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The Sick Kitten Rachel Dean BVMS DSAM(fel) MRCVS, Recognised RCVS specialist in feline medicine Associate professor in Feline Medicine, Director of the Centre of Evidence Based Veterinary Medicine, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus. LE12 5RD Tel: 0115 951 6575 Email: [email protected] Kitten – young cat, sick – afflicted with ill health or disease, ailing There are many conditions that can affect a kitten during the first 6 months of life. No matter how small the kitten is a complete clinical examination and history is vital. If the kitten is still with its litter mates or mother, then clinical examination of all ‘in contacts is recommended. These notes will focus on the first 3 months of life. Feline neonates Neonatal kittens that are presented to the veterinary surgeon during the pre-weaning period provide a diagnostic challenge. In the absence of a major congenital defect, clinical examination is often unrewarding. Abnormalities frequently detected in neonates e.g. hypothermia are non-specific and therefore provide little information about the underlying aetiology of the condition. Furthermore, by the time the breeder has recognised a problem and brought the kitten to the surgery, he/she is already critically ill. As a consequence of the above, targeted treatment is often impossible and therefore response to treatment is poor. This is further confounded by altered drug tolerance and metabolism in young neonates, which limits the number of safe therapeutic options available to the veterinary surgeon (see later). It is important to remember that one ill neonatal kitten may reflect a greater problem within a cattery. Establishing the extent and frequency of kitten losses to assess whether it is acceptable is often warranted. The neonatal period, from birth to 34weeks of age, is critical. More kittens are lost during this period than any other time. An acceptable kitten mortality rate is about 10% where approximately half of these are stillbirths, however if the mortality rate is much higher then further investigations are required. Post-mortem examination of any neonate can provide invaluable information, particularly as neonatal kittens can show minimal clinical signs or die unexpectedly. The physiology and the main causes of death of neonatal kittens will be considered but it is important to understand kitten development when approaching a breeder/cattery/shelter with a high rate of pre-weaning kitten mortality. Neonatal Thermoregulation o Kittens less than 3 weeks of age cannot regulate their own body temperature and the shivering reflex does not start to develop until the kitten is at least one week of age. The range rectal temperatures of new born kittens are approximately: Week 1: 35 - 37oC (95 - 99 oF) Weeks 2 and 3: 36 - 38oC (97 - 100 oF) Week 4: 38 - 39oC (100 - 102 oF) o Hypothermia is a major contributing factor to neonatal mortality and kittens’ body temperature will drop rapidly if separated from the queen. As soon as body temperature starts to fall depression of the suckling reflex occurs and the resultant hypoglycaemia is life threatening. Neonatal Metabolism o The metabolic rate of neonates is 2 - 2.5 that of adult cats. o Neonates are very vulnerable to hypoglycaemia and regular suckling is necessary to maintain normoglycaemia. o Hypoglycaemia is self-perpetuating as a decrease in blood glucose leads to suppression of the suckling reflex exacerbating the hypoglycaemia and hypothermia. At birth, kittens on average should weigh 100g, depending on the breed (i.e. average Main Coon kitten weighs 120g, smaller oriental breed kittens weigh 80g). Most kittens will lose weight during the first 24hours of life, if this exceeds 10% bodyweight or if the weight loss continues for a longer period then supplementary bottle-feeding should be instituted. o Young kittens should to sleep for 90% of the day – a very active noisy kitten is an indication of problems in the litter. Neonatal Haematology o Foetal red blood cells are still present until approximately 4 weeks of age. They are larger than normal red blood cells (rbc) but there are fewer of them so initially the PCV of a neonatal kitten is the same as an adult cat. However the PCV of neonatal kittens decreases during the first 2-4 weeks of life. This is a physiological anaemia due to the short lifespan of foetal rbc in circulation, haemodilution due to expanding blood volume and a reduced rate of erythropoeisis compared to an adult cat. The anaemia is not associated with decreased oxygen carrying capacity as the concentration of 2,3diphosphoglycerate increases shifting the oxygen-haemoglobin curve to the right. At 4 weeks of age foetal rbcs are replaced by neonatal rbcs and by 8 weeks of age a kitten will have a PCV similar to that of adult cats o The haemoglobin oxygen diffusion curve in neonates is shifted to the right, compared to adult cats. This maximises the efficiency of oxygen transfer, which coupled with their relative tolerance to hypoxia makes it worth persisting with kittens that are reluctant to breathe following parturition. Neonatal Nephrology o The glomerular filtration rate of kidneys in the neonate is approximately 1/3 – ¼ of that of an adult cat. This is due to a combination of smaller capillary beds at the glomeruli, decreased permeability of the glomerular epithelium and/or decreased systolic pressure. The concentration of neonatal urine is only 1.5 times the plasma osmolality. Hence kittens will drink more than an adult cat and up to 200ml/kg can be normal for a neonate. o Neonatal kittens are therefore highly susceptible to dehydration. Neonatal Immunology o In the neonatal period the immune system is poorly developed, with decreased number of lymphocytes, no T-helper cell activity, no memory cell production and reduced complement and neutrophil function. o Maternally derived immunity (MDI) is an important aspect of neonatal resistance to infection. Negligible amounts of maternally derived antibodies cross the placenta, so kittens are reliant on passive transfer via the milk. Kittens can absorb antibodies up to 72 hours following parturition but the first 16 – 24 hours are considered the most vital. Regular booster vaccination of queens, particularly just prior to mating, will help optimise MDI The major causes of death in neonatal kittens can be split into 5 main categories: 1. Maternal factors 2. Management factors 3. Bacterial infections 4. Congenital disorders 5. Neonatal isoerythrolysis (NI) 1. Maternal Factors From pregnancy through to weaning the queen plays a vital role in survival of the neonate. Dystocia can be a significant factor in neonatal mortality. Particular attention should be paid to the health of the queen, as she provides energy and warmth to the underdeveloped neonates. The provision of MDI via colostrum is also the major mode of protection against infectious diseases in the first few weeks. Paradoxically the queen can act as a source infection either via the milk (mastitis), vagina or by the introduction of umbilical infections (See bacterial infections below). 2. Management Factors If a high neonatal death rate occurs during the first few days of life it is possible there is a basic management problem and a visit to the cattery should be considered. As hypothermia and hypoglycaemia are major causes of neonatal death (see above), environmental and management factors should be investigated. Environmental temperature, humidity, hygiene and privacy for the queen should all be considered. Kittens need to suckle regularly and rely on the queen for warmth. If the environment is inappropriate the queen/kittens will spend time moving rather than feeding/sleeping predisposing the kittens to hypoglycaemia and hypothermia. Nutrition of the queen is important to avoid obesity during pregnancy, which has been associated with increased rates of dystocia, and to ensure adequate production of milk and minimise weight loss during lactation. 3. Bacterial infections Infection is a relatively unusual cause of neonatal death. However bacterial septicaemia can occur and the most important route of infection is via result umbilical cord (omphalophlebitis). This infection may be from the vaginal during parturition, from the queen’s saliva or from the environment. Omphalophlebitis can rapidly extend to hepatic abscessation, peritonitis and septicaemia through haematogenous spread via the umbilical vein. A kitten with bacterial septicaemia will deteriorate rapidly with minimal clinical signs, and often several within a litter will be affected. If infection is suspected and the causal agent is unclear, a broad-spectrum antibiotic with efficacy against gram-positive and gram-negative organisms is advised. Neonatal Pharmacology Neonatal kittens have different susceptibilities to the toxic effects of some regularly used drugs. This is due to different enzyme systems, altered renal function, reduced plasma protein levels and increased permeability of the bloodbrain barrier, which can influence blood and tissue loads. They also have a large surface area:weight ratio, so any drug which impairs thermoregulation is hazardous. Foetal haemoglobin is also more susceptible to oxidation as levels of methaemoglobin reductase are reduced, so oxidant drugs such as sulphonomides and phenothiazines should be used with caution. Antibiotics: If there is suspicion of sepsis in a neonatal kitten, ampicillin, penicillins and cephalosporins are considered relatively safe. Tetracyclines, sulphonamides, aminoglycosides, and chloramphenicol are considered unsafe due to toxic side effects and impaired secretion. N.B. Viral infections are more likely to affect kittens during the post-weaning period as MDI wanes prior to vaccination (see later). 4. Congenital disorders Many body systems can be affected by congenital disorders, some are clinically obvious physical defects and others e.g. metabolic defects, will go unnoticed. The abnormalities can arise from genetic disorders or from teratogenic drugs (e.g. griseofulvin). If the defect is severe then it may result in neonatal death, however other cats can live a normal life with quite severe abnormalities e.g. pericardialperitoneal hernia. A congenital defect should be suspected in any kitten that is failing to thrive or has a reduced growth rate A note on Flat-chested kittens (FCK) and Pectus excavatum (PE) These conditions are the most common congenital chest wall abnormalities, and both defects can potentially reduce thoracic volume and compress the heart and lungs. FCK becomes apparent during the first few weeks of life, and is seen as an angulation of the ribs at the costachondral junction making the ventral part of the thoracic cavity flat. Mildly affected cats will be asymptomatic; moderate to severely affected kittens will have poor weight gain and exhibit difficulty breathing. Severely affected individuals die as neonates. PE is an upward displacement of the sternum towards the thoracic spine. If the defect is severe dyspnoea, weight loss or failure to thrive may become apparent. A less severely affected kitten may have reduced growth rates but can survive to adulthood. With both conditions if the kitten survives, the defect will become less pronounced as the cat matures. 5. Neonatal isoerythrolysis (NI) Cats have 2 major blood groups – type A and types B. Type A cats have low levels of naturally occurring antibodies against type B rbc, but type B cats often have significant levels of naturally occurring antibodies against type A rbc. Blood type A is dominant to blood type B. NI occurs when a type B queen is mated with a type A tom, which will result in some (dependant on whether the tom in homogenous or heterogeneous type A) type A kittens. The kittens are born healthy however once they start to suckle maternally derived antibodies are transferred via colostrum. These antibodies rapidly led to the destruction of foetal rbcs and within 2 - 3 days of parturition kittens will stop feeding and become weak, jaundiced, have haemoglobinuria, or die suddenly. NI can be avoided by blood-typing both queen and tom prior to mating, and avoid mating type A toms with type B queens. Rapid vet H blood typing cards (DMS laboratories) have made the determination of a cat’s blood type readily available to veterinarians. Certain pedigree breeds e.g. British shorthair and Devon rex, have a much higher prevalence of type B cats so blood typing these cats prior to breeding is advisable. An alternative strategy is to identify the type A kittens by using drops of blood from the umbilical cord. The kittens should then be removed from the queen for the first 16-24 hours and receive colostrum from another queen. The ‘older’ kitten The disease seen in the kittens if they progress beyond the neonatal period are often due to infectious pathogens. This is due to: Waning (or lack of) maternally derived antibodies Increased exposure to potential pathogens due to increased activity, outdoor access, rehoming etc Management factors similar to those for neonatal cats It is possible that other congenital defects such as portosystemic shunts, peritoneopericaridal hernia, metabolic and cardiac defects may be noted at this age but often these conditions remain silent until later in life. The nutrition of cats at this age is very important. The diet must be of good quality, be a complete diet and be the correct kitten formulation. It is essential to provide adequate nutrition throughout the weaning period to ensure there are enough nutrients for growth. Whatever the clinical problem kittens of this age are extremely vulnerable and can deteriorate rapidly if their clinical signs go unnoticed. These notes will give a brief overview of the pathogens which may affect kittens from 6 – 12 weeks of age. The majority of pathogens which affect kittens of this age will either lead to gastrointestinal signs, predominantly vomiting, and respiratory tract signs. The exception is feline infectious peritonitis, due to feline coronavirus which is most situations causes transient diarrhoea. This pathogen will be covered in other notes. Common pathogens that may lead to gastrointestinal clinical signs include: Isospora and Cryptosporidium spp Infection with these two pathogens is often asymptomatic and is most commonly encountered where there are high numbers of cats. Severe diarrhoea and weightloss is sometimes seen in compromised individuals; hence underlying disease should be looked for if infection persists. Often with adequate nutrition (sometimes a prescription highly digestible diet is helpful) the kitten will respond without treatment. Effective antibiotic treatment for kittens with these infections is problematic. Remember that Cryptosporidia has zoonotic potential Bacteria spp e.g. Campylobacter spp, Salmonella spp, Clostridium difficile and E. Coli Bacterial causes of diarrhoea are probably less common than viral or protozoal infections, but infection with certain pathogens can have serious consequences. Avian strains of Salmonella typhimurium have been recently reported to cause diarrhoea and in some cases mortality in cats in the UK. The cases occurred between September and February and the syndrome has been termed ‘songbird fever’. A positive culture can also be found in asymptomatic acts, so faecal cultures should always be interpreted with caution Tritrichomonas foetus This pathogen is relatively ‘new’ to feline medicine and can cause severe large intestinal diarrhoea. It is often seen in young cats but they are mostly over 12w of This pathogen can be distinguished from Giardia on a fresh faecal smear due to its ‘jerky forward’ movements as it is propelled by the three flagellae that give this pathogen it’s name. There are now PCRs available to diagnose this pathogen and the author often does this if the clinical signs are suspicious of T. foetus and a faecal swab is negative. The current treatment of choice is Ronidazole (similar to Metronidazole which has no activity against T foetus) which can be difficult to source and then dose accurately and reversible neurotoxicity has been reported following overdosing of cats. Cats with T foetus infection can have diarrhoea for months. Giardia spp Infection in young kittens often leads to an acute diarrhoea. Infection is most common in cats kept in large groups. A recent study of faecal samples from 250 (adult) cats in the USA showed a prevalence of Giardia of 13.6% using faecal flotation and immunoflourescence. This is much higher than previous studies. Also 75% of the cats shedding Giardia spp were also shedding Cryptosporidium oocysts (Vasilopulos et al). Giardia can be difficult to diagnose on faecal examination. It is worth collecting at least 3 consecutive faecal samples from a cat that you are suspicious may have Giardia. Giardia has a ‘falling leaf’ motility which differentiates it from T. foetus. Helminths Toxocara cati and Toxascaris leonina are the most common helminth infections that cause diarrhoea in cats and are readily eliminated by routine anthelmintics. Feline panleukopenia virus (FPV) FPV is now rarely seen in countries where routine vaccination in commonplace. However if vaccination is not available clinical signs are seen and can be devastating. Sudden death is a common presentation, though some cats will have peracute diarrhoea. A cat with severe diarrhoea and a marked lymphopenia, should be treated as an FPV unless proved otherwise. Once FPV is in a household or shelter the effects can be devastating. Feline coronavirus (FCoV) Most kittens will have antibodies to FCoV as this is a highly contagious pathogen that is common in open cat populations and normally causes mild transient diarrhoea. A positive antibody titre DOES NOT indicate a cat has feline infectious peritonitis (FIP) – a rare consequence of FCoV infection. Common pathogens that lead to upper respiratory tract infections in young kittens include: Feline herpesvirus (FHV) Feline Calicivirus (FCV) Chlamydophila felis (C felis) Bordetalla bronchiseptica Mycoplasma spp All of these infections will give none specific clinical signs and without further diagnostics it is not possible to be certain which is causing disease. FHV, FCV and C. felis are most commonly encountered, and a kitten is often infected with more than one pathogen at once. Disease is often seen in vaccinated cats as the vaccines do not create a sterilising immunity and if the viral load is high the immune system can be overcome. Tips for diagnosing and treating these infections include: FHV causes ocular lesions as well as respiratory signs, most commonly dendritic corneal ulcers FCV causes lingual ulceration as well as respiratory signs Skin lesions are also seen occasionally with FHV infection C felis is purely an ocular pathogen than only affects the conjunctiva and will not cause corneal ulceration. Polymerase Chain Reactions are reliable for the diagnosis of FHV and C.felis, but are more problematic when diagnosing FCV, so virus isolation is recommended for diagnosing this pathogen Supportive and symptomatic treatment is paramount for kittens with FHV and FCV. Anti-viral treatment has limited success. Kittens with C felis should be treated with systemic antibiotics, 10mg/kg SID Doxycyline for 4 weeks is the treatment of choice. Clavulonate-potentiated amoxicillin can be used as an alternative if there is concern of enamel discoloration. The role of Bordetella and Mycoplasma in respiratory tract disease is often debated as there is little evidence in the literature about these infections. Upper and lower respiratory tract signs can be observed with these infections and the infections can be lethal