Urs Giger, PD,, Diplomate, ACVIM,

Margret L. Casal, and Andrea Niggemeier, DVM

Philadelphia, Pennsylvania

Although a small number of kitten losses is unavoidable when breeding cats and raising kittens, the relatively high kitten morbidity and mortality rate is of great concern and has a considerable economic impact. In a large survey of purebreed catteries, mortality from birth to one year of age averaged 34.5%. One-third of these losses were stillborn kittens and of the live-born kittens, one-half died during the first week of life. In a specific pathogen-free domestic shorthair breeding colony, the preweaning kitten mortality was 14.8% and nearly all deaths occurred within the first week of life. In our own cat colony at the University of Pennsylvania, the overall kitten mortality up to 12 weeks of age averaged 23.9%, but varied markedly from one year to the other. One-fifth were apparently stillborn and of the live-born kittens, one-third died within the first week of life. Overall, the kitten mortality appears to vary greatly between catteries, breeds of cats, and individual queens.

These fading kittens are often not presented to the veterinarian, and therefore, the cause of death remains generally unknown. Some of the major reasons for neonatal morbidity and mortality are listed in table 1.

Table 1. Causes of the fading kitten syndrome and kitten mortality complex

Management and environmental problems are readily recognized by obtaining a detailed description, or even better, by inspecting the cattery. Inappropriate temperature, poor hygiene, overcrowding, and exposure to chemical toxins should be considered. Maternal problems are revealed by physical examination, ultrasound of the queen, and laboratory tests and may include fetal retention, endometritis/pyometra and other infections, and mastitis or agalactia. Under these circumstances the entire litter is generally affected. Although maternal neglect of newborns and cannibalism may be associated with maternal problems and may be readily corrected by helping the queen deal with kittens, such behavior may just as well be induced by illnesses of the kittens.

Kittens may be stillborn and may show developmental retardation and congenital malformations. Others are born alive prematurely, weak and unable to nurse, and will likely die of dehydration, hypothermia, and hypoglycemia. However, many newborn kittens appear healthy, active and very keen to nurse only to fade during the first few days or weeks of life. Sudden death may be caused by trauma, bleeding, congestive cardiomyopathy, sepsis, metabolic disturbances, and neonatal isoerythrolysis. Infections may be systemic or involve the respiratory tract (including ophthalmia neonatorum), gastrointestinal tract as well as the skin including umbilical cord. Queens may be asymptomatic carriers that shed virus under stressful circumstances (lactation, introduction of new cats, overcrowding).

Table 2. Infections in kittens

Upper respiratory infections (feline rhinotracheitis)  Skin infections 


Flea infestation 


Mycrosporium caninum 


Bacterial omphalitis 



Gastrointestinal infections  Systemic infections 

Toxocara, Isospora, Giardia, Dipylidium  

Bacterial sepsis 

Salmonella, Campylobacter, and other bacteria 


Panleukopenia virus 

Toxoplasma gondii 

Corona virus 

Although congenital malformations may be acquired, e.g., cerebellar hypoplasia due to intrauterine parvovirus infection, many have a hereditary basis. They include many developmental disorders leading to musculoskeletal defects, hernias, and cardiovascular disorders. In addition, many inborn errors of metabolism have been described that affect the intermediary metabolism. They include many storage diseases that lead to neuromuscular disorders. Hereditary disorders that may contribute to fading kitten syndrome and kitten mortality complex are listed in table 3.

Table 3. Hereditary diseases associated with fading kitten syndrome and kitten mortality complex


Feline porphyria 


Hemophilia A and B 

Spina bifida 

Vitamin-K dependent coagulopathy 

Pharyngeal polyps 

Hypotrichosis congenita with thymus atrophy 

Cleft palate  

Ehlers-Danlos syndrome 

Midfacial dysmorphia  

Lactic aciduria 

Osteogenesis imperfecta 

Methylmalonic aciduria 

Muscular dystrophy 

Primary oxaluria 


Primary hyperlipidemia 

Ventricular septal defects 

Portosystemic shunts 

Endocardial fibroelastosis 


Patent ductus arteriosus 

Gangliosidosis I, II 


Mucopolysaccharidosis I, VI, VII 

Diaphragmatic hernia 

Glycogenosis IV 

Umbilica hernia 

Globoid cell leukodystrophy 

 Atresia ani



The transfer of immunoglobulins by colostrum from the queen to the neonatal kittens does not only provide protection from infection, but maternal antibodies also attack the erythrocyte of the newbown, thereby being responsible for fatal incompatibility reactions known as hemolysis of the newborn or neonatal isoerythrolysis. Thus, colostrum may protect from or contribute to the fading kitten syndrome or kitten mortality complex, and therefore, can be considered a friend or foe.

Feline Neonatal isoerythrolysis (NI)

The AB blood group system: Thus far, only one blood group system with 3 blood types has been recognized. Although type A is by far the most common blood type, the frequency of type A and B in domestic shorthair cats varies worldwide and markedly among breeds. The allele for type A is completely dominant over the allele for type B. Thus, type B cats are homozygous for the B allele (B/B), whereas type A cats can either be homozygous (A/A) or heterozygous (A/B). Type AB, the third feline blood type, occurs extremely rarely in domestic shorthair and purebred cats, and could be explained by a third allele. A simple in-practice blood typing card test is now available (DMS Laboratories, Inc., 2 Darts Mill Road, Flemington, NJ 08822; 1-800-567-4367).

Naturally occurring alloantibodies: In contrast to dogs, cats have naturally occurring antibodies against the blood type they are lacking in their plasma. Type A cats have weak anti-B alloantibodies with titers typically only 1:2 and rarely reaching 1:32. However, all type B cats have very strong anti-A alloantibodies with hemagglutinin and hemolysin titers of 1:64 to 1:2064. Neonatal kittens acquire maternal alloantibodies of the IgG class via colostrum during the first day of life and begin to produce their own alloantibodies between 6 to 10 weeks of age. These alloantibodies, particularly anti-A antibodies, are responsible for transfusion reactions and neonatal isoerythrolysis (NI).

Pathogenesis of NI: Colostral anti-A alloantibodies are responsible for NI, i.e., type A and AB kittens born to type B queens are at risk of developing NI during the first week of life. Since all type B queens have high anti-A antibody titres, even primiparous queens can have litters with NI. No case of NI in a type B kitten born to a type A queen has been documented. The hemolysis may occur intra- as well as extravascularly and may cause anemia, nephropathy, as well as other organ failure.

Clinical signs of NI: Kittens with type A or AB blood born to type B queens may develop signs of NI immediately following colostrum intake. The hallmark sign of NI is severe pigmenturia due to hemoglobinuria. Other clinical signs include sudden death, failure to thrive (stop nursing), anemia, icterus, and tail tip necrosis.

Prevention of NI: Despite removing the kittens from their queen as soon as the first clinical signs develop, the mortality rate is high. NI is best prevented by avoiding incompatible matings between type B queens and type A toms. In blood incompatible matings, kittens at risk for NI should not be allowed to nurse from their type B queen for the first 24 hours. Cord blood could be used to determine the kitten's blood type or to perform a crossmatch with serum from the queen. Kittens with blood type B could be immediately placed back with their queen. Type A (or AB) kittens may safely receive milk or colostrum from a type A queen:.

Table 4: Blood type A and B frequency and risk for neonatal isoerythrolysis in the United States

  Blood frequency (%)    Allele frequency (A+B=1)     Proportion of matings 
  Type A  Type B   A allele  B allele  at risk for NI (%) 
Abyssinian 86  14    .63  .37  12 
Birman 84   16  .60  .40  13 
British shorthair 60  40  .37  .63  24 
Burmese 100  0  1.0  .00  0  
Cornish Rex   66   34  .42  .58   23 
Devon Rex   59  41  .36   .64  24 
Domestic shorthair  99   1  .90  .10   1 
Himalayan   93   7   .74  .26   6 
Japanese Bobtail   84   16   .60  .40   13 
Maine Coon 98   2   .86   .14   2 
Norwegian Forest   93  7   .74   .26  6 
Persian 86  14  .63  .37   12  
Scottish Fold  82   18  .58    .42 15 
Siamese 100   0   1.0   .00   0  
Sphinx 82   18  .56  .44   16  
Somali 83   17  .59   .41   14  
Tonkinese 100   0   1.0  .00  0 

Supported in part by grants from the Feline Winn Foundation and the National Institutes of Health (HL02355, RR02512).