 2-16 days); kittens recognize queen by sight by about 4 weeks;  iris remains blue-gray until 4-6 weeks; ear canal at birth is blocked by ridges of skin but widens and opens by about 9 days of age (range 6-17 days); newborn kittens have a good sense of smell;  pain perception is present at birth.

w        Crawling is well developed by 7-14 days; walking begins about 2 weeks of age; elimination of urine and stool is a reflex stimulated by the queen; voluntary urination and defecation appear at about 3 weeks.

Examination of the Neonatal Kitten

w        Observe kitten’s response to environment, body condition, mentation, posture, locomotion, and breathing; ill kittens may be isolated from the group and neglected by queen.

w        Normal body temperature for new-born kittens is 95-97^oF; temperature then rises slowly, reaching 100^oF by about 4 weeks of age; for first few weeks of life, kittens cannot regulate their body temperature; they lack a shiver reflex until about 6 days old.

w        Normal heart rate can be over 200 beats per minute (range 220-260); normal breath rate 15-35 breaths/minute.

w        Inspect for obvious abnormalities: cleft palate/lip, umbilical hernia/infection, open fontanels, limb deformities/contractures, abnormal urinary or rectal openings, etc.

w        Umbilical cord should be dry and free of discharges; normally falls off by day 3.

w        Check for normal urination/defecation by stimulation of rear end with soft moist cloth or cotton ball; check for constipation or diarrhea (present in about 60% of sick kittens), as well as urine colour.

w        First baby teeth to appear are incisors and canines at 3-4 wks of age; premolars appear 5-6 wks of age.

w        Coat should be clean and shiny; healthy neonatal kittens may have dark pink or red gums until 7 days old, whereas sick neonates often have pale, gray, or bluish gums.

w        Full abdomen is normal in well-fed kitten, but swollen abdomen in an ill kitten may indicate swallowed air.

Therapeutics

Hypothermia (low body temperature):

w        Occurs when rectal temperature is 78-95^oF; associated with poor breathing, impaired immune system function, slow heart rate, poor intestinal function, coma.

w        Rewarm slowly using: incubator, heat lamp, hot water bottle; room temperature should be 85-95^oF with 55-65% humidity; turn often and monitor rectal temperature carefully to avoid over-warming.

w        Never attempt to feed hypothermic kittens until they are rewarmed (risk of aspiration).

Hypoglycemia (low blood sugar):

w        Common due to immature liver function and rapid depletion of energy stores in the body.

w        If not hypothermic or dehydrated, smear dab of corn syrup on gums, or give dextrose solution (from your vet) orally (1/4 ml per ounce body weight).

Dehydration:

w        Gums should be moist and either dark red or pink.

w        Pale gums and slow capillary refill time (have your vet show you how to do) may indicate 10% dehydration or more.

w        Normal neonatal urine is clear and colorless; in dehydration, urine is dark yellow.

w        Use warmed oral electrolyte solution (such as Pedialyte) when kitten is not hypothermic,  not seriously dehydrated.

w        if unstable/seriously ill, dehydration must be corrected at the vet clinic with IV fluids.

Kitten Losses

w        Rates vary from 4% (in disease-free research colonies) to over 30% (in some pedigreed catteries).

w        Pre-weaning losses of over 20% should be vigorously investigated.

w        Typical time periods for losses: during pregnancy (absorptions, abortions), at birth (stillborns), in the first 2 weeks of life, and the period immediately after weaning.

w        Investigation requires examination/treatment of individual kittens, diagnostic testing, full necropsies (including cultures and histopathology); kittens that die at home should be refrigerated until necropsy (not frozen).

w        Most common factors: low birth weight, congenital defects, trauma, inadequate nutrition, maternal neglect, environmental factors, infectious diseases and parasitism, neonatal isoerythrolysis (NI).

Low Birth Weight (under 90 grams/3 ounces)

w        Multiple causes, may be hard to determine:  prematurity, inherited diseases (i.e. inborn errors of metabolism), birth defects, in utero infections, and others.

w        Kittens under 75 grams (2-1/2 ounces) at birth have very high death rate.

w        Kittens losing more than 10% of their body weight after birth have a poor prognosis.

Congenital defects

w        Defects present at birth, may be due to multiple causes (i.e. genetics, drugs, infections, etc.)

w        Up to 20% of live-born and stillborn kitten deaths involve major anatomical abnormalities.

w        Defects include: cleft palate, craniofacial defects (i.e. Burmese, American Shorthair head defects), heart defects, open abdomen, skeletal abnormalities, incomplete twinning.

Trauma

w        Up to 10% of kitten losses attributed to trauma during birth (insufficient oxygen) or the first 3 days of life.

w        May be due to maternal neglect or cannibalism.

Inadequate nutrition

w        Kittens should nurse within 2 hours of birth, colostrum only absorbed within first 16 hours.

w        First born kitten may be subjected to a long wait before nursing if delivery is prolonged.

w        Difficult births may produce kittens that are too exhausted and traumatized to nurse effectively.

w        Inadequate milk production associated with: first time queens, aged queens, queens who are sick or malnourished, difficult labors, familial trait, mastitis, litters of small weak kittens .

Environmental Factors

w        Environmental stressors (overcrowding, noise, poor ventilation, etc.) may compromise maternal care.

w        Temperature fluctuations may be harmful to neonatal kittens; high room temperatures combined with high humidity promote some infectious diseases (pneumonia, mastitis).

Infectious Diseases

w        Highest death rates from infectious diseases are in the first 2 weeks of life and post-weaning period.

w        Pathogens include: Strep, Mycoplasma, herpesvirus, calicivirus, parvovirus, FeLV, FIV, FIP, Toxoplasma, E. coli, Pasteurella, Staphylococci, Bordetella, Chlamydia. Most important are Strep. canis (Group G, beta-hemolytic) and coliform bacteria (i.e. E. coli).

w        Strep. canis may be significant cause of kitten losses, especially between 5-10 days of age:

·        carried in vagina of young queens and in prepuce of toms, uncommon in older queens.

·        associated with internal and external umbilical abscesses, septicemia, peritonitis.

·        diagnosis by culture of umbilicus, liver, abdominal cavity, lungs at necropsy; treat remaining litter mates with oral amoxicillin .

·        preventative management program for catteries experiencing confirmed losses to S. canis:

§         kittens: single SC injection of 0.25 ml of 1:6 dilution in sterile 0.9% saline of product containing 150,000 IU/ml benzathine and procaine penicillin G.

§         queen: one SC injection of 150,000 IU of the same product (undiluted).

§         single dose given to queen at parturition may temporarily suppress the S. canis population.

Neonatal Isoerythrolysis (NI)

·        Responsible for up to 50% of deaths in some pedigreed catteries.

·        Two main blood types, A (dominant) and B (recessive); third blood type is rare (AB).

·        Most non-pedigreed cats are blood type A (95-98%), some breeds may be over 30% type B.

·        Antibodies are naturally occurring; no previous pregnancy or transfusion is necessary.

·        Type B cats have strong antibodies against type A red blood cells.

·        NI occurs in blood type A kittens born to a type B queen mated to a type A male.

·        Kittens are born healthy; some die suddenly; others stop nursing within first 3 days with suggestive signs: failure to thrive, red-brown urine, jaundice, anemia.

·        Treatment: kittens with severe anemia require transfusion with washed type B blood (preferably from the queen); despite treatment, death rate is high.

·        Prevention: remove kittens from queen for first 16-18 hrs and foster nurse kittens with type A queen if available or hand feed milk replacer; plan breedings carefully; blood type all breeding cats; record blood type on pedigrees.

Tube Feeding

w        Hand feeding kittens can be accomplished by bottle feeding or tube feeding:

·        bottle feed kittens who are vigorous with a good sucking reflex; avoids overfeeding, but more time consuming than tube feeding; use small pet nurser, Catac^® nurser, or a nipple on a 3 cc syringe .

·        tube feeding is method of choice for weak kittens with a poor sucking reflex; quickest method of feeding orphans; best choice if a large litter must be hand raised.

·        problems occur if formula is fed too cold, fed too rapidly or in too large a volume; may result in  regurgitation, aspiration, bloating, diarrhea (common).

·        to resolve diarrhea, milk replacer volume should be diluted 50% with water or electrolyte solution for next several feedings; formula can then be gradually increased to full strength; also helpful to reduce volume of formula fed for several feedings; in general, better to underfeed slightly rather than overfeed; consider using probiotics.

·        weigh kittens frequently to assess progress; aim for weight gain of about 10 grams daily and production of normal stool (firm and somewhat yellow).

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Los Korats son una de las razas originarias de Thailandia, con pocas variaciones morfológicas a lo largo de los últimos 400 años. El orígen del standard FIFe se remonta al trabajo de la Scandinavian Korat Association (uno de los primeros clubs europeos dedicados a esta raza, liderado por Elfi Kleive), que tradujeron el standard CFA que luego aprobaría FIFe.

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* EC & EP Primpraus Meo Mao (FIFe WW 1999/2000). Criadora: Camilla Baird (Primpraus Cattery), Propietaria: Donatela Mastrangelo (Jadeye Cattery)

* Guan-yin v. Baan Thai (Baan Thai Cattery)

* Guan-yin v. Baan Thai y compañía (Baan Thai Cattery)

* Pu-ying Galanos (Galanos Cattery)

* Sirikit Si-Sawat (Galanos Cattery)

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