Kitten deaths have been reported in households of fully vaccinated cats, possibly because of exposure to large amounts of virus in the environment.Infection occurs when the virus enters the body through the mouth or nose. Whether illness results or not depends on the immunity in the victim vs. the number of individual virus particles (i.e. the amount of virus) entering the body. Clinical signs
The clinical manifestations of FPLV are variable based on the dose of the virus, the age of the cat, potential breed predispositions, and prior immunity from maternal antibodies, previous exposure, or vaccination. Most infections are subclinical, as evidenced by the high seroprevalence of anti-FPV antibodies among some populations of unvaccinated, healthy cats. The cats that become clinically ill are usually less than one year old, but older cats are also at risk. There is high mortality in clinically affected kittens and sudden death can occur.Clinical signs usually develop in 4–6 days after exposure, but can show in 2–14 days. The virus infects and destroys actively dividing cells in bone marrow, lymphoid tissues, intestinal epithelium, and—in very young animals—in the cerebellum and retina. The virus primarily attacks the lining of the gastrointestinal tract, causing internal ulceration and, ultimately, total sloughing of the intestinal epithelium. Primary signs include: 

anorexia
lethargy
profuse watery to bloody diarrhea (bloody diarrhea is more common in dogs with parvovirus than cats)
vomiting (most common in cats)Clinical laboratory findings include (but are not limited to):
electrolyte and total protein concentrations that reflect dehydration, vomiting, and diarrhea.
A further editorial reply in the British Journal of Anaesthesia discusses changes in the face and airway structure making it more difficult to secure the airway under anaesthesia, however, complications appeared in a minority of cases, and routine methods of airway control in the operating room appears to be successful. They recommended close individual evaluation of Rubinstein–Taybi patients for anaesthetic plans.A 2009 study found that children with RTS were more likely to be overweight and to have a short attention span, motor stereotypies, and poor coordination. The study hypothesized that the identified CREBBP gene impaired motor skills learning. Other research has shown a link with long-term memory (LTM) deficit.It is diagnosed when a heterozygous pathogenic variant of the CREBBP gene is identified in the individual. It exhibits an autosomal dominant inheritance pattern, but some documented cases show heterozygous individuals exhibiting germline mosaicism. This condition affects men and women equally, and is often misdiagnosed with other diseases or disabilities that result in delayed mental development. Genetics
Rubinstein–Taybi syndrome is a microdeletion syndrome involving chromosomal segment 16p13.3 and is characterized by mutations in the CREBBP gene. Varying amounts of material are deleted from this section of the chromosome and accounts for the spectrum of physiological symptoms.The CREBBP gene makes a protein that helps control the activity of many other genes. The protein, called CREB-binding protein, plays an important role in regulating cell growth and division and is essential for normal fetal development.