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Medical Concerns for Orphan and Fading Kittens
Julie K. Levy, DVM, PhD
Diplomate, American College of Veterinary Internal Medicine
College of Veterinary Medicine
University of Florida
Neonatal kittens face a number of hurdles before they are weaned at 6-8 weeks of age. Studies of kitten mortality in large, well-run breeding facilities confirm the obvious: the best chances for survival of kittens born without birth defects to healthy queens with good maternal instincts and milk supply. Kitten mortality is these settings is often 15-30%, which is higher than for many other domestic and laboratory animal species. The differential diagnoses for kitten losses can largely be narrowed based on the age of the affected kittens, since certain disease processes affect specific age groups of neonatal cats. The immature immune and metabolic systems of neonates often leads to rapid deterioration of ill kittens. Medical intervention instituted after the development of clinical signs of disease may be ineffective. On the other hand, recognition and correction of risk factors before obvious illness develops is often successful.
A survey of kitten mortality over a four-year period in a large breeding facility revealed that low birth weight is the most significant risk factor for death. The average birth weight of surviving kittens is 100 g ± 10 g, and they typically gain 90-100 g/week for the first 6 weeks of life. Wasting and non surviving kittens may be smaller at birth with reduced weight gain or even weight loss. The cause of low birth weight or poor growth is usually difficult to determine but may include immaturity, inborn errors of metabolism, birth defects, infections, nutritional deficiencies, and maternal neglect. Risk of kitten loss was also associated with obese queens, single kitten litters, and for the first kitten born in a litter. In some cases, death is unavoidable, and such kittens should be euthanized as soon as possible to avoid unnecessary suffering. In others, medical intervention and good nursing care may reverse the disease process.
The perinatal period
About half of all kittens that fail to survive to weaning are stillborn or die within the first three days of life.
Factors implicated in perinatal deaths include prematurity, in utero infection with viruses such as feline herpes, feline infectious peritonitis, panleukopenia, and feline leukemia virus, anatomic birth defects (found in about 10% of non surviving neonates), birth trauma, inadequate nutrition, maternal neglect, and environmental stresses. In the breeding cattery, good husbandry practices, including vigorous surveillance for infectious diseases, selection of appropriate breeding stock, strict separation of cat groups by life stage, proper nutrition, and a hygienic environment should reduce or eliminate most infectious causes of perinatal kitten death. If possible, queening should be observed. The higher rate of death of the first kitten born suggests that the queen may not care for her first born as readily as the following kittens. Some queens may not allow nursing until the delivery of the entire litter is complete, thereby subjecting the first born kittens to delayed milk intake. Extended or difficult labor may result in birth trauma, in kittens that are too weak to nurse, or in ill or exhausted queens that are unable to care for their kittens. Although the normal body temperature of newborn kittens is approximately 95 F during the first two weeks of life, they lack a shiver reflex and are only able to raise their temperature about 12 degrees higher that ambient temperature. Thus, they are very dependant upon outside heat sources such as the queen for warmth and will chill rapidly if separated or abandoned. If the core temperature drops below 94 F, they may cease nursing, and if it falls below 90 F, the digestive tract becomes nonfunctional. As the kittens chill further, heart rate, respiration, and metabolism slow, and dehydration and hypoglycemia develop. Regardless of the cause of fading. weak and chilled kittens are resuscitated similarly. Chilled kittens should be warmed slowly to allow the cardiopulmonary system to recover before warmed tissues demand increased oxygen. Because gastroenteritis develops during hypothermia, kittens should not be fed until they are warmed to more than 90 F. Blood glucose should be checked if possible, and hypoglycemia treated as needed by parenteral or oral glucose solutions. Most intravenous solutions and medications may be easily administered by the intraosseous route for rapid effect. Alternatively, glucose can be given empirically to weak kittens. If kittens still refuse to nurse after warming, tube feeding is indicated.
Nursing failure
Milk let-down typically occurs about a day before the delivery, but may be delayed until after birth in some cats. Poor milk production occurs more commonly in primiparous, sick, or undernourished queens. Adequate milk production can be confirmed by expressing milk from each mammary gland. Queens with inflamed mammary glands suggestive of mastitis should not be allowed to nurse their kittens. Colostrum is the first milk produced in the mammary gland. For the first 2-5 days of lactation, the mammary gland actively concentrates immunoglobulin of all three antibody classes, especially lgG. While human babies obtain their antibodies before birth, the structure of the feline placenta almost entirely prevents antibody transfer from queen to kitten in the uterus. Thus, the kitten is dependant on quality colostrum for antibodies that will protect it from infection for the first few weeks of life while the neonate's immune system develops. The kitten can absorb intact antibodies for only the first day of life, after that, the intestinal tract is unable to absorb the large antibody molecules. For these reasons, it is very important for newborn kittens to receive an adequate meal of colostrum during the first hours of life. If the kitten is orphaned or otherwise unable to nurse, serum from a healthy cat can be substituted for colostrum. Five milliliters of serum can be administered orally in the first day of life. If given later, the same volume should be administered subcutaneously or intraperitoneally. If there is concern about adequate passive transfer of maternal antibodies, serum IgG levels may be measured. Following ingestion of colostrum, IgG levels in the neonate generally reach 10-30 mt/mi within 24 hours, which is higher than that of the queen. The half-life of passively acquired antibodies is shorter than that of endogenous immunoglobulin and varies depending upon the inducing antigen. Immunoglobulin levels steadily decline in kittens to a nadir of 5-10 rng/ml at 3-6 weeks before the kitten's own endogenous immunoglobulin levels begin to increase.
Neonatal isoerythrolysis (NI)
Incompatible blood types of the parental cats have recently been implicated as a cause of feline neonatal mortality. This incompatibility arises when queens with Type B blood give birth to kittens who inherited the sire's blood Type A. Type B is rare in mixed breed and Siamese cats, but is much more common in certain purebreds such as British shorthair and Devon rex cats. Type B cats have naturally-occurring anti-A antibodies. When the kittens nurse and absorb these antibodies, the kittens' own red blood cells are hemolyzed, leading to anemia and organ failure. The clinical course is determined by the severity of the hemolytic reaction. In all cases, the kittens are born healthy and nurse vigorously. Some kittens may die suddenly in the first day, while others linger longer and fade during the first week of life. Clinical NI is suggested by dark red-brown urine and confirmed by documenting hemolytic anemia and the blood types of the parents. If NI is suspected, the kittens are removed from the queen and fostered on a Type A queen or bottle-fed for the first two days of life. NI can be avoided in catteries by testing the blood types of breeding animals and avoiding matings of Type B queens with Type A toms. Some breeders are actively attempting to eradicate Type B carriers from their bloodlines. For a complete discussion of feline NI, refer to the Feline Blood Typing lecture by Dr. Cynda Crawford.
One to four weeks of age
While congenital, nutritional, and environmental factors are the most common contributors to perinatal morbidity and morality,
bacterial infection plays a larger role in apparently healthy kittens that fade after the first week of life. It is interesting that in a large survey of 95 specific pathogen free kittens that failed to survive to weaning, only one died after one week of age, while a much higher proportion of kittens died after one week in purebred catteries. This suggests that infection takes a significant toll on kittens reared in conventional settings. The incubation period of various infections accounts for the delay in clinical signs observed following exposure. Typically, an entire litter is affected by the same infection. Thus, it is imperative to perform complete necropsies with microbial culture and sensitivity testing on dead kittens to enable appropriate treatment of the remaining littermates. Although viruses and protozoa claim some kittens during this period, bacterial infections are the most common. At the time of birth, the kitten leaves its sterile uterine protection and enters an environment crowded with bacteria. The kitten's defense against overwhelming bacterial colonization is primarily nonspecific innate immunity and passively acquired maternal antibody. Kittens with failure of passive transfer are especially susceptible to bacterial sepsis. The most common bacterial pathogens cultured from septicemic kittens of this age range are Streptococcus canis and gram negative enteropathogens.
Healthy queens may carry S. canis on the vaginal mucosa asymptomatically and transmit the infection to kittens during birth. Affected kittens are apparently healthy and then die one after the other in the first 1-2 weeks of life. Necropsy olden reveals visceral abscessation and pneumonia. Catteries with a history of S. canis infections can decrease kitten mortality by dipping the umbilical cord in iodine and administering a parenteral dose of penicillin at birth. The queen is given a 1-mi SC injection of a product containing 150,000 IU benzathine penicillin and 150,000 IU procaine penicillin per mi. At birth, each newborn kitten receives 0.25 mi SC of a 1:6 dilution of the same product, and their navels are dipped in a 2% solution of tincture of iodine.
Gram negative infections arise from the normal enteric flora of the queen. Healthy kittens with adequate IgG levels should be able to resist these organisms, but nutritional, environmental, and other stresses can increase their susceptibility. As in S. canis septicemia, kittens with gram negative sepsis frequently appear healthy and vigorous up until a few hours of death. In some kittens, dyspnea from pneumonia may be the only clinical sign. Affected kittens usually decline rapidly, ceasing to nurse and become chilled and inactive. The queen may refuse to care for the kitten and reject efforts to place the sick kitten back with its litter mates. Although there is frequently little external evidence of bacterial infection, necropsy usually reveals widespread sepsis with abscessation of the liver, spleen, and lungs. An abscess internal to the umbilical stump may mark the point of entry in some kittens. Bacterial culture and sensitivity are essential to guide therapy for the remaining kittens.
Because gram positive and gram negative infections are difficult to distinguish clinically and may occur in combination, and because the entire litter is at risk, it is advisable to treat the remaining litter mates prophylactically with antibiotics while awaiting final necropsy and culture results. The decision to treat kittens already showing signs of sepsis or dyspnea should take into consideration the likely advanced state of infection and poor prognosis for survival these kittens have. Suspected sepsis should be treated initially with antibiotics selected for coverage of both gram positive and gram negative organisms and then modified if culture results become available. Enrofloxacin (5 mg/kg) with cephalexin (22 mg/kg) provide excellent coverage for most commonly cultured organisms. The antibiotics are administered subcutaneously once daily until 2 weeks of age, and then twice daily for older kittens. Enrofloxacin may cause areas of baldness at injection sites. Antibiotics may be given orally, but absorption is less predictable, and normal intestinal flora is more likely to be disrupted. Careful maintenance of fluid balance, blood glucose, and body temperature is essential. Cessation of nursing behavior is a serious warning sign that necessitates tube feeding and increased nursing vigilance.
Other infections
There is a wide variety of pathogenic organisms that threaten kittens in this age group, and frequently entire litters are affected. Toxoplasma gondii, acquired prenatally or through the milk, may cause severe disseminated disease. Treatment with sulfa antibiotics or clindamycin is recommended for T. gondii infection. Tyzzer's Disease caused by Bacilluspiliformis, can also affect suckling kittens, causing diarrhea and hepatic necrosis, but effective treatment has not been described. Mycoplasma spp and Bordetella bronchiseptica may also disseminate or result in pneumonia. These and other infections likely represent opportunistic agents in kittens with waning immunity due to poor passive transfer, malnutrition, concurrent disease states, or environmental stresses.
Four to seven weeks of age
While congenital defects and environmental challenges are the most likely causes of morbidity and mortality in neonatal kittens,
and bacterial infections are the primary threat to kittens during the next few weeks of life, viral infections and weaning stresses increase in weanling kittens. Kittens are unable to generate a fever in response to infection until they reach 6 weeks of age. This may make it difficult to monitor response to therapy in younger kittens and may enhance the virulence of infections. Respiratory infections caused by herpes virus and calicivirus, which rarely kill adult cats, may become life-threatening in young kittens. Nasal congestion, oral ulcerations, and polyarthritis ("febrile limping kitten syndrome"), may cause kittens to stop nursing or eating solid food, resulting in rapid weight loss and dehydration. Death in this setting is usually due to secondary effects and inanition, rather that to direct viral pathogenesis. Coronaviruses, agents of enteric diarrheal disease and feline infectious peritonitis (FIP), can spread throughout a cattery, causing vomiting, diarrhea, and dehydration, although "outbreaks" of classic FIP do not occur. Kittens that acquire FeLV infection transplacenta!ly or during nursing may begin to fade during this period, especially if other medical or environmental stresses are present. Kittens infected with FeLV may be seronegative for several weeks to months following infection, so repeat testing may be necessary to identify FeLV infection in fading kittern that initially test negative. On the other hand kittens are rarely infected with FIV from their positive mothers. Because FIV infection is diagnosed with an antibody test, kittens that have nursed from FIV-positive queens will initially test positive themselves from the maternal antibody absorbed with the colostrum, even though the kittens are not truly infected with the virus. This FIV-specific maternal antibody may be detected as long as six months after birth. Therefore, a diagnosis of FIV infection should not be made from an antibody test prior to 6 months of age. The superb efficacy of vaccines against feline panleukopenia virus has drastically reduced the incidence of this lethal viral infection in the past few decades. When panleukopenia infection does occur, it is in kittens that are exposed to the hardy virus during the vulnerable period in which maternal antibody is declining but endogenously produced antibodies produced in response to vaccination have not yet reached protective titers.
Parasitic infections also reach pathogenic levels in this age group of kittens. Coccidia infection, which may be inapparent in adults, can cause severe diarrhea and malnutrition, resulting in rapid weight loss, hypoglycemia, and dehydration. Coccialia are highly contagious and survive in the environment despite extensive decontamination efforts. Coccidia infection is readily diagnosed by fecal floatation and should be considered in kittens that develop diarrhea in this age range or older. Treatment is with sulfadimethoxine (50 mg/kg PO first day, then 25 rog/kg PO q day for 5-20 days until asymptomatic and fecal flotation negative) which is coccidiostatic, not coccidiocidal. Recovery from coccidia infection requires an intact immune response, so treatment failures can often be traced to concurrent immunosuppressive conditions such as malnutrition, overcrowding, and poor hygiene. If coccidiosis is diagnosed in a group of cats, all of the animals should be treated. Ascariasis (round worms) also becomes significant in this age group, and large worm burdens can lead to malnutrition and poor growth. Because maternally acquired ascaridiasis is so common, all kittens should receive routine de-worming treatments with pyrantel pamoate (10 mg/kg orally, repeated in two weeks), regardless of fecal test results. Flea infestation becomes important in kitten health because severe blood loss from the blood-sucking insects may result in life-threatening anemia. Infested kittens should be bathed in a shampoo labeled for use in young kittens and kept in a flea-free environment. Sprays and dips with residual activity are generally avoided in very young or debilitated kittens.
Weaning stress - Kittens of the same age or within the same litter may mature at different rates, so it is not possible to enforce rigid weaning schedules on all kittens. Healthy kittens will generally show interest in solid food at 4-5 weeks of age. Weak, unthrifty kittens will grow more slowly, and tooth eruption may be delayed, resulting in kittens that physically lag behind their true age and require prolonged nursing. Hand reared kittens may become very attached to bottle feeding and resist solid food well beyond normal weaning ages. In these cases, prolonging the interval between feedings and offering formula in a dish will usually entice the kittens to begin eating on their own. In general, housing orphaned and weanling kittens in small groups improves activity and weaning success, but careful attention must also be paid so that less outgoing kittens are not crowded out by cage mates and to ensure that each cat in the group continues to thrive.
Principles of neonatal kitten care
As mentioned above, passive immunity is critical for survival of young kittens. If kittens are suspected not to have nursed, or if measured IgG levels are below normal, supplemental immunoglobulin can be provided in the form of serum. Ideally, the serum donor will share the same environment with the kittens, so that the transfused antibodies will be specific for the organisms the kittens are exposed to. However, since kittens are often overwhelmed by ubiquitous cutaneous and enteric flora, most senun sources will offer protection. Frozen serum may be stored for at least a year, so banking 5 mi aliquots of senun doses in advance is a convenient means of assuring a ready supply for use in breeding facilities or for orphan kittens. Once signs of infection occur, it is doubtful that serum administration will be beneficial to the individual, but treating the remaining litter mates may prevent further losses. If IgG measurement is impractical, an alternative practice is to administer serum empirically to all kittens at risk: orphans, poor nursers, fading kittens, and littermates of kittens that have died of infectious disease.
Intravenous administration of blood products, fluids, glucose, and medications is the most reliable method of delivery, but venous access may by limited in very small or debilitated kittens or in kittens treated outside of the clinic. The intraosseous route is approximately equivalent to intravenous administration, although some solutions, such as concentrated glucose, should be diluted before use. A 22-gauge needle is easily placed in the proximal humerus or femur, and can be bandaged into place for repeated use. As for intravenous catheter placement, strict aseptic technique is observed to prevent nosocomial infection. Other possible routes of administration include intraperitoneal, subcutaneous, and oral, but absorption is slower and less predictable.
Regardless of the cause of illness, sick neonatal kittens frequently stop nursing or eating, and can rapidly dehydrate, loose weight, and become hypothermic. Because kittens have limited fat and glycogen stores, inanition occurs quickly, often leading to death in kittens that did not originally suffer from fatal disease. Regular weight measurements should document steady weight gain of approximately 100 g/week during the first weeks of life. If weight loss or fading is observed, supplemental feeding should be started early. In very young kittens, orogastric is the simplest method. Selection of the largest possible soft rubber feeding tube (eg. 8 French) is recommended, since inadvertent tracheal intubation is less likely with a larger tube. If prolonged tube feeding is anticipated (eg. very sick kittens, or following orofacial surgery) nasogastric tubes may be left in place to avoid the stress of repeated tube placement. Nasogastric tubes are easily placed in even newborn kittens (3.5 French).
Queen's milk is the obvious diet of choice, and orphan kittens should be fostered onto lactating queens whenever possible. Good queens with inadequate milk supply may still be valuable mothers, performing housekeeping and socialization duties while the kittens are fed by bottle. Kittens raised by queens frequently have better social development than hand-reared kittens. Vigorous orphan kittens will usually readily accept bottle feedings, if kittens are to be reared completely by hand, urination and defecation must be stimulated by rubbing the perineum with a damp cotton ball. Kittens develop the ability to urinate and defecate on their own by 5 weeks of age.
Poor maternal behavior can often be corrected by reducing stress and distraction in a quiet, safe environment flee of human interference. If the queen still neglects the litter, she should be confined to a small space with kittens. Resting benches and other alternatives to the nest box should be removed. If necessary, the queen may be restrained to allow the kittens to nurse. Queens often accept their litter after several nursing sessions. If the queen is highly distracted or agitated, mild sedation may encourage maternal behavior. Hand-rearing or transfer to a foster queen may be required if bonding is unsuccessful.
Used with permission.
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