Congenital defects of newborn puppies, most common in the French Bulldog breed. Death of newborn puppies Causes of deformities in puppies
Hypothermia(as well as overheating) is one of the most dangerous factors threatening the life of newborn puppies. As already noted, for the puppies to function normally, it is necessary to maintain an optimal temperature in the nest. In the first week of life it is 20°C; Depending on the type of coat, fluctuations of 1.5°C are permissible. If the puppy’s body temperature is below the age norm, then this is hypothermia. In this case, it must be warmed up urgently. It is best to place the puppy against your own body under a sweater or jacket. It takes a long time to warm him up: for example, if the body temperature is 34.4 0 C, then warming up will take two to three hours. Under no circumstances should puppies be warmed up quickly using a hot heating pad, as the skin vessels expand and additional heat loss occurs from the surface of the body, as a result the puppy has to expend additional energy. A chilled puppy should not be fed either mother's milk or artificial food, since the stomach and small intestines will not be able to cope with the load in this case. During the warming process, he is given a 5-10% solution of glucose with water at the rate of 3.5 ml per 100 g of body weight per hour. Instead of glucose, you can use a solution of honey, or, in extreme cases, sweetened water: 3/4 teaspoon per 100 ml of water.
Insufficient weight gain. Normally developing puppies gain weight daily, and by the 8th to 10th day their weight doubles. If the puppy does not gain weight, you need to carefully examine him and find out the reason. If there are several such puppies in the litter, then we can assume that the problem is in the mother (toxic milk, inflammation of the uterus, insufficient milk production). The puppy may be born underdeveloped (hypotrophic). Such puppies at birth have a low weight (25% lower than that of their littermates), they have underdeveloped muscles and subcutaneous tissue, shallow breathing and they suck inactively. Their ability to thermoregulate is even less advanced than that of normal puppies. Such puppies are artificially fed and raised in an incubator. A sudden drop in weight accompanies diarrhea, which is associated with loss of water from the body. In this case, it is urgent to replace the loss of water and electrolytes, otherwise the puppy will die from dehydration. To combat dehydration, Ringer-Locke solution is used, mixed in half with a 5% glucose solution. The dose is 1.8 ml per 100 g of body weight per hour. The solution is dispensed from a bottle, syringe or pipette. It is more effective to administer this mixture subcutaneously. At the same time, the puppy is warmed up. Puppies that are not gaining weight due to lack of food whine, tremble, and look lethargic. Such puppies are immediately transferred to artificial feeding and warmed up, since dehydration quickly occurs with insufficient nutrition.
Hypoglycemia(decreased blood glucose levels) is most often observed in puppies of toy breeds aged 6-12 weeks. This condition is usually preceded by stress: change of place of residence, transportation, etc. Symptoms arise unexpectedly: the puppy refuses to eat, chills, apathy, and indigestion appear. Then muscle weakness and tremors develop (especially in the facial muscles). In milder cases, the puppy appears weakened and his gait is unsteady and unsteady.
Attention! This condition is very dangerous and can result in seizures and death of the puppy. Therefore, treatment must be started immediately to avoid the death of the animal! If the puppy’s consciousness is preserved, a 5-10% glucose solution, honey solution or sweetened water is poured into his mouth. The condition should improve within half an hour. If the puppy is unconscious, emergency medical attention is required. To prevent repeated attacks, the puppy must be fed more often (at least 3 times a day) high-quality food with added sugar or honey, and given food in small portions.
Gastrointestinal disorder due to errors in feeding. A normally developing puppy gains weight daily, appears calm, and has normal stools—hard, yellowish in color. Usually there is stool after each feeding. Underfeeding or overfeeding bottle-fed puppies immediately affects the nature of their stool and the frequency of bowel movements. The first sign of overfeeding is loose stools. If overfeeding is insignificant, then the stool is yellow in color. With severe overfeeding, it acquires a greenish color, due to the presence of unchanged bile due to the accelerated movement of food masses through the intestines. In these cases, it is sufficient to dilute the feeding mixture with water in a 1:1 ratio. After the color and consistency of the stool are restored, the concentration of the mixture is gradually adjusted to the original concentration. If overfeeding was prolonged and there was a violation of the enzymatic function of the intestines, then the diarrhea becomes gray. The most severe condition is when food is not digested at all., then the feces resemble curdled milk. In this case, dehydration occurs very quickly. (For the fight against dehydration, see above.) In this case, puppies are given 1 teaspoon or 1 tablespoon (depending on weight) of smecta every 3-4 hours, and the feeding mixture is diluted with water in a 1:1 ratio.
Toxic milk syndrome. In some cases, milk from lactating bitches can be toxic. One of the main causes of illness in bitches: inflammation of the uterus or mastitis. This can also be caused by taking drugs or medications. When puppies get into their bodies with milk, toxins cause digestive upset. This is usually seen in puppies between 3 and 14 days of age. The most typical symptoms are diarrhea and bloating. These puppies whine, look exhausted, and may drool. In the case of toxic milk syndrome, puppies are immediately weaned from the bitch and transferred to artificial feeding. Puppies are given smecta internally, warmed up and treated for dehydration. The bitch is given a scarf around her chest and belly. If the puppies are in satisfactory condition, the mothers allow them to be cared for.
Cardiopulmonary syndrome or neonatal circulatory failure, observed in puppies during the first five days of life. It is caused by various stressful situations, to which newborn puppies are very unstable (cold, overheating, insufficient milk, etc.). All this causes a drop in temperature, respiratory rate and heart rate. As a result, food digestion is disrupted or stops completely. If the body temperature drops to 34.5 °C and below, then there is an even greater depression of vital functions, which soon becomes irreversible. To prevent the death of puppies, immediate measures must be taken to normalize vital functions. The symptoms of cardiopulmonary syndrome, regardless of the cause, are the same: puppies begin to drool, they scream, and make swallowing movements. Puppies become weak very quickly, stop moving and lie on their sides. The heart rate is reduced to 40 beats per 1 minute, and the respiratory rate is reduced to 4 times per 1 minute. This leads to impaired cerebral circulation, which manifests itself as seizures. Convulsions are accompanied by cessation of breathing. Blood may appear in the stool and urine, and fluid may leak from the nostrils. If this happens, it means that the changes have become irreversible.
Attention! Cardiopulmonary syndrome requires emergency medical care!
Inflammation of the navel. The umbilical stump can become a gateway to infection in newborns. The reasons for its inflammation are the handling of the navel after the birth of the puppy with contaminated instruments or dirty hands, an insufficiently clean living environment for the newborn, or diseases of the mother’s teeth (if she chewed the umbilical cord). An inflamed navel looks red, swollen, and can fester. Since the navel vessels are connected to the liver, this condition poses a real threat to the health and life of the puppy - he may develop sepsis. The navel is treated with hydrogen peroxide and antibiotic ointment. If necessary, the doctor prescribes antibiotics orally or intramuscularly. A sick puppy can pose a danger to littermates, as it is a carrier of the infection.
Puppy septicemia(puppy death syndrome) The disease is usually observed from the 4th to the 40th day of life. Its causes may be the mother's infected birth canal, infected mother's milk and navel diseases. Place of entry of infection - gastrointestinal tract. The first symptoms resemble toxic milk syndrome: the puppy screams, his stomach is swollen and tense. Subsequently, the abdomen swells even more and becomes hard as a board. The skin of the abdomen acquires a dark red or bluish tint, which indicates the development of peritonitis. The puppy develops chills, weight loss, and dehydration. The disease very quickly ends in the death of puppies. If you take the puppies away from their mother in time and start treatment (antibiotics, combating dehydration, artificial feeding), then recovery is possible.
Herpesvirus infection of puppies - It is an acute, non-febrile infection of newborn puppies, usually occurring before 14 days of age. Infection occurs during the passage of the mother's birth canal. The virus develops at low body temperature (less than 36.7°C). Hypothermia contributes to the development of the disease. The puppies stop sucking, scream, they develop chills, bloating (the abdomen is painful and soft), and the stool is liquid and yellow-green in color. Coordination of movements may be impaired. There is no cure. Animals die within 24 hours after the onset of the disease. Infected puppies raised in an incubator may survive if their body temperature is above 7.8 °C. Recovered puppies may develop kidney failure by 8-10 months. No vaccine has been developed for the herpes virus.
Swimmer puppy. Normally developing puppies begin to stand at two weeks of age and walk confidently by three weeks of age. If the puppy does not begin to walk within this time frame, then he will be a “swimmer”. Such puppies have limbs turned outward, and they resemble sea turtles. This pathology can be congenital (especially in cocker spaniels) and acquired (in obese puppies of breeds with massive bones). Slippery floors contribute to the development of this pathology. As a rule, the pathology is incurable.
Pyloric stenosis(narrowing of the pyloric opening). This is a congenital pathology in which the muscle ring of the pyloric (outlet) opening of the stomach is thickened. Often found in boxers. With pyloric stenosis, puppies vomit after sucking, while they suck actively. Puppies can eat vomit, but the vomiting is repeated. Such puppies are retarded in growth and development. The diagnosis is confirmed by x-ray. Treatment is surgical.
IntroductionBirth defects are abnormalities in the structure or functioning of organs that are already present at the time of birth. Such defects, found in most breeds of dogs and cats, arise as a result of pathological processes occurring at certain stages embryonic development. Contrary to popular belief, they are not always the result of genetic disorders and can be caused by various factors. The term “congenital” does not mean “hereditary”, although there are pathologies that are both congenital and hereditary. Many defects cannot be detected without clinical or laboratory examination. It is estimated that a combination of birth defects that pose a threat to the life of the newborn occurs in 1-2% of purebred puppies. Unfortunately, the incidence of congenital pathologies has been determined in only a small number of studies.
Hereditary diseasesObviously, if among animals raised in the same nursery or representing a certain breeding line, there is an increase in the number of cases of hereditary defects, then research into the causes of their occurrence is required. For this purpose, it is necessary to collect a family history and conduct a pedigree analysis. It is extremely important to establish which of the deviations are explained by genetic factors and to exclude carriers of these genes from breeding. However, in some cases, if a genetic disorder is suspected, to confirm the diagnosis, it is recommended to carry out control matings to establish the type of inheritance and the carrier of the defect. It is to be expected that genetic screening tests will be available to enable identification of underlying defects.
Types of inheritanceDifferent forms of a gene located on a specific part of a chromosome are called alleles. The specific location of a gene on a chromosome is called a locus. The term "gene" is usually used to mean an allele or locus. Although any animal can have a maximum of two different alleles at a single locus, the number of different alleles in a population can exceed this figure, in which case the locus is said to have multiple alleles. The transfer of genes from one generation to another is called inheritance.
Genetic diseases are caused by the transmission of a pair of mutant genes, one mutant gene, or polygenic inheritance. The phenotypic manifestations of a genetic defect may change depending on external conditions or under the influence of other genes.
Recessive inheritanceSimple autosomal recessive inheritance is the most common pattern of gene transmission. In this case, identifying hereditary characteristics is difficult due to the fact that the defect becomes obvious only in homozygous individuals ( ahh), who received mutant gene alleles from each of the heterozygous ( Ahh) apparently healthy parents. With continued crossing of animals that carry the trait, the defect appears in 25% of the offspring, while 50% of the offspring turn out to be healthy carriers. In table Table 13.1 shows the calculated results of matings of carriers of a single autosomal recessive trait.
Table 13.1. Predicted results of all possible matings relative to a single autosomal recessive traitBy excluding carriers of the defective gene from breeding, it is possible to reduce the incidence of anomalies transmitted by a recessive type.
Dominant inheritanceWith dominant inheritance, a distinctive trait appears in heterozygous individuals, so diseases inherited according to a dominant type can be easily prevented by excluding carrier animals from breeding. Disorders such as coagulopathies due to deficiency of factors X and XI are rare.
Incomplete dominant inheritanceSometimes genes have multiple alleles but do not function in a dominant/recessive pattern of inheritance, in which case heterozygotes exhibit the effects of both alleles. In this case, all carrier animals should be excluded from breeding. Crossing healthy animals and carriers of severe forms of the defect produces only sick offspring. Crossing animals with minor deviations produces 25% healthy offspring, 50% with minor deviations and 25% with severe congenital disease.
Incomplete penetranceIn some cases, the gene is not fully expressed. If we are talking about a dominant gene, then the combination AA will appear the same way Ah, because the A is dominant in relation to A. If A has 100% penetrance, then the offspring will have three different genotypes ( AA, AA And ahh) and two phenotypes ( AA And ahh), because the A always shows himself to be dominant. However, if the combination Ahh sometimes gives external manifestations of the phenotype ah, speak of incomplete penetrance. If heterozygotes Ahh the dominant trait is expressed in 75% of cases, talking about 75% penetrance. The reasons for incomplete penetrance are unknown.
Table 13.2. Hereditary pathologies of the musculoskeletal systemPolygenic inheritancePathology - Comments
Head:Cleft palate/lip - It occurs in various breeds, especially brachycephalic breeds and Siamese cats. A simple autosomal recessive pattern of inheritance in the English Bulldog. May be caused by hypervitaminosis A or medicines, such as griseofulvin and corticosteroids.
Overshot (retrognathia) or undershot prognathia) - It is inherited in an autosomal recessive manner in long-haired dachshunds and cocker spaniels. Prognathia (according to the breed standard) is observed in Burmese and Persian cats.
Cranioschisis - Non-fusion of the cranial vault; observed in cocker spaniels as a lethal recessive trait.
Otocephalic syndrome - Described as an autosomal recessive trait in beagles; in a mild form, it is characterized by partial agnathia, hydrocephalus and fontanel defects, and in a high degree of severity - by the absence of all cranial structures located in front of the medulla oblongata.
Axial skeleton:Spinal pathologies:
Atlantoaxial instability - Congenital hypoplasia of the odontoid process and/or non-fusion with C2; observed in small breeds (Pomeranian Spitz, Chihuahua).
Spina bifida - Absence of the dorsal part of the vertebrae. Occurs in rare cases; described in Maltese dogs and Siamese cats.
Dewclaws on the hind legs - An autosomal dominant trait in most breeds.
Muscles:Myopathy - In Golden Retrievers, the defect appears at 6–8 weeks of age and consists of severe muscle atrophy of the tongue/diaphragm; inherited as a sex-linked trait. Myopathy in Labradors develops from 3 months of age and is inherited in an autosomal recessive manner. In male Irish Terriers, sex-linked hereditary myopathy appears from 8 weeks of age.
Myotonia - Hereditary defect associated with impaired intracellular calcium transport (chow chow, Staffordshire bull terrier).
Abdominal wall defects:Umbilical hernia - Inherited as a threshold trait in the Basenji, Airedale Terrier, Pekingese and Weimaraner.
Inguinal hernia - Inherited as a threshold trait in the West Highland Terrier, Basenji, Basset Hound and Pekingese.
Polygenic inheritance is an inheritance in which a trait is determined by several genes, but each gene has a relatively small effect, and in addition, external factors play a significant role, under the influence of which the inherited trait can manifest itself to a greater or lesser extent.
Threshold signsSome traits are controlled by many genes but have a narrow range of expression depending on the number of genes involved. Thus, there is a threshold at which an inherited trait can change from one form to another; an example is non-occlusion of the ductus arteriosus, which can be complete or partial. Other examples are cryptorchidism and umbilical or inguinal hernia.
Sex-linked inheritanceAny trait controlled by a gene located on the sex chromosome is, by definition, associated with gender. As far as we can tell, the Y chromosome is relatively inert. The X chromosome carries the hemophilia A gene and some other defects. A female can pass the hemophilia gene to offspring of either sex, while a male can only pass it on to females because male offspring do not inherit the father's X chromosome.
Sex-limited inheritanceWe are talking about the inheritance of a trait characteristic of only one sex, for example, lactation is observed exclusively in females, but the inheritance of this ability is determined by genes transmitted to both sexes; Cryptorchidism can be transmitted by females, but only appears in males. With limited sex inheritance, the trait is not linked to the X or Y chromosome, but its manifestation is limited by gender.
Chromosomal aberrationsChromosome aberrations are rare in dogs and cats. Such disorders occur spontaneously, are inherited or develop under the influence of external factors. Sometimes a violation of the chromosome set occurs as a result of duplication or loss of a chromosome. Either a single chromosome or an entire chromosome set can undergo duplication. It is likely that most chromosomal abnormalities result in embryonic death rather than the development of birth defects. Chromosome abnormalities may affect sex chromosomes; Thus, the appearance of XXX, XXY and other combinations leading to intersexuality has been described in Weimaraners and Cocker Spaniels.
Non-genetic causes of birth defectsThe first of these reasons is the use of pharmaceutical drugs during pregnancy: under the influence of griseofulvin, microphthalmos can occur in kittens and cleft palate in puppies; progestogens prescribed at the beginning of pregnancy cause masculinization of the external genitalia in female puppies, including clitoral hypertrophy; corticosteroids increase the risk of developing generalized edema of the subcutaneous tissue in puppies of brachycephalic breeds and can lead to deformation of bone tissue; The formation of congenital heart defects, cleft palate, microcephaly and other abnormalities is associated with the effect of anticonvulsants. Therefore, when prescribing any medications to pregnant females, it is necessary to take into account the likelihood of teratogenic effects.
Table 13.3. Hereditary malformations of the reproductive systemDefect - Comments
Gonadal agenesis or hypoplasia - The defect is unilateral or bilateral; obviously not inherited. True or pseudohermaphroditism. Disorders of sexual differentiation: abnormalities of X/Y chromosomes, gonads and phenotype.
Intersexuality - Intersexuality may be hereditary or caused by nongenetic factors (eg, exposure to exogenous progestogen in utero).
Hypospadias - Displacement of the urethral opening caused by incomplete fusion of the urethral folds.
Persistent Müllerian duct syndrome - Typically seen in dogs with cryptorchidism, but also occurs in normal male dogs. From the inside, both testes are attached to the cranial ends of the bicornuate uterus.
Cryptorchidism - Unilateral or bilateral, considered a hereditary defect, usually seen in dwarf and brachycephalic breeds (Persian and other cat breeds).
In some cases, the development of pathologies is associated with exposure to food: hypervitaminosis A (125,000 mg/kg) between 17 and 22 days of pregnancy can cause cleft palate, kinked tail and deformed ears in kittens. Excess vitamin D causes tissue calcification, intrauterine fontanelle fusion, hypoplasia of tooth enamel and supravalvular stenosis.
It is assumed that some chemicals that pollute the environment have a teratogenic effect, but it is quite difficult to prove the validity of this hypothesis. In some cases, birth defects are caused by infection, for example, feline parvovirus causes cerebral hypoplasia in kittens. Observations show that the teratogenic effect depends on the stage of intrauterine development. Exposure at the stage of organ formation in the first trimester of pregnancy leads to the development of defects in the brain, organs of vision, hearing and heart disease. vascular system. Exposure during the transition period, i.e. after the 26th day of intrauterine development, causes mainly defects of the palate, cerebellum, of cardio-vascular system and/or genitourinary system.
In many cases, it is not possible to determine the causes of birth defects; Sometimes such anomalies are of a single, isolated nature.
Types of Birth DefectsBirth defects may affect a single structure or function, but they are often a syndrome of multiple defects and are often breed related. The true prevalence of birth defects is unknown because they are not always detected at birth and many cause fetal death. For example, heart defects become apparent as the puppy grows older and begins to move more; Such a defect of the visual organs as progressive retinal atrophy manifests itself only in adult animals. Some defects are detected at autopsy or biochemical/hematological studies.
Inborn errors of metabolism are based on genetically determined enzyme deficiency. Any metabolic process can be disrupted due to a defect in the gene responsible for the synthesis of the corresponding enzyme. As a rule, such a defect is autosomal recessive or gender-related. There are two main types of enzyme deficiency: the first leads to an abnormal accumulation of metabolic intermediates; the second is characterized by a deficiency of lysosomal enzymes responsible for the decomposition of complex carbohydrates. Many metabolic disorders remain undetected or are not recorded for economic reasons. The most commonly reported birth defects involve damage to the central nervous system, vision, musculoskeletal and cardiovascular systems. According to a study conducted by the author on the problems of newborn mortality, the most common malformations of bone tissue (cleft palate, cleft lip). Genetically determined congenital defects are more often observed in purebred dogs.
Information on the most common birth defects occurring in puppies and kittens in the first 3 months of life is given in Tables 13.2–13.12 (data taken from Leipold, 1978; Willis, 1992; Jubb et al, 1993; Casal, 1995; Hoskins, 1995 a, b). Cases where the hereditary nature of the disease is known are reflected in the “Comments” column. The predominance of certain pathologies in various breeds is not indicated in the tables, and the order in which breeds are listed is in no way related to the frequency of lesions. The fact is that the prevalence of hereditary animal diseases in different countries varies, so data from studies may not be consistent. The hereditary nature of some diseases has been confirmed, but in many cases the defects are characteristic only of a specific breeding line.
PUPPY EXHAUSTION SYNDROME
DefinitionPuppy fading syndrome is a serious problem for breeders and veterinarians. There are various assumptions about the reasons for its occurrence, and many experts doubt that extinction syndrome is a separate disease. On the other hand, an unsuccessful attempt was made to include in this syndrome all pathologies that lead to weight loss in the first month of life.
Table 13.4. Congenital pathologies of the central nervous systemTable 13.5. Hereditary pathologies of the urinary tractPathology - Comments
Malformation:Cerebral hypoplasia - One of the most common birth defects of the central nervous system. Has an obvious hereditary character in the Chow Chow. May be of viral origin (parvovirus infection in cats); it is assumed that in some cases it occurs under the influence of toxins. Cerebral dysfunction is evident from birth. Not progressing.
Cerebral abiotrophy - Early or accelerated degeneration of formed elements. Ataxia and hypermetria are observed from 12 weeks of age. Registered in a number of breeds (Airedale Terriers, Scottish Setters, Border Collies). Hereditary degeneration of brain tissue in the area of the striatum - substantia nigra and cerebellum - olive is observed in Kerry Blue Terriers, probably as an autosomal recessive trait.
Hydrocephalus - It is observed mainly in Chihuahuas, cocker spaniels, and bulldogs; sometimes caused by non-genetic causes (for example, inflammatory processes). Found in Siamese and other cat breeds.
Spinal dysraphism - Duplication, absence or underdevelopment of the central canal; appears from 4–6 weeks of age; noted in Weimaraners, probably as an autosomal recessive trait.
Myelinopathies:Hereditary myelopathy - Progressive ataxia; observed in Afghan hounds (3–12 months). Inherited as an autosomal recessive trait. Myelin lysis and cavitation formation occur mainly in the thoracic spinal cord.
Hereditary ataxia - It is observed in Fox Terriers and Jack Russell Terriers and is inherited as a simple autosomal recessive trait. It appears from 2–4 months and progresses rapidly.
Central hypomyelination and demyelination - Generalized tremor occurs from 2–3 weeks of age. Occurs in Chow Chows, Springer Spaniels, Samoyed Laikas, Weimaraners and Bernese Mountain Dogs. X-linked inheritance in springer spaniels.
Hypertrophic neuropathy - Described from the Tibetan mastiff. Disruption of myelin formation affects only peripheral nerves. Develops as a result of primary metabolic defects of Schwann cells. Appears at 7–10 weeks. Recessive inheritance.
Axonopathies and neuropathies:Progressive axonopathy - It is observed in boxers and is inherited in an autosomal recessive manner. The posterior brainstem and spinal cord are most affected. Appears from 8 weeks of age.
Lysosomal storage diseases:Globoid cell leukodystrophy. Galactocerebroside-?-galactosidase deficiency - Appears from 3–6 weeks of age; in Cairn and West Highland Terriers, as well as in Miniature Poodles, it is inherited as a simple autosomal recessive trait; accompanied by impaired myelination. It is also observed in domestic mongrel cats, in which it manifests itself from 2 weeks of age.
Gangliosidosis - German Shorthaired Pointers, Portuguese Water Dogs, Japanese Spaniels and Mixed Breeds; Siamese, Korat and domestic mongrel cats.
Glucocerebrosidosis - Australian Silky Terriers.
Sphingomyelinosis - Dwarf poodles, domestic mongrel cats, Siamese and Balinese.
?-L-fucosidosis - Springer Spaniels; autosomal recessive inheritance; appears from 6 months of age.
?-L-iduronidosis - Domestic cats are not purebred.
Amylo-1,6-glucosidosis - German shepherds, mongrel domestic cats.
Phosphofructokinosis - English Springer Spaniels.
Ceroid lipofuscinosis - Many breeds including English Setter, Chihuahua, Dachshund, Saluki, Border Collie, Tibetan Terrier, mixed breed dogs and Siamese cats.
Table 13.6. Hereditary diseases of the cardiovascular systemPathology - Comments
Kidneys:Renal agenesis - Double-sided/one-sided. It is observed in beagles, Scottish shepherds, and Doberman pinschers. May be combined with abnormalities of the reproductive tract.
Renal hypoplasia - Appears sporadically; the kidneys appear as miniature versions of normal ones and contain a reduced number of histologically normal nephrons.
Renal dysplasia and aplasia - Dysplasia means the presence of segmental anomalies, aplasia is a malformation of the entire kidney. Dysplasia occurs as a hereditary disease in the Sealyham Terrier, Lhasa Apso, Shih Tzu and Small Poodle. It is also believed to be hereditary in Keeshonds, Chow Chows and Miniature Schnauzers. Some cases of renal dysplasia in dogs have been linked to the herpes virus.
Polycystic kidney disease - Formation of fluid-filled cysts in the renal parenchyma. It may develop as an autosomal disease or as a consequence of progressive renal failure. Found in Persian cats and Cairn terriers.
Ectopy and fusion of the kidneys - Congenital displacement of one or both kidneys; fusion is the union of normal kidneys. The etiopathogenesis is unknown.
Formation of duplex or accessory buds - The presence of one or more accessory kidneys or a duplex - an organ containing two kidneys, the renal pelvis and the ureter. Rarely observed.
Fanconi syndrome - Generalized tubular kidney dysfunction. It is observed in Basenjis, Norwegian Elkhounds, Schnauzers and Scottish Shepherds. The hereditary nature has not been confirmed.
Primary glycosuria - Impaired reabsorption of glucose in the renal tubules. Found in Scottish Terriers, Norwegian Elkhounds and mixed breeds. The type of inheritance is unknown.
Cystinuria - Impairment of renal tubular transport of cystine and other two basic amino acids. It is observed in many breeds, especially in males. In Irish and Scottish Terriers, it is probably inherited in a recessive manner.
Hyperuricuria - Hyperuricuria is increased production of uric acid caused by urease deficiency. It is observed in Dalmatians and is inherited in an autosomal recessive manner.
Primary hyperoxaluria - Acute renal failure caused by oxalate deposition in the tubules. It is observed in domestic outbred shorthaired cats.
Nephrogenic not diabetes - Severe polyuria; nocturia and growth retardation in puppies.
Ureters:Agenesis - Bilateral or unilateral (the latter is observed more often and is accompanied by ipsilateral renal aplasia).
Duplication - Associated with the formation of a duplex and additional buds.
Ureteral valves - They are caused by the preservation of transverse folds of the rudimentary mucous membrane and smooth muscles.
Ectopic ureters - Single-sided or double-sided; may be intra- or extramural and combined with other malformations of the genitourinary tract. It is more often observed in mixed breeds, but there is a predisposition in huskies, Labradors, Newfoundlands, English bulldogs, West Highland terriers, white, Skye and fox terriers, Welsh corgis, golden retrievers, miniature and toy poodles.
Urethrocele - Congenital cystic expansion of the submucosal layer of the ureter (terminal section) with protrusion into the lumen of the bladder.
Table 13.7. Hereditary diseases of the endocrine systemDisease - Comments
Non-infection of the arterial (botallian) duct - The most common congenital heart defect - inherited as a polygenic threshold trait; in poodles it is inherited with a high degree of probability. It is often found in Pomeranians, collies, Maltese dogs and English springer spaniels, but can also be found in other dog breeds, as well as Siamese, Persian and other cat breeds.
Subaortic stenosis - The second most common vice. Usually has subvalvular localization. Inherited as a polygenic trait in Newfoundlands. It is observed in golden retrievers, Rottweilers, and boxers.
Pulmonary artery stenosis - The third most common vice. Most often observed in beagles, chihuahuas, English bulldogs, fox terriers, Samoyed huskies and miniature schnauzers; usually caused by dysplasia of the pulmonary valves; is inherited in beagles as a polygenic trait.
Anomalies of the vascular ring - The fourth most common defect. There is a breed predisposition in German Shepherds and Great Danes. Includes a number of anomalies caused by impaired embryonic development of the aortic arches. The most common anomaly of this type is non-closure of the right arch (with preservation of the right ductus arteriosus).
Ventricular septal defect - It usually occurs as a single septal defect located just below the tricuspid and aortic valves. No breed predisposition has been identified. Often combined with other anomalies.
Tetralogy of Fallot - Includes ventricular septal defect, right ventricular outflow tract obstruction, right ventricular hypertrophy, and dextraposition of the aorta, which receives blood from both ventricles. Polygenic threshold inheritance has been confirmed in the Keeshond.
Tricuspid valve dysplasia - Described in dogs of large breeds.
Mitral valve disease - Found in Great Danes and German Shepherds.
Heartbreaking vices - Atrial septal defects; usually combined with other congenital defects.
Endocardial fibroelastosis - Congenital defect - characterized by proliferation of elastic and collagen fibers of the endocardium. It is observed mainly in young cats, especially Burmese and Siamese breeds, and sometimes occurs in puppies, often in combination with other heart defects.
Congenital rhythm disorders - Ventricular extrasystole can occur as an isolated pathology or be accompanied by congenital anatomical defects; Fatal ventricular arrhythmia is inherited in some lines of German Shepherds. Atrial arrest syndrome has been described in young springer spaniels, Siamese, Burmese and domestic mongrel shorthair cats. Hereditary AV node stenosis with sinus delay occurs in pugs.
Alpha-glucosidase deficiency causes myocardial dysfunction in the Lapland dog, and mucopolysaccharidosis I (lysosomal enzyme deficiency - L-iduronidase) - in young plothounds.
Extracardiac arteriovenous fistulas - The defect can be congenital or acquired and occurs anywhere in the vascular system, but usually in large vessels, internal organs, or distal parts of the extremities.
Table 13.8. Hereditary skin diseasesDisease - Comments
Juvenile diabetes mellitus - Insulin-dependent diabetes appears before the age of 12 months. In Keeshonds, the disease is caused by hereditary B-cell atrophy and is inherited as an autosomal recessive trait with incomplete penetrance. Apparently, it is also inherited as a recessive trait in golden retrievers.
Hypoplasia of the pituitary gland - Pituitary dwarfism is transmitted as an autosomal recessive trait in German Shepherds and Karelian Laikas.
Congenital idiopathic diabetes - Described from a male toy poodle.
Congenital hypothyroidism - It occurs as a result of dysgenesis of the thyroid gland, disturbances in the formation and serum transport of thyroid hormones, their congenital deficiency and severe iodine deficiency. The mode of inheritance in dogs has not been established. In Abyssinian cats it is inherited in an autosomal recessive manner.
Table 13.9. Hereditary diseases of the respiratory systemDisease - Comments
Imperfect epitheliogenesis - A rare congenital defect of squamous epithelium.
Ichthyosis - Extreme degree of keratosis. It is observed in Doberman Pinschers, West Highland Terriers, Irish Setters, Collies, Bull Terriers, Boston Terriers, Labrador Retrievers, Jack Russell Terriers.
Congenital seborrhea - Found in English Springer Spaniels. Puppies develop areas of hyperkeratosis and peeling skin.
Nevus - Focal skin defects arising from epithelial or dermal structures or a combination of both.
Dermoid sinus or cyst - It is localized mainly along the midline of the back, running down to the supraspinous ligament. The defect is caused by incomplete separation of the neural tube from the skin during embryogenesis. Characteristic of Rhodesian Ridgebacks, in which it is probably inherited in an autosomal recessive manner.
Hereditary alopecia and hypotrichosis (ectodermal defects and dysplasia) - A rare disease that manifests itself in newborns; characterized by alopecia of varying severity. In the affected areas, the number of adnexal structures is reduced. The disease can manifest itself in isolation or in combination with other ectodermal pathologies, for example, with impaired formation of the dentition. Sex-linked inheritance is assumed in males of the poodle, basset, beagle, Labrador retriever and bichon frise breeds, in females - the Labrador retriever and Rottweiler breeds; the disease has also been described in cats of the Sphynx, Cornish, Devon Rex, Mexican Hairless, Siamese and Burmese breeds.
Ehlers-Danlos syndrome - Structural defects of collagen leading to hyperextensibility of the skin; It is found in dogs of the English springer spaniel, beagle, boxer, German shepherd, greyhound, dachshund, St. Bernard, mixed-breed dogs, as well as in Himalayan cats and a number of other breeds. It can occur as a result of a spontaneous mutation or be inherited as a dominant autosomal trait.
Acrodermatitis - Described in American Bull Terriers. Affected puppies are stunted, have weaker pigmentation than normal, and have difficulty swallowing. By the 6th week of life, skin lesions develop on the paw pads, ears, face and around natural openings.
Epidermolysis bullosa - Occurs in newborn toy poodles.
Pigmentation defects associated with deafness - Partial or complete albinism may be accompanied by deafness, especially in white bull terriers, Sealyham terriers, white and black collies and Dalmatians, as well as in white cats; may be combined with eye defects. Autosomal dominant type of inheritance with incomplete penetrance.
Vitiligo and poliosis - It is observed in Rottweilers, especially in adults, less often in puppies.
Leukotrichia (poliosis) - Premature graying; found in Labrador Retriever puppies.
Table 13.10. Hereditary diseases of the digestive systemDisease - Comments
Hypoplasia of the larynx - It is inherited in an autosomal recessive manner in Skye Terrier dogs.
Tracheal hypoplasia - It appears during the first 2 months of life, most often in English bulldogs.
Congenital hiatal hernia - May be inherited in an autosomal recessive manner.
Primary ciliary dyskinesia - Dysfunction of the ciliated epithelium of the respiratory tract, leading to decreased mucociliary clearance. It is observed in English Pointers, Springer Spaniels, Border Collies, English Setters, Dalmatians, Doberman Pinschers, Golden Retrievers, Old English Sheepdogs, Chihuahuas, Chow Chows, Bichon Frizes.
Table 13.11. Hereditary diseases of the blood and lymphatic systemDisease - Comments
Digestive tract:Congenital megaoesophagus (enlargement of the esophagus) - Apparently, this pathology is caused by developmental disorders or underdevelopment of neuromuscular structures. It is found mainly in Great Danes, German Shepherds and Irish Setters, less commonly in other breeds. It is considered a hereditary disease in miniature schnauzers. Inherited in an autosomal dominant manner or with 60% penetrance in an autosomal recessive pattern.
Segmental aplasia of the digestive tract Absence of anus - Leads to death soon after birth. Most often, the author observed this pathology in the small intestine.
Congenital pyloric stenosis - Found in boxers, Boston terriers, and Siamese cats.
Liver:Portosystemic venous shunt and intra-renal arthrio-portal fistula - The most common congenital anomaly of the hepatobiliary system. Manifested by a violation of portal circulation.
Inborn errors of metabolism - Diseases accompanied by the accumulation of mucopolysaccharides. Copper storage disease in Bedlington Terriers (autosomal recessive inheritance).
Table 13.12. Hereditary visual impairmentsDisease - Comments
Congenital coagulopathies:Coagulation factor VIII deficiency (hemophilia A) - One of the most common defects of the blood coagulation system. An X-linked recessive type of inheritance has been identified in the Irish Setter, St. Bernard, Scottish Sheepdog, Beagle, Collie, German Shepherd, English Setter, Greyhound, Weimaraner, Chihuahua, Cairn Terrier, Samoyed Laika and Husky. It appears in a less pronounced form in cats.
Coagulation factor IX deficiency (hemophilia B) - Recessive, X-linked trait; less common than factor VIII deficiency. Known in Cairn Terriers, St. Bernards and mixed-breed dogs, as well as in British Shorthairs, Siamese and domestic mongrel shorthair cats.
Coagulation factor VII deficiency - Found in miniature schnauzers, malamutes, boxers, bulldogs, beagles; manifests itself as a mild coagulopathy.
Coagulation factor X deficiency - In cocker spaniels it is inherited in an autosomal dominant manner. Severe hemorrhagic diathesis occurs in newborns and young dogs, but in older older animals the disease is mild.
Insufficiency of coagulation factor XI (precursor of blood plasma thromboplastin) - In the English Springer Spaniel, it is inherited as an autosomal dominant trait with incomplete penetrance or as an incomplete recessive trait. It manifests itself as episodes of mild bleeding, which, however, can become severe during surgical interventions. Occurs, although relatively rarely, in Pyrenees Mountain dogs, Weimaraners and Kerry Blue Terriers.
Congenital disorders of exogenous platelet functionFunctional disorders:
von Willebrand's disease - The disease is caused by deficiency or absence of von Willebrand factor (factor VIIIR); in dogs, this is the most common of all hereditary blood clotting pathologies. It has also been described in the Himalayan and a number of other cat breeds. It is inherited according to an autosomal type with incomplete dominance (in most dog breeds), less often - according to an autosomal recessive type. Factor VIIIR is required for platelet adhesion to the subendothelial surface.
Congenital disorders of endogenous platelet functionFunctional disorders:
Canine thrombopathy - Known among Basset Hounds.
Thrombasthenic thrombopathy - It is inherited in an autosomal recessive manner in Otterhounds. Characterized by the presence of giant platelets.
Spitz thrombopathy - Observed in two female Spitz breeds.
Cyclic hematopoiesis - An autosomal recessive disease in gray collies. Characterized by cyclical fluctuations in the concentration of circulating neutrophils, reticulocytes and platelets, which is caused by a congenital stem cell defect bone marrow. Most puppies die within the first 6 months of life.
Anemia:
Pyruvate kinase deficiency - It is inherited in an autosomal recessive manner in Basenjis. Nonspherocytic hemolytic anemia.
Hemolytic anemia - It is manifested by a decrease in the life expectancy of erythrocytes and chondrodysplasia inherited in an autosomal recessive manner. Specific for Malamute dogs.
Non-spherocytic hemolytic anemia - It is severe in poodles and beagles, in which it ends in death in the first 3 years of life. The reason is unknown.
Phosphofructokinase deficiency - Chronic hemolysis with hemolytic crises and mild myopathy. Specific to Springer Spaniels.
Defects - Comments
Eyelids:Ectropion - It is inherited in St. Bernards, Bloodhounds, Bulldogs, Chow Chows, Irish Setters and Cocker Spaniels, but can also develop as a secondary disease due to injuries and conjunctivitis.
Entropion - Inherited in dogs of the Chow Chow, Bloodhound, Great Dane, Labrador, Bulldog, Bullmastiff, Spaniel (Springer and Cocker), Papillon, St. Bernard, Golden Retriever and Pomeranian breeds; Along with this, it can be an acquired disease. Also observed in Persian cats.
Diamond-shaped deformation of the eyelid - A predisposition has been identified in St. Bernards and Clumber Spaniels.
Districhiasis - Formation of a double row of eyelashes; it is inherited among Pekingese, poodles, cocker spaniels, collies, and dwarf long-haired dachshunds.
Trichiasis - Eyelash growth in the wrong direction; described in Pekingese dogs. It can also be an acquired disease that developed as a complication of a mild form of entropion.
Entropion of the third century. - A predisposition has been noted in the German Shepherd and Great Dane.
Agenesis - Absence of certain areas of the edges of the eyelids; may be combined with other hereditary eye defects, such as iris coloboma and dermoids; It occurs in various breeds of dogs, as well as in domestic (mongrel) shorthaired and Persian cats.
Underdeveloped or imperforate lacrimal puncta - Found in Bedlington Terriers, Cocker Spaniels, Sealyham Terriers, and Golden Retrievers.
Eyeball:Microphthalmia (in rare cases - complete absence of the eyeball) - May be combined with other eye malformations. It is inherited in a number of dog breeds, such as the Miniature Schnauzer, Old English Sheepdog, Akita Inu, Cavalier King Charles Spaniel, and is observed in puppies obtained from gray-black parents.
In the Australian Cattle Dog, microphthalmia occurs together with multiple colobomas and is inherited as an autosomal recessive trait linked to color. The development of microphthalmia has been reported in the offspring of cats treated with griseofulvin during pregnancy.
Divergent strabismus - Described in brachycephalic dog breeds, including Boston Terriers.
Convergent strabismus - Typical for Siamese cats.
Spontaneous nystagmus - In Siamese cats; caused by an abnormal development of the visual pathways.
Cornea:Deep corneal opacification - Formed as a result of fusion of the remainder of the embryonic pupillary membrane with the inner part of the cornea; It is inherited in Basenji dogs. In other breeds it occurs in rare cases.
Epibulbar dermoids - They occur in dogs of various breeds, but St. Bernards, German Shepherds, Dachshunds and Dalmatians appear to have a predisposition. Also described in cats - Burmese, Burmilla and domestic short-tailed.
Corneal dystrophy - Familial bilateral symmetrical corneal opacities not associated with any previous eye damage.
In most cases, corneal stromal dystrophy (with lipid deposition) is clinically evident in dogs over 1 year of age. Progressive corneal dystrophy has been described in Manx cats. It is characterized by swelling and ulceration of the stroma in kittens from 4 months of age. It is assumed that the disease is inherited in an autosomal recessive manner.
Anterior chamber of the eyes:Preservation of the pupillary membrane - Hereditary disease of Basenji dogs.
Iris cysts - Formation of fluid-filled vesicles in the endothelium of the iris; They are usually found in the anterior chamber of the eye.
Pupil abnormalities - Corectopia (non-centered position of the pupil). May be combined with multiple eye malformations. It is inherited among Australian Cattle Dogs.
Heterochromia of the iris - Difference in the color of the irises of an individual; most often observed in subalbino animals. The pathology is typical for Persian and Angora cats. In dogs, multiple eye development disorders are often combined with partial albinism and deafness.
Malformations of the iris and cornea - Congenital preservation of mesoderm remnants in the iridocorneal angle. In Basset Hounds.
Lens and vitreous body:Changes in the size and shape of the lens - Because the embryonic lens influences the development of the eye, lens abnormalities are often associated with multiple ocular defects.
Congenital cataract - It may be hereditary or occur during intrauterine development. Congenital cataracts occur in dogs of the Beagle, Cocker Spaniel, Cavalier King Charles Spaniel, Old English Sheepdog, Australian Cattle Dog, Bedlington Terrier, Sealyham Terrier, and Labrador Retriever breeds. Juvenile cataracts develop from the neonatal period until animals reach 6 years of age. Heredity plays a major role in the pathogenesis of this pathology, although cataracts can also develop as a consequence of inflammatory processes, metabolic disorders, malnutrition, intoxication and injury. This pathology has also been described in domestic (mongrel) shorthair cats and in Persian, Burmese and Himalayan breeds.
Hyaloid residual deformation - The most common disorder of the formation of the vitreous body.
Persistent primary vitreous hyperplasia and secondary glaucoma - The presence of a fibrovascular membrane on the posterior surface of the lens; observed in different breeds. The hereditary nature of the disease has been established in dogs of the Doberman Pinscher, Staffordshire Bull Terrier and Bouvier des Flanders breeds. Autosomal dominant inheritance has been identified in border collies and terriers (in particular, wire-haired fox terriers, Jack Russell terriers, Sealyham terriers, Tibetan terriers, wire-haired and smooth-haired dwarf bull terriers).
Goniodysgenesis of the pectineal ligament and glaucoma - It is inherited in dogs of the Basset Hound, Siberian Husky, American Cocker Spaniel, Cocker Spaniel, Dandie Dinmont Terrier, Elkhound, Great Dane, Welsh Springer Spaniel and Welsh Terrier breeds.
Retina and optic nerve:Collie eye abnormality - A hereditary disease of rough and smooth collies, Scottish collies, border collies, and Australian cattle dogs. Inherited in an autosomal recessive manner, it is characterized by chorioretinal hypoplasia, optic disc coloboma and retinal detachment.
Multifocal retinal dysplasia - It is inherited in English Springer Spaniels and Labrador Retrievers as an autosomal recessive trait, including multifocal retinal folding and retinal detachment. Isolated or in combination with other eye development disorders, it occurs in a number of other dog breeds (American Cocker Spaniel, Beagle, Akita Inu, Australian Cattle Dog, Doberman Pinscher, Old English Sheepdog, Rottweiler, Yorkshire Terrier, German Shepherd, Cavalier King). Charles Spaniel, Hungarian Puli, Elkhound and Field Spaniel). Congenital retinal dysplasia may also be non-hereditary.
Generalized retinal dysplasia - It is inherited in Bedlington Terriers, Labrador Retrievers and Sealyham Terriers.
Hemeralopia - Hereditary day blindness (absence of cones; fundus without features), characteristic of Malamute dogs; begins to appear at the age of 8–20 weeks, also described in the toy poodle (onset at the age of 12 weeks). Autosomal recessive trait.
Congenital permanent night blindness - Clinically manifested in Briard and Tibetan Terrier puppies at the age of 6 weeks. Presumably inherited as an autosomal recessive trait.
Optic nerve hypoplasia - Reducing the size of an optical disc, single-sided or double-sided. Occurs in dogs of any breed.
Generalized progressive retinal atrophy (PARA) - Hereditary disease. The generalized form of PAS develops in dogs aged from several months to several years (depending on the breed). Registered in Rough Collies, Miniature Schnauzers, Gordon Setters, Irish Setters, Miniature Poodles and Toy Poodles, American Cocker Spaniels, Norwegian Elkhounds, Longhaired Miniature Dachshunds, Chesapeake Bay Retrievers, Golden Retrievers, Tibetan Spaniels, Cardigan Vellip Corgis , Irish Wolfhounds and Akita Inu. Autosomal recessive type of inheritance. Feline hereditary retinopathy has been sufficiently studied only in Abyssinian breed. In these animals, the disease can occur in 2 forms: 1) an early-onset form (kittens become blind already in the first 2 months of life), developing as a consequence of rod and cone dysplasia and inherited in an autosomal dominant manner; 2) a late-onset form (cats go blind at the age of 5–10 years), developing as a result of degeneration of the affected rods and then cones and inherited in an autosomal recessive manner.
According to the data obtained by the author, highest scores Neonatal mortality occurs in the short period of time between 3.5 and 5 days after birth. A picture emerges in which the puppy’s weight at birth corresponds to the breed standard, other parameters also indicate favorable development prospects, and yet such a puppy suddenly stops gaining weight and dies for no apparent reason, usually between the third and fifth days of life. The condition of the female is, as a rule, good; pregnancy and childbirth proceeded without any special features. The development of the syndrome is not associated with dystocia, lack of maternal instinct or milk deficiency.
Vulnerability of newbornsTo adequately assess the appearance and reactions of newborns, one should first take into account the fact that a newborn puppy is an immature animal, different from an adult; within 3 weeks the cub is completely dependent on the mother and is very vulnerable. The four main reasons for its vulnerability are given below.
Problems with thermoregulation. The mechanism of thermoregulation in puppies is poorly developed. During the first day after birth, body temperature is 35.5 °C, by the seventh day it rises to 38? C, and by the fourth week - to 38.5? C. Normal temperature fluctuations are considered to be between 27.5°C and 36°C. Initially, temperature is maintained by the breakdown of brown fat, which occurs under the control of the sympathetic nervous system (non-yeast thermogenesis). Heat production due to trembling (muscle contraction) appears by 6–8 days; by 4 weeks, the puppy’s thermoregulatory mechanism has fully developed. While the puppies are in close contact with their mother, they receive enough warmth to maintain the required body temperature. If there is no such contact (the bitch does not care for the cubs well, or the puppies are raised without a mother), there is a danger of hypothermia.
Risk of developing dehydration. Water makes up 82% of a newborn's total weight, but the puppy's kidneys are still functionally immature. Glomerular filtration increases from 21% at birth to 53% by the 8th week of life, and tubular secretion is finally formed by the 8th week. The daily fluid requirement is 60–90 g/450 g live weight per day, and fluid turnover is almost twice that of adult animals. Glucosuria is typical for newborns under 2 weeks of age. It is important to provide newborns with regular feedings to maintain hydration.
Risk of developing hypoglycemia. Puppies are born with a relatively low glycogen reserve (located primarily in the liver). Lack of food leads to a rapid reduction in this reserve and the development of hypoglycemia on the second day. It is necessary that puppies gain weight daily from the first day of life. Normally, weight should double by day 10.
Immaturity of the immune system. It is important that puppies receive colostrum within the first 12 to 24 hours of life, since only 5% of maternal antibodies pass through the placenta. Despite its immaturity, the immune system is susceptible to stimulation. The development of the immune system is completed by 3–4 months of age.
Normal behavior and appearance newbornsNewborns spend most of their time sleeping, interrupted by short periods of feeding; from 4 weeks of age this behavior is replaced by activity. Lack of active sleep indicates a painful condition. During the first 3 weeks of life, the central and peripheral parts of the nervous system mature, so the neurological reactions of newborns differ from those of adult animals. The predominance of flexor tone observed at birth is replaced by the predominance of extensor tone by the third day of life. At 3 weeks of age, the puppy can already stand, demonstrating normal tone and postural reflexes. The eyes open by 10–15 days, but vision remains poor until 4–5 weeks of age. The external auditory canals open by 12–14 days, which can be determined by the appearance of a pronounced reaction to a sharp sound. A healthy newborn screams only when scared or hungry; Excessive vocalization indicates the presence of some abnormalities. The puppy strives to move and purposefully crawls towards the nipple; The sucking reflex occurs when the mouth comes into contact with the nipple. A healthy puppy has a round belly, a full but not bloated stomach, a smooth coat, a warm body and supple skin.
The immaturity, small size and vulnerability of newborns force their condition to be assessed using criteria different from those used for adult animals. Criteria used include changes in behavior, signs of dehydration and/or cooling, and weight loss or failure to gain weight. Examination of the newborn includes looking for birth defects (eg, cleft palate, missing anus), injuries (swelling, rib/limb fractures, hemorrhages), or symptoms of inflammation of the umbilical cord and eyelids (ophthalmia neonatorum). Newborns need their mother to lick them regularly to ensure regular bowel and bladder movements and to keep their genitals clean. Dirty, matted fur indicates an undeveloped maternal instinct in the female.
Puppy Fading Syndrome; clinical and pathological signsExtinction syndrome is expressed in the fact that, despite the absence of abnormalities at birth, puppies lose weight (in many cases during the first day of life), demonstrate a reduced sucking reflex and general lethargy, or, conversely, are excessively restless and continuously squeak pitifully; gradually they weaken and die. Sudden, unexpected death is not typical for this syndrome. Postmortem examinations reveal a decrease in weight compared to birth weight and the absence of food debris in the stomach and intestines; There are no signs of any diseases or developmental defects. The ratio of liver weight to total body weight ranges from 1:10 to 1:20. Pathomorphological examination of the main organs does not reveal any infectious diseases or other specific injuries.
Impact of the care systemAccording to the data available to the author, mortality is not associated with the care system or breed characteristics, although certain trends can be traced: in many nurseries there are bitches whose litters regularly die from puppy extinction syndrome, while the remaining bitches successfully raise their offspring.
Research methodsDue to the absence of specific symptoms, post-mortem examinations should be carried out in order to exclude other causes of death (septicemia, birth defects, maternal injury). To obtain representative data on the causes of neonatal mortality, studies are carried out on dead puppies from different litters obtained over a fairly long period of time. Even puppies from the same litter can die from various causes. Before autopsy, corpses are stored at +4 °C, but not frozen, since freezing and subsequent thawing damages the integrity of the tissue. According to the author, the most common causes of death of puppies (about 50% of cases) include the following:
Infectious diseases(mainly bacterial);
Factors associated with care (underdeveloped maternal instinct in the female);
Low birth weight;
The presence of congenital pathologies.
When establishing the cause of death, it is necessary to take into account the identified clinical signs of disease and the characteristics of housing, which also include caring for the female, especially during childbirth and the postpartum period. The following are considered important factors:
The design of the enclosure and the room intended for litter;
Heating system, presence of drafts, risk of hypothermia;
Practice of care and monitoring of newborns, especially during the first 2–3 days;
Hygiene measures;
Availability of qualified personnel;
Presence of infection vectors (birds, mice);
Risk of infection associated with newly arrived animals (eg studs);
The nutritional level and health status of animals used for breeding;
Timely deworming;
Timely vaccination.
Apparently, the first five factors deserve the most attention, since they largely determine the conditions in which the first critical days of puppies’ lives pass.
It is important that the breeder carefully records all data regarding the litter, including details such as birth weight and daily weight gain for the first 3 weeks; Subsequently, such records will allow an objective assessment of the situation. A study of one deceased puppy, conducted several months or even years after the death of the litter, can hardly be regarded as informative.
Despite all the efforts made by the author, in approximately 50% of cases the specific cause of death of the puppies could not be determined. Nevertheless, based on the autopsy results, it was possible to outline a general clinical picture. It was established that the puppies died in a large group in a short period of time, and no signs of infectious damage were found; death probably resulted from a process that began on the first day of life or even before birth. Therefore, in the absence of other assumptions, it seems logical to group these cases under common name"Puppy Fading Syndrome"
Possible Causes of Puppy Fading SyndromeWhen studying the composition of lung surfactant, a significant decrease in the content of phosphatidylcholine (lecithin) was found; similar changes were identified in sudden infant death syndrome. Pulmonary surfactant is essential for normal respiratory adaptation and maintenance of breathing after birth. Changes in surfactant composition lead to difficulty breathing/sucking and predispose to the development of hypoxia. It remains unclear, however, whether this disorder is the main cause of death or only accompanies some other pathology, for example, respiratory failure of central origin.
The manifestation of extinction syndrome in the first 24 hours after birth suggests that puppies are born with reduced viability and that there are undetected prenatal factors leading to death. As already mentioned, the offspring of some bitches are at risk, while other bitches have puppies that survive well. It can be assumed that there is a genetic predisposition, however, judging by the fact that the death of puppies (sometimes entire litters) is observed in all breeds and is not associated with closely related breeding, it cannot be explained only by genetic reasons.
Treatment approachesThere are no data on successful treatment of the syndrome. The use of antibiotics, as a rule, does not bring the desired result. Since the deadly problems of dehydration, hypoglycemia and weight loss occur soon after birth, it is likely that the main problem lies in the baby's lack of contact with its mother and its weak sucking response. Assessing this possibility requires research into the physiology of postnatal adaptation in puppies and their sucking reflexes in the first 24–48 hours of life. It should be noted that early administration of supplemental nutrition to puppies suspected of developing fading syndrome appears to improve survival. Unfortunately, in practice, maintenance therapy is prescribed too late in most cases.
LITERATURE
Blunden A. S. (1983) Neonatal and Perinatal Mortality in the Dog: Clinical, Pathological and Managemental Studies. PhD Thesis, London.
Blunden A. S. (1988) Diagnosis and treatment of common disorders of newborn puppies. In Practice10 , 175–184.
Blunden A. S., Hill C. M., Brown B. D. and Morley C. J. (1987) Lung surfactant composition in puppies dying of fading puppy complex. Research in Veterinary Science42 , 113–118.
Casal, M. L. (1995) Feline pediatrics. Veterinary Annual35 , 210–228
Detweiler D. K., Hubben K. and Patterson D. (1960) Survey of cardiovascular disease of dogs. 21 , 329–359.
Evans J. M. (1978) Neonatal mortality in puppies. In: Refresher Course in Canine Medicine. Proceedings No. 37. University of Sydney, Sydney, pp. 127–139 Fox MW (1970) Inherited structural and functional abnormalities in the dog. Canadian Veterinary Journal11 , 5.
Hodgman S. F. J. (1963) Abnormalities and defects in pedigree dogs. An investigation into the existence of abnormalities in pedigree dogs in the British Isles. Journal of Small Animal Practice4 , 447.
Hoskins, J. D. (1995a) Congenital defects of the cat. In: ed. S. J. Ettinger and E. C. Feldman, pp. 2106–2114. W. B. Saunders, Philadelphia.
Hoskins, J. D. (1995b) Congenital defects of the dog. In: Textbook of Veterinary Internal Medicine: Disease of the Dog and Cat, 4th edn, ed. S. J. Ettinger and E. C. Feldman, pp. 2115–2129. W. B. Saunders, Philadelphia.
Hoskins J. D. (1995c) Puppy and kitten losses. In: Veterinary Pediatrics, 2nd edn, ed. J. D. Hoskins, pp. 51–55. W. B. Saunders, Philadelphia.
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Roth J. A. (1987) Possible association of thymic dysfunction with fading syndromes in puppies and kittens. Veterinary Clinics of North America: Small Animal Practice17 , 603–616.
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ETIOPATHOGENESIS AND FEATURES
Characteristics.
It occurs with a specific symptom complex.
Clinical signs.
Most or all of the litter dies suddenly or within a few days. The puppies quickly weaken, scream, and refuse to suckle.
Etiopathogenesis.
This is due to many reasons given below.
Herpes virus infection.
This is an acute, feverless, viremic disease of newborn puppies.
Age. Appears before 14 days of age.
Transmission. It is transmitted transplacentally from the mother or during childbirth when the fetus passes through the birth canal.
Pathogenesis.The development of the virus in the body provokes hypothermia in puppies. Chilled puppies, consuming increased oxygen, fall into a state of hypothermia, which owners mistake for sleep.
Clinical signs.
In addition to nonspecific signs of the disease, puppies develop shortness of breath, nasal discharge, their abdomen is painful and soft, and their feces are greenish-yellow. Ataxia occurs later. The incubation period lasts 1-2 days, puppies die a few hours after the onset of symptoms of the disease.
Puppy death syndrome (infection with beta-hemolytic streptococcus).
Etiopathogenesis.
This is an acute septic condition of newborn puppies, resulting from infection of the mother's birth canal. Infection can also be caused by staphylococci and Escherichia coli, which form hemolysins.
Clinical signs.
Puppies are born healthy, but after 2-3 days they become weak, dehydrated, their abdominal skin is colored bluish-red. Then they die.
Infectious hepatitis.
Characteristic.
This is a lightning-fast disease with sudden death of newborns.
Clinical signs.
After 2-6 days, sudden death occurs without any warning signs. Severe vomiting and bloody diarrhea may occur for a short time. Almost all cases of sudden death of newborns after 14 days of life can be attributed to infectious hepatitis. It is difficult to recognize the disease.
Death of newborns due to intoxication and sepsis in a female.
Clinical signs.
It proceeds in the same way as in previous cases. A distinctive feature is the simultaneous illness of the female and puppies.
Puppy deformities.
The quick death of puppies is caused by deformities such as “cleft palate” (puppies cannot suckle, milk is aspirated into the lungs, and pneumonia develops), atresia of some parts of the digestive tract, and vascular abnormalities.
Clinical signs.
A few puppies die. Sometimes the pathology is clearly visible visually.
Treatment.
Not developed.
Puppy death syndrome (infection with beta-hemolytic streptococcus).
Treatment.
Newborns are given antibiotics (except tetracycline) and transferred to artificial feeding.
Forecast.
If the puppies are taken away from the female and fed artificially, then both she and the puppies will remain healthy.
Infectious hepatitis.
Treatment.
Animals that exhibit the disease are treated with prednisolone, antibiotics, and glucose. There are no preventive measures.
Death of newborns due to intoxication and sepsis in a female.
Treatment.
Transferring puppies to artificial feeding
Puppy deformities.
Prevention. If deformities often begin to appear in the nursery, it is necessary to check heredity and exclude carriers of the trait from breeding work. It is cheaper to prevent the disease than to do expensive tests to determine the causes of death.
Undead puppies with deformities should be immediately euthanized by intrapleural injection of 100-200 g of sodium thiopental.
To avoid stagnation of milk in the female, if possible, not the entire litter is destroyed; 1-2 puppies are left for 10-14 days.
All newborn puppies should be examined for birth defects and deformities. Experience shows that cubs with serious pathologies cannot be saved anyway; they die in any case. Ultimately, they have to be euthanized, so making puppies suffer while prolonging their lives is simply heartless. Very rarely, deformities such as the absence of a head or front paw, or inverted hind limbs are encountered.
Non-union of the abdominal wall
This is a developmental disorder of the fetus in which the intestines and other internal organs are not located inside the abdominal cavity. Breeders often call these puppies “squeezed tubes” because the intestines come out of a hole in the abdominal wall and really resemble toothpaste squeezed out of a tube. It is possible to save newborns with such a pathology only if they were born through caesarean section ensuring sterility. The internal organs are set, the hole in the abdominal wall is sutured. During natural childbirth, while passing through the birth canal, an infection inevitably enters the puppies' body, and subsequently peritonitis develops. They must be euthanized immediately.
Umbilical hernia
A hernia looks like a swelling at the site of the navel. You can get rid of it with a simple surgical operation, but this is not always necessary.
An umbilical hernia can be congenital or acquired. Weakness of the tissue in the navel area can be caused by genetic reasons. Hereditary predisposition is easy to recognize if you carefully observe the puppies and the behavior of the mother: the tendency of the bitch to carry puppies by grasping the umbilical cord with her teeth is genetically determined. However, a hernia sometimes occurs during childbirth if the bitch or person pulls hard on the umbilical cord. In this case, it is associated with trauma, and not with heredity.
If the hernia is repaired every time the puppy is picked up, it sometimes disappears on its own. Pressure bandages and adhesive bandages, for example the Vetrap brand, have proven themselves well. Typically, as the puppy grows, the hernia will decrease. This defect only bothers dogs when it is large. In bitches that are planned to be used for breeding, umbilical hernia must be operated on without fail.
Cleft palate/cleft lip
A cleft lip (cleft lip) is very easy to notice - the upper lip appears to be severely cleft. Sometimes the cleft also involves the nose. In the case of a cleft palate (cleft palate), a gap is formed in the upper palate. All newborn puppies should be examined with a flashlight or by palpating the mouth with a finger. Sometimes the cleft is located very deep, almost at the very throat. These developmental defects occur quite often, both individually and together.
When puppies suckle, some of the milk flows out of the nose without going into the stomach. They often die from exhaustion or inflammation of the lungs; fluid enters the respiratory tract. Sometimes the baby can be saved if fed through a stomach tube. Surgical correction of defects is possible, but in practice it is used very rarely.
Anasarca
This pathology is also called dropsy of the skin, congenital lethal edema.
Newborns with anasarca are often called “walrus babies,” due to the fact that they have bloated bodies, as well as “water puppies,” “rubber puppies,” or “monsters.” They can weigh more than 1.2 kg at birth! Often, due to such pathology of the fetus, the bitch is not able to give birth on her own, and surgical intervention is required. The defect is caused by impaired lymph circulation and may be associated with congenital diseases of the thyroid gland. In severe cases, the outcome is fatal. If the case is mild, breeders can sometimes relieve swelling by administering diuretics immediately after birth and 12 hours later.
Anal atresia
Puppies suffering from this rare birth defect become bloated and scream constantly within the first 4 to 6 days after birth. They have no anus, and the intestines end blindly.
There is a known case in which a ten-day-old Bernese Mountain Dog puppy underwent surgery to remove the rectum and create an artificial anus. Later, throughout his life, he had to carefully monitor the activity of his intestines. If a breeder wants to keep such puppies alive, he must realize that caring for the dogs that grow up from them will not be easy. In the first days of the puppies' life, the anomaly cannot always be noticed, since the mother carefully licks them. In order to make sure that everything is fine with newborns, they need to insert a thermometer into the anus
Swimmer's syndrome in puppies
This puppy developmental disorder (otherwise known as pectus excavatum, sunken chest, or pectus excavatum) can be diagnosed by anyone who has ever seen a swimmer. Puppies have a wide, flat chest; the limbs move to the sides instead of standing straight under the body, so the puppies move by crawling. Their actions resemble the movements performed by swimmers. Sometimes the legs are stretched back, and the babies “swim” like seals. Although in some cases this syndrome develops due to slippery flooring or exposure to other factors environment, most often it is caused by a hereditary defect.
Since such cubs cannot, like other puppies, place their paws straight, they walk (if they walk at all) with a wobbling gait. If this violation is not corrected, the puppies will never walk normally, moreover, they will become crippled and will have to be euthanized. Because they have a sunken chest, they may develop lung and heart disease.
However, this defect can be successfully corrected. If the puppy is taught to stand and walk correctly, his chest gradually restores its normal size and shape. If no measures are taken, it will remain flat, and under the growing weight of the body it will flatten more and more.
In order to get rid of swimmer's syndrome, the cubs are picked up every day and their chest is massaged, trying to give it the correct shape. Rolled towels or rugs are laid out on the floor, creating hills and valleys so that the puppies can pump up their muscles while overcoming obstacles. Such exercises will also be beneficial for their healthy littermates.
One breeder of Sussex spaniels and English bulldogs, breeds in which swimmer's syndrome is often observed, raises their babies on cardboard boxes with cells intended for transporting eggs, which are covered with an easy-to-wash cloth on top. in order to get to the mother, babies have to work and develop muscles all the time
Another way to correct the defect is swimming in water, which promotes the development of muscles and the respiratory system. When puppies sleep, they should be repositioned so that they lie on their sides, not on their bellies. Every time the breeder enters the room, they must turn them over.
In severe cases, it is necessary to tie the puppy's front legs at the elbows so that they assume a normal position. If the hind legs are not positioned correctly, they are also tied. Such puppies should not be overfed. The earlier the correction begins, the easier it is to correct the defect.
Hydrocephalus
This disease begins to appear as the puppies grow. Due to the accumulation of fluid in the skull, pressure on the brain increases, its development slows down and death occurs. This anomaly is more often observed in small decorative and brachycephalic breeds of dogs.
With hydrocephalus, the skull is disproportionately large and has a strongly convex shape. The eyes are bulging and slanted (strabismus). Sometimes there is a divergence of the cranial sutures, covered by soft tissues. It looks like an ungrown fontanel, although it has nothing in common with it. Puppies have impaired coordination of movements, there is a delay in mental development
Heart defects
In some cases, puppies have congenital abnormalities or heart defects. Sometimes they are small and do not appear at all. Other, more serious disorders in the structure and function of the heart have a variety of symptoms.
Immediately after birth, respiratory failure may occur, and in older cubs, exercise intolerance may occur. At the same time, breathing is rapid, shallow, labored, without deep breaths. It is very easy to notice, since normal breathing of healthy puppies is practically inaudible. Sick puppies cough and sniffle, and if the lesion is severe, the mucous membrane of the mouth and paw pads become bluish. Taking such a baby in your arms, you can hear extraneous noises in the chest or feel an abnormal heartbeat rhythm.
During the examination, the veterinarian should be sure to listen to the puppies' chest using a stethoscope.
Some heart defects can be corrected surgically, after which dogs can live a long and happy life. Naturally, animals with heart disease, both genetically determined and non-hereditary, should be excluded from breeding, since pregnancy, birth and raising puppies are too stressful.
Deafness/blindness
Hereditary deafness sometimes occurs in pure white dogs (such as the Dogo Argentino), as well as in double merle dogs. To ensure that puppies have normal hearing, hearing is tested weekly starting at 14 days of age. In this case, it is necessary to ensure that there are no air vibrations (for example, you cannot clap your hands), it is better to knock on the pan, ring a bell or blow a whistle.
Deaf puppies do not turn their ears towards the source of sound and bark differently than their hearing littermates. In breeds where hereditary deafness is quite common, all puppies are tested using a baby test when they stop feeding on their mother's milk. Those who are deaf in one ear need to be removed from the breeding program and neutered, but they are quite capable of living full life as pets.
The causes of blindness can be congenital juvenile cataracts and microphthalmia (reduction in the size of the eyeball). Puppies should be seen by a veterinary ophthalmologist at 8 weeks of age.
INFLAMMATION OF THE BUTTON
Pathogenic bacteria can enter the puppy's body through the belly button and then spread through the bloodstream. As a result, the liver and joints are affected, and a generalized infection occurs.
To avoid infection, during childbirth the umbilical cord must be treated with an alcohol solution of iodine or another disinfectant. It happens that the navel becomes inflamed or becomes wet, in which case the skin around it should be washed twice a day with antibacterial soap and rinsed thoroughly. If this doesn't help, go to your veterinarian. Generalized infection is treated with antibiotics administered parenterally.
HERPES VIRUS INFECTION
Herpesvirus is a highly contagious (contagious) infection and has few symptoms in adult dogs. However, if this infection develops in an unvaccinated pregnant bitch, the virus attacks the fetuses, causing the death of 50-100% of the pups; in this case, miscarriages occur, dead or non-viable puppies are born, which quickly die. Cubs infected from the mother during childbirth or before reaching three weeks of age inevitably die. In the fourth week of life, they have a chance to resist infection.
The virus attacks the kidneys and liver, causing internal bleeding. Infected puppies behave restlessly, trembling, then suddenly go limp, refuse to eat and squeak pitifully. Body temperature may be low, yellow-green diarrhea is observed, and the abdomen is painful. Most babies die within 24 hours. Take one of the dead puppies to a veterinarian to determine the exact cause of death.
The only way to save an infected litter is good feeding combined with antibiotic treatment to prevent the development of secondary infections and measures to combat dehydration. Puppies are removed from the bitch and artificially fed. The room is treated with diluted liquid laundry bleach, and the temperature in it is increased.
At the age of 8-10 months, surviving puppies sometimes experience kidney failure as a result of infection by the herpes virus. The only consolation for the breeder is the fact that all subsequent litters will be protected from herpes virus infection, since the mother’s body develops a strong immunity against it. Since the infection can be spread not only sexually, but also by airborne droplets, to prevent the disease it is better to avoid contact of a pregnant bitch and suckling puppies with other dogs.
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