on line desde enero 2002

junio 2004

	La reunión anual de la Federation Internationale Féline (FIFe) tuvo lugar los pasados  27 y 28 de mayo en Albufeira (Portugal), organizada en colaboración entre el comité de FIFe y el club portugués CPF.      A continuación presentamos un resumen no oficial de las decisiones acordadas; en cursiva azul el texto nuevo, y tachado el eliminado. FIFe publicará las actas oficiales próximamente, pero mientras se puede leer una versión muy completa (no oficial) publicada por Mundikat (NL).

     El "Club Français du Bleu Russe et couleurs associées" está desarrollando una intensa actividad en los últimos meses. El pasado 16 de mayo organizó una especial de raza en Saverne, cerca de Estrasbourg (F), en el marco de la exposición internacional felina organizada por Les Chats de France (LOOF). Aprovecharon también la ocasión para entregar los premios a los ganadores de la Challenge 2003 del CFBR:

     El club colaborará en la organización de otras 3 especiales: en septiembre, octubre y noviembre 2004. En ésta última, el club de raza Russisch Blau IG conmemorará sus 10 años de existencia:

.

Introduction 

     Feline infertility can be due to a variety of environmental, behavioral, infectious, neoplastic or congenital factors, all of which can be present alone or in combination. From a practical standpoint, the most frequent presenting complaints for infertile queens are: (1) the queen does not show heat; (2) the queen cycles regularly and breeds, but does not conceive; and (3) the queen conceives, but experiences spontaneous abortion. This article discusses these three presenting complaints.

Failure to show heat

     Anestrus can be primary (delayed puberty in younger queens) or secondary (lack of cyclicity in postpuberal animals). The majority of queens go through puberty between 5 and 10 months of age, although the first heat can be as early as 4 months and as late as 21 months depending on the breed. Such a large variation is accounted for by factors, such as body weight (it should be R2/3 of adult’s weight or at least 2.3–2.5 kg), season of the year (during Summer and early Fall, queens typically show anestrus) and genetics (long-haired breeds show a tendency toward a delayed puberty). Secondary anestrus can either be due to a behavioral problem, a disease affecting the reproductive system or other organs, or a silent heat.

Primary anestrus

     A clinical investigation for the absence of signs of puberty should not be undertaken until: (1) the queen has reached 14–21 months of age (depending on breed); (2) the queen has reached at least 2.3 kg of body weight; and (3) the feline breeding season has started. A photoperiod of at least 14 h of light is necessary for the hypothalamus–pituitary axis to start producing gonadotropins. Also, it is always advisable to house prepuberal queens with cycling queens to provide anestrous animals with the stimulating action of pheromones. 

     Potential causes for lack of cyclicity in queens who have satisfied the previously mentioned three conditions are premature gonadal failure (relatively common), pathology of the reproductive tract (common) or hypothyroidism (uncommon) (Table 1).

     An abnormal karyotype (37,X0; 37,X0/74,XX00; 37,X/39,XXX; 37,X/38,XX) is not an uncommon finding in queens with primary anestrus and has been reported previously (Johnston et al 1983; Norby et al 1974; Berepubo and Long 1983). Diagnosis is hampered by cost and availability of  laboratories where animal karyotypes is offered as a service. Congenital hypothyroidism as well as other congenital diseases causing anestrus are either poorly documented or not reported in the queen. Other pathological conditions of the feline female reproductive system causing primary anestrus are also poorly documented (except for ovarian cysts) and diagnosis needs to be confirmed through laparotomy/laparoscopy.

     Periods of prolonged anestrus during the breeding season in postpuberal queens can be: (a) normal in some long-haired breeds whose reproductive patterns are still not very well known; (b) due to pseudopregnancy (a progestational phase lasting for about 45 days) occurring after non-coital ovulation (Lawler et al 1993; Romagnoli et al 1996); and (c) due either to diseases of the reproductive system, such as pyometra, ovarian cysts or ovarian tumors, or to a subclinical disease of the endocrine system, such as diabetes or Chushing.

     Cyclicity with no signs of behavioral heat due to social stress can be observed in queens with a very low social rank, especially if living in a crowded colony. Low intensity of heat signs is known to occur either in younger queens or in queens who are overweight, highly inbred, sedated or treated with drugs, such as progestins.

     To confirm diagnosis of anestrus, one or more vaginal smears and blood samples should be collected so as to rule out vaginal epithelial cornification or a progestational phase (characterized by serum/plasma progesterone concentrations R2.0 ng/ml). Although poorly documented in the cat, assay of follicle stimulating hormone (FSH) and luteinizing hormone (LH) (which require a specialized veterinary endocrine laboratory) may allow differentiation between normal queens (FSH–LH values %10 ng/ml) and queens with non-functional ovaries (R100 ng/ml). Once anestrus is confirmed, etiology should be investigated performing a karyotype (normal is 38,XX) and/or evaluating thyroid function (normal is T3
60–200 ng/dl, T4
1.0–4.0 mcg/dl) based on clinical indications. If results are normal, pharmacological induction of estrus can be attempted: FSH at the dose of 2 mg daily IM for 3–7 days until onset of estrus is considered an effective treatments, which should be followed by natural mating or administration of 150–250 IU human corionic gonadotropin (hCG) or of 25 µg gonadotropin releasing hormone (GnRH) (Chakraborty et al 1979; Wildt et al 1978). A more recent protocol, which seems to give better results consists of administering 150 IU PMSG IM followed by 100 IU hCG 84 h later (Swanson et al 1996).

     Ovarian biopsy performed under laparotomy or laparoscopy can be used as a last resort if estrus induction protocols fail. Silent heats should be managed trying to reduce the source of stress, using an experienced tomcat, trying different tomcats if necessary, and also housing the queen with cycling females.

     Causes for failure to conceive in cycling queens are listed in Table 2 and discussed in subsequent sections.

     In the majority of queens, ovulation occurs following a copulation-induced pituitary LH peak, which is directly proportional to the number of breedings. Ovulation occurs in only 50% of queens bred just once, while it occurs in 100% of queens bredR4 times. Breeding too early (1st day of heat) or too late (R5th day of heat) also may not induce ovulation as the follicles may not be mature enough or might be undergoing atresia, respectively. Failure of the tomcat to achieve complete intromission, which can be due to a vaginal abnormality (persistent hymen, adhesion, neoplasia) or to a penile problem (hair-ring, etc) can also lead to an incomplete LH peak.

     Cystic endometrial hyperplasia (CEH) develops normally during a luteal phase and then regresses during periods of uterine quiescence. Exposure to repeated luteal phases might cause CEH to persist and predispose the queen’s uterus to develop a pyometra, which tends to be more common in adult or older animals, especially in nulliparous. Open cervix pyometra often compromises future fertility.

     Total oviductal aplasia (often accompanied by ipsilateral ovarian and uterine horn aplasia) is reported as a cause of feline infertility. Oviductal villous hyperplasia as well as utero-tubal junction hyperplasia are also reported in the queen and can cause infertility. Hydrometra (accumulation of serous, clear or opaque noninflammatory fluid in the uterus) has also been occasionally reported as a cause of feline infertility.

     Lack of experience or presence of a hair-ring may prevent the tomcat from achieving a complete penetration, therefore, causing insufficient or no LH peak in the queen. Less common and poorly reported causes for failure to conceive in the feline are lack of ejaculation or poor semen quality.

     Feline serum progesterone concentrations start rising between 76 and 100 h following ovulation. In order to diagnose ovulation failure, P4 can be assayed between the 1st and 4th week following breeding. The cause of ovulation failure can be investigated by: (a) carefully collecting history relative to number and time of observed breedings during heat, and evaluating whether or not administration of hCG (100–250 UI IM) or GnRH (50 µ IM) at subsequent breeding may be advisable; (b) performing a vaginoscopy using an otoscope with the queen, under general anaesthesia to check for vaginal abnormalities; and (c) checking the tomcat’s penis for the presence of hair-rings. 

     Diagnosis of pyometra in the queen is based on the presence of one or more of the following signs: leukocytosis, uterine enlargement, abdominal enlargement, purulent vulvar discharge, anorexia, fever. Open cervix pyometra can be treated with specific antibiotic therapy and administration of natural prostaglandin F2alpha compounds (0.2–0.5 mg/kg BID until uterine size has returned to normal). Developmental defects of the reproductive tract can be diagnosed through ultrasound, contrast radiographic studies of vagina, cervix and uterus, or through laparoscopy/laparotomy. The role of the male can be investigated performing a vaginal smear or a vaginal lavage with sterile saline, right after the breeding to check for presence of spermatozoa.

     Mid-term abortion is not an uncommon event during the feline pregnancy, and infectious agents play a major role in determining death of the conceptus. Data on incidence of feline abortion are relatively scarce, while neonatal mortality is estimated to occur in 6–12% of pregnancies, although in some catteries such value may be as high as 50%. Because of the negative effect of an infectious disease outbreak in a cattery, small animal practitioners must know how to confirm and characterize a diagnosis of infectious abortion and how to differentiate it from abortion due to endocrine insufficiency or abnormal fetal development. Other causes of feline abortion, such as use of drugs, toxic agents, trauma, uterine torsion or nutritional problems will not be dealt with in this discussion. Feline pregnancy loss can be due to infection, fetal defect or maternal endocrine imbalance. Viral causes include panleukopenia virus, feline rinotracheitis virus, feline leukemia virus, and perhaps feline infectious peritonitis. Embryonic/fetal pathology depends on the stage of gestation at time of infection, and can go from abortion to stillbirth, neonatal death or cerebellar hypoplasia. Abortion can also be caused by a nonspecific secondary reaction to viral infection of the mother, as has been observed in experimental abortions induced by IV or IP inoculation of feline rinotracheitis virus. Feline leukemia virus infection of the feto-placental unit has not been reported, although fetal resorption or abortion is documented in FeLV positive queens. 

     Bacterial causes of embryonic/fetal loss in the queen include Brucella spp, Salmonella cholerae suis, Escherichia coli, Streptococcus spp and Mycoplasma felis. Incidence of feline abortion following bacterial infection is unknown. As in the bitch, queens may carry to term viable fetuses in one horn and have a pyometra in the other horn.

     Toxoplasmosis probably causes abortion or fetal loss only because of systemic maternal compromise following acute disease, as no evidence of uterine lesions or fetal infection has ever been produced in queens. Transplacental infection could not be demonstrated when queens were experimentally infected with Toxoplasma gondii before or during pregnancy, although neonatal death prior to 1 month of age has been attributed to the presence of well developed T gondii cysts (which take 4 weeks to form in experimental infection) in dead kittens. Spontaneous chromosomal errors are reported as the cause of abortion or fetal death in the feline.

     Abnormal karyotypes such as 37,XO or trisomy of autosome D-2 have been reported in aborted feline fetuses or found at laparotomy in normal or consistently subfertile queens. Inadequate maternal environment causing endocrine imbalance in pregnant queens may result from cycling during pregnancy, from luteal insufficiency or from noninfectious placental disease. Most of the reported cases of feline abortion (often occurring around day 40) are not associated with any recognized infectious disease, suggesting maternal endocrine imbalance. Recurrent feline abortion in which viral, bacterial, parasitic infections or chromosomal abnormalities have been ruled out has been successfully treated with 1.0–2.0 mg/kg repositol P4 IM every 7 days until 7 days before parturition.

     However, such treatments should never be used in impending abortions or when other causes of embryonic/fetal loss cannot be excluded, such as in first-time spontaneous abortions, as, in general, the effect of a progestational drug may be harmful to the mother whose dead or irreversibly compromised fetuses must be expelled.

     Clinical signs of pregnancy loss in the cat depend on the cause of the problem and are highly variable, ranging from absence of signs to evidence of systemic illness with severe maternal compromise, with or without a 1–2-day course of bloody/purulent vulvar discharge. Diagnosis is based on observation of abortion following a positive pregnancy diagnosis. Fetal and vulvar discharge culture and histology, as well as karyotype of aborted fetuses should always be attempted. The dam should be monitored with a haemogram; serology (FIP, FeLV, toxoplasmosis) should be performed to rule out infective causes, and supportive therapy should be instituted if necessary. Early or late abortions are not considered life-threatening diseases in the feline, unless uterine hemorrhage occurs, which may cause maternal death. Prognosis for both life and fertility is guarded to good.

Chakraborty PK, Wildt DE, Seager SWJ (1979) Serum luteinizing hormone and ovulatory response to luteinizing hormone releasing hormone in the estrous and anestrous domestic cat. Laboratory Animal Science 29, 338–344.

Johnston SD, Bouen LC, Madl JE, Weber AF, Smith FO (1983) X-chromosome monosomy (37,X0) in a Burmese cat with gonadal dysgenesis. Journal of the American Veterinary Medical Association 182, 986–989.

Lawler DF, Johnston SD, Hegstad RL, Keltner DG, Owens SF (1993) Ovulation without cervical stimulation in domestic cats. Journal of Reproduction and Fertility. Supplement 47, 57–61.

Norby DE, Hegreberg GA, Thuline HC, Findley D (1974) An X0 cat. Cytogenetics and Cell Genetics 13, 448–453.

Romagnoli S, Vannozzi I, Ferdeghini M, Pollera C, Merico A, Bigalli L (1996) Spontaneous ovulation in domestic queens kept in a laboratory environment. In: Reproduction in dogs and other carnivores. Satellite Meeting of the 13th International Congress on Animal Reproduction, Sydney, Australia, July 5,

Swanson WF, Graham K, Horohov DW, Thompson DL, Godke RA (1996) Ancillary follicle and secondary corpora lutea formation following exogenous gonadotropin treatment in the domestic cat and effect of passive transfer of gonadotropin-neutralizing antisera. Theriogenology 45, 561–572.

Wildt DE, Guthrie SC, Seager SWJ (1978) Ovarian and behavioural cyclicity of the laboratory maintained cat. Hormones and Behavior 10, 251–257.

Berepubo NA, Long SE (1983) A study of the relationship between chromosome anomalies and reproductive wastage in domestic animals. Theriogenology 20, 177–190.

Cline EM, Jennings LL, Sojka NJ (1981) Feline reproductive failures. Feline Practice 11 (3), 10–36.

Concannon PW, Hodgson B, Lein DH (1980) Reflex LH release in estrous cats following single and multiple copulations. Biology of Reproduction 23, 111.

Dow C (1962) The cystic hyperplasia–pyometra complex in the cat. The Veterinary Record 74, 141–147.

Johnston SD (1989) Premature gonadal failure in female dogs and cats. Journal of Reproduction and Fertility. Supplement 39, 65–72.

Stabenfeldt GH, Pedersen NC (1991) Reproduction and reproductive disorders. In: Feline Husbandry. Disease and Management in the Multiple-Cat Environment. Pedersen NC (ed), Goleta, CA: American Veterinary Publications, pp. 129–162.

Stein BS (1955) Abortion in cats. Modern Veterinary Practice 55, 597.

Swanson WF, Roth TL, Brown JL, Wildt DE (1995) Relationship of circulating hormones, luteal luteinizing hormone receptor and progesterone concentration, and embryonic mortality during early embryogenesis in the domestic cat. Biology of Reproduction 53, 1022–1029. 

Wilson HC (1964) Pyometra in the cat. The Veterinary Record 76, 438. 

.

© 2003 ESFM and AAFP. Published by Elsevier Science Ltd.

* Catopuma badia, o

Gato de Borneo

 

 

STANDARD MANX & CYMRIC

.

. .