The Breed History
The early Persian type cats likely reached us via European trade originating in Iran (formerly Persia) during the 1600s. The Himalayan was the result of crossing Persian with Siamese later in breed development (1920s-1930s) to add the colorpoint pattern, and is a division of Persian in some registries-a separate breed in others (see Himalayan chapter). The Persian cat is always amongst the most popular of cat breeds. Historically, Persian cats had a less foreshortened face. The current British Longhair (Persian) standard has more moderate facial features. Persians were first registered in CFA in 1909. No out-crossing is allowed.
Weight: 8-15 lb (3.5-7 kg)
Coat: The thick soft undercoat is overlain by a profuse standoff outer coat of long soft hairs. Well-developed ruff and frill, and tail is heavily haired. Coat texture should not be wooly.
Eyes: The large wide-set eyes are copper or orange. In shaded silver, golden and chinchilla, they are blue-green or emerald green. In Europe, a copper-eyed shaded silver is termed Pewter. Variable colored eyes are present in Persian white cats.
Points of Conformation: Persians have a heavy cobby build, small ears with rounded tips. A very short upturned nose and muzzle, with a well defined stop or break between the eyes is present. Persian cats have a large rounded broad head. Paws are rounded, tufted, and large. Tail is short, and carried low. The neck is short. Peke-faced is a subtype that is extremely foreshortened, similar to a Pekingese dog, while doll-faced cats are more moderate in their brachycephalic head conformation. The Peke subtype is specifically described in only certain registries. In ACFA for example, the Peke-faced is recognized as a head indented between eyes, creases following cheekbone; forehead, nose and chin form a perpendicular line.
Grooming: High grooming requirements are typical for Persian cats. Once to twice daily grooming to prevent matting is helpful; allow 15 minutes minimum daily. Regular baths are also used to help maintain the coat in excellent condition. Daily removal of tears to prevent staining and dermatitis in medical canthus area and facial folds may be required.
Recognized Behavior Issues and Traits
Reported breed characteristics include: Gentle, easygoing, placid, affectionate, quiet voiced, adaptable, playful, not big jumpers and climbers, get along well with children and other cats, and best as indoor cats. Himalayan cats are considered on average a bit more active than Persian cats due to infusion of Siamese blood.
Normal Breed Variations
Need to watch food intake and exercise to prevent obesity. Heavy shedding especially when coat changes.
B Blood Type: There is geographic variation in prevalence of B blood type cats, but overall, the trait is present at sufficient rates that blood typing should be done prior to mating or transfusions. In a study of blood type distribution in the USA, Persian cats (n=230) had 9.6% type B blood. In another American study, 41/170 or 24% were B type. Prevalence of 14% type B was also reported.In a small UK survey, 12% were type B cats.
Epiphora: Secondary to face conformation rather than due to any unusual anatomic defects in the lower punctum.
B Blood Type: There is geographic variation in prevalence of B blood type cats, but overall, the trait is present at sufficient rates that blood typing should be done prior to mating or transfusions. In a study of blood type distribution in the USA, Persian cats (n=230) had 9.6% type B blood.In another American study, 41/170 or 24% were B type. Prevalence of 14% type B was also reported. In a small UK survey, 12% were type B cats.
Epiphora: Secondary to face conformation rather than due to any unusual anatomic defects in the lower punctum.
Hair coat genetics: The long hair phenotype in cats is a recessive Mutation (AM412646:c.194C>A) Somali, Persian, Maine Coon, Ragdoll.
None reported in the literature
Autosomal Dominant Polycystic Kidney Disease (ADPKD): This condition leads to formation of cysts within the kidney parenchyma, and is often associated with eventual renal failure. Cyst size and number gradually increase over time in most cats. PKD is the most commonly seen inherited disorder in cats, affecting approximately 38% of Persian cats worldwide, and since there is a large population of Persian cats (Persian and Persian-related cats are about 80% of the cat fancy), about 6% of all cats have this disorder. Recently the gene for autosomal dominant PKD (ADPKD) has been identified. No homozygotes have been seen which suggests two copies of this gene lead to in utero lethality. A genetic test is available. Signs of the condition are variable in age of onset and degree of expression/rate of progression. Even within closely related families, expression can be significantly different. Multiple cysts may be found in both medulla and cortex. Smooth and round, and of variable size, these hypoechoic structures can be easily visualized with ultrasound using a 7.5 MHz transducer (10 MHz in kittens). By ultrasound evaluation, it was determined that in some kittens as young as 7 weeks old, cysts were already present. Many cats have good longevity, while about one quarter of seriously affected cats die before 5 years of age. Those living a full lifespan may harbor a few small cysts, so normal health does not preclude presence of cystic condition. Age of onset of clinically significant renal disease ranges from 3-10 years, with a mean of 7 years of age. Concurrent tubulo-interstitial nephritis of variable severity and distribution occurs. Neither the brachycephalic head conformation nor longhair genes segregate with the PKD gene. No increased probability of hypertension was reported associated with ADPKD. Another study reported increased mean arterial pressure (MAP) and aldosterone:renin ratio in Persians over 4 years of age with PKD. Note that absence of cysts at 6 months of age is strongly correlated with a low risk of development of cysts in the future. Note that cysts may also be found in the liver and pancreas in some cats. In a study in the Netherlands, of 27 affected cats, 68% had cystic changes in the liver or congenital hepatic fibrosis, and pancreatic cysts or pancreatic fibrosis. One report mentions associated peritoneopericardial hernias. That same report suggests that for screening purposes, the cutoff for positive PKD status be set at three or more cysts found in two kidneys by US evaluation. Cysts range in size from 1 mm to over 1 cm, and as they grow, pressure on the surrounding tissues leads to dysfunction-renomegaly and renodynia may occur. Late stage, the surface of the kidney may become irregular. Cysts derive from both distal and proximal nephron. Persian cat ADPKD strongly resembles ADPKD in humans.
Feline Hypertrophic Cardiomyopathy (HCM): The pattern of inheritance is unclear in this breed. Left ventricular outflow obstruction, left ventricular (LV) diastolic dysfunction, LV wall/ septum hypertrophy, myocardial hypertrophy, interstitial fibrosis and ischemia lead to typical signs of heart failure; also may see aortic thromboembolism. Dyspnea and crackles, arrhythmias, and murmurs are typical findings.16 Persian cats are overrepresented so perhaps there is a genetic influence. Average age of onset is 6.5 years. Over 75% of cases are in males, usually sudden death or acute left sided heart failure is the terminal event. Concurrent pulmonary edema is distributed in a patchy pattern diffusely through the lung field (not necessarily perihilar, as is typical in dogs), and they are not usually hypothermic. Histologic examination shows one quarter of cats have myofiber disarray. Growth hormone excess may play a role in this condition.
In a study of a partially inbred colony of cats with Persian ancestry, plasma atrial natriuretic factor was elevated; an autosomal dominant inheritance was suspected.
PDA: Increased breed incidence was reported; may be associated with septal and valvular defects.
Congenital Portosystemic Vascular Shunts: Persian and Himalayan together accounted for 16% of cases out of 98 cats in one report. Signs were noted by 6 months of age; a single extrahepatic portocaval anomaly was the most common type of defect seen.
Neonatal Isoerythrolysis (NI): Prevalence of B blood type makes NI a concern in this breed. All B type cats have circulating anti-A antibodies and even primiparous queens carry these. Type B queens bred to type A toms can result in fatal red cell lysis in A blood type offspring with undetected NI. Kittens with NI can be distinguished from other fading kittens because of pigmenturia; anemia and icterus will also be present; not all kittens at risk for NI will develop overt clinical symptoms. The proportion of matings at risk for NI was reported to be 0.12.
FIP Susceptibility: Pedigree analysis indicated a high heritability (> 0.54) in a selection of catteries, with perhaps a polygenic trait controlling susceptibility to development of clinical FIP. There was no correlation between FIP death and inbreeding.
FeLV Susceptibility: Feline leukocyte antigen (FLA), important for control of immune response, is represented by a set of genes and polymorphism here may play a role in susceptibility.
Corneal Sequestration (SYN: Black body or cornea nigrum): In early phases, an amber colored corneal stromal opacity may be noted. It gradually develops distinct raised borders; the surrounding cornea is cloudy and neovascularized; chemosis, blepharospasm, mucopurulent ocular discharge, and hyperemic conjunctivae may also be noted. Surface of sequestrum does not stain with fluorescein dye but does retain rose bengal stain. Exophthalmic conformation is thought to play a role in susceptibility. It is central or paracentral in distribution, and Persian cats are over-represented. When matured, this is a brown to black pigmented lesion; often surrounded by a loose collarette of poorly adherent corneal epithelium. Lesions may extend into shallow or deep stroma, or even to Descemet's membrane. Sloughing and corneal healing may take 2-6 months; surgical debridement is an option. Most often they are unilateral, but can be bilateral; it is a corneal stromal necrosis. Topical glucocorticoids are contraindicated; some cases may be associated with feline herpesvirus infection; if suspected, do a PCR test for the virus on excised black body tissue. Recurrence, or involvement of the second eye in previously unilateral cases may occur. Mean age of affected Persians is 5 1/2 years.
Non-healing Corneal Ulcers: In a retrospective study of cats with refractory ulcers, the Persian was found to be overrepresented. These indolent ulcers involve only the superficial epithelium and unless complicated, do not extend into the stroma. During extended treatment regimens averaging 5 weeks, the same cats were also predisposed to corneal sequestration.
Cervical Neck Lesions: Increased risk for Persian cats was reported. Of cats with in one study, 47% afflicted were Persians.
Lower Urinary Tract Disease: Increased risk of calcium oxalate urolithiasis was reported. A retrospective study (3,498 urolithiasis cases) found increased risk for calcium oxalate (CaOx) uroliths but reduced risk for forming Magnesium Ammonium Phosphate (MAP or struvite) crystals. Persian cats were found to be 3.2 times more likely to develop CaOx stones, and 1.4 times as likely to develop MAP as cats of other breeds in another report. In a retrospective analysis of 22,908 LUTD cases (1980-1997), Persian cats were reported to be at increased risk of congenital defects as well. A new type of uroliths was reported, consisting of Mg, K, and inorganic pyrophosphate; a possible dysfunction of the pyrophosphate-hydrolyzing alkaline phosphatase enzyme was proposed (perhaps a genetic defect) as a reason for the novel stone structure.
Dystocia: A survey of 2,928 litters of multiple cat breeds was carried out to ascertain prevalence of dystocia, and over-representation of Persian breed cats was found. There were 939 Persian litters analyzed. Average dystocia rate in a mixed breed colony was 0.4%, and 7.5% in the Persian group.
Cryptorchidism: There is some variation between practitioners on the cutoff age to be considered failure to descend. A common definition of cryptorchidism is when testes fail to descend into the scrotum by 7-8 months of age. Persian cats were the breed with the highest reported incidence of cryptorchidism, accounting for 20% of cases in one study. In a study (1980-89) of 1,345 cats admitted for orchiectomy, 29% of Persians were cryptorchid versus 1.4% in non-Persians.
Brachycephalic Syndrome: A flat-face conformation and rounded skull can result in stenotic nares, jaw changes, elongated soft palate, and distorted nasopharynx. Because of the sedentary lifestyle of cats, many cats can live with this conformational defect, but in severe cases surgical therapy is required.
Transfusion Reactions: Due to prevalence of B blood type, natural allo-antibodies markedly increase the risk of transfusion reactions so donors and recipients should be blood typed.
Idiopathic Facial Dermatitis (Dirty Faced Persians): In the UK, and sporadically in the US, black exudates that mat in hair and on skin, with frequent self excoriation secondary to pruritis, and associated skin erythema have been noted. Often ceruminous otitis externa is present simultaneously. A genetic basis is suspected; histology shows dyskeratotic basal epithelial cells, acanthosis and crusting with mixed inflammatory infiltrate and sebaceous hyperplasia. Mean age of onset is 1 year of age, with a symmetric pattern around eyes, mouth, chin and ears, and may be associated with submandibular lymphadenopathy. Mucoid ocular discharge may be noted. Though inflammatory cells are often noted, and bacteria and yeast may be isolated, the condition is not antibiotic or glucocorticoids responsive.
Separation Anxiety Syndrome: Of a study group of 136 cats, Persians accounted for 12% of the cats. Associated clinical signs in Persians were that females urinated, and males urinated and defecated out of place.
Hereditary Deafness: Is associated with the dominant gene for white cat (W); may be found in white cats of this breed.
Hip Dysplasia (HD): This condition is much more prevalent than was previously thought. In a 1998 report, in a nonrandom group of 78 cats of different breeds, 32% of this pooled group of cats, and 60% of Persians had HD using OFA-like criteria. A positive correlation with joint laxity and HD was identified. A study (1991-1995) found that based on VD hip radiographs, (684 Cats, 12 breeds) HD prevalence was 5.8% in unregistered versus 12.3% in purebred cats. Persian cats had a 15.8% rate (3/19). Classic radiographic signs were found to be different than in dogs, with minimal remodeling of the femoral neck. Instead, shallow acetabulum and remodeling of the cranio-dorsal acetabular rim were noted.
Rare and Isolated Reports
Chediak-Higashi Syndrome: Chediak-Higashi has an autosomal recessive inheritance pattern. This condition affects dilute blue smoke Persian cats. Iris is pale and yellow-green, thin, and the fundus hypopigmented due to loss of retinal pigmented epithelial cells. CHS also leads to tapetal cell dysmaturity and gradual loss of tapetal cells leading to lack of visible tapetum. Cataracts may also form. A membrane defect is thought to be the underlying defect in CHS, leading to increased unsaturated fatty acid levels. Essentially a lysosomal defect is associated with this dilute partial oculocutaneous albinism. CHS is associated with bleeding tendency, and granules staining pink to magenta with Romanowsky stain in leukocytes. Also granules are present in melanocytes. Bleeding tendency is due to a platelet storage pool deficiency. Cats may be photophobic, and mild neutrophilia may also occur. Cats with this condition should not enter breeding programs. Normal lifespan is expected.
Alpha Mannosidosis: Lysosomal enzyme О±-mannosidase deficiency, an autosomal recessive disorder, leads to progressive storage disease. Leukocyte morphology changes include vacuolation of lymphocytes and monocytes. Cells such as neurons accumulate partially processed N-linked oligosaccharides.46 Signs begin in the first month of life and are progressive, with death frequently occurring a few months later. Tremors, facial dysmorphia, ataxia, seizures, reduced vision (cataracts), organomegaly, behavior changes and skeletal deformities may occur. Three families of Persians have been reported with this rare storage disease (in the USA, Switzerland, and Belgium). The mutation was characterized, and resulted in zero enzyme activity. In DSH cats, milder phenotype and 2% enzyme activity has been reported. Corneal opacification may result in frosted appearance of the eyes by 11 weeks of age; marked pathology occurs in the RPE, but is not visualized clinically. Lens shows characteristic Y-suture pattern of cataract-appearance is granular to feathery.
Entropion: Suspected to be hereditary, present at an early age; high prevalence in Persian; all or part of lower palpebral margin is affected, and is often bilateral.
Eyelid agenesis: Most commonly seen in the temporal upper palpebral.
Cataracts: Congenital or juvenile cataracts have been reported.
Heterochromia Iridis: Variations in iris and retinal pigment epithelium and choroid may occur.
Retinal Degeneration: Begins as foci of hyperreflective tapetum, then coalesce to become generalized; leading to blindness.44 In one report, two litters from the same parents developed visual deficits, and fundus abnormalities on ophthalmoscope exams were noted by a few months of age. Diffuse outer segment degeneration occured. A recent report strongly suggests this is an autosomal recessive rod cone dysplasia. By 3 weeks of age in offspring of homozygous cross with heterozygous parents, pupillary light reflexes were abnormal, by 6 weeks the tapetum hyperreflective, and by 15 weeks of age, the retinal degeneration was advanced; all were blind by 16 weeks old.
Hyperlipoproteinemia/Hyperlipidemia: Pattern is familial. High circulating triglycerides and hyperchylomicronemia occur. Signs may include: iridocyclitis, lipemia retinalis (pink or creamy retinal vasculature), xanthomata (lipid granulomas of skin), and lipid aqueous humour. Nerves may become impinged due to xanthomata, leading to paresis or paralysis. Anterior chamber contents may have a creamy or white appearance when hyperchylomicronemia is present, and opalescence when hypertriglyceridemia alone is present. Arcus lipoids cornea and lipid keratopathy can also be seen with hyperlipoproteinemia. Uveitis has also been described. Concurrent atherosclerosis of abdominal vessels, aorta and coronary vessels also occurred. Deficiency of lipoprotein lipase enzyme is thought to be the underlying defect responsible for the hyperlipoproteinemias. In another report of kittens with severe hypertriglyceridemia, anemia was also evident.
Dystrophic Epidermolysis Bullosa: This is a collagen VII defect leading to reduced anchoring fibrils, so trauma leads to formation of blisters that progress to ulcers; an easily torn off skin is the result. Sloughing of foot pads and oral mucosa occurs in addition to loss of hairy skin.
Primary Hereditary Seborrhea Oleosa: First signs are noted at only 2-3 days of age and are severe and quickly progressive, with no coat color predilection. Greasy, scaly skin and a rancid odor are present. Orthokeratotic hyperkeratosis is found on biopsy. A primary keratinization defect is thought to be the underlying condition. To date, no effective treatment options have been reported.
Multiple eyelid cysts: Histology is similar to apocrine hidrocystomas of humans. In one report, these were described as multilocular cysts; PAS+, diastase resistant granules were seen in the cytoplasm of affected cells. Blepharospasm, epiphora and masses/color changes of eyelids were the chief complaints. In another case, unilocular cysts in a senior Persian were reported and were characterized as cystadenomas.
Progressive Retinal Atrophy PRA: Kittens are 2-3 weeks of age at onset, autosomal recessive. By about 4 months of age, they have severe photoreceptor loss.
Miscellaneous: Dermatophytosis, Otitis Externa, Umbilical Hernia, Peritoneopericardial hernia, Portosystemic Shunt, Cryptorchidism, Lymphocytic Cholangitis, Hemophilia A.
Mannosidosis Genetic (Direct) Test Josephine Deubler Genetic Testing Laboratory, (PennGen) at the University of Pennsylvania Veterinary Hospital offers testing. Minimum of 1-2 ml EDTA blood processed within 48 hours. Is not necessary to cool; and do avoid freezing. Test request form is available online. Can do concurrent blood typing on the same sample. Can also submit a pair of buccal swabs for testing.
PKD: Direct genetic test is available at UC-Davis VGL and the Animal Health Trust. Ultrasound screening of kidneys should be done with transducer of 7.5 MHz for adults, 10 MHz for kittens. In older cats, cysts are larger and thus easier to detect. Typical findings are spherical cysts with smooth sharp outline, anechoic internally, with through transmission of larger cysts. Recommend scan breeding stock at 10 months of age in 2 planes; both kidneys, and again at 2 years old if early US is equivocal (single cyst or a few in one kidney only), or if negative since may not pick up PKD at 10 months of age if very small cysts or no changes. In some patients, renomegaly may be visible on routine radiographs. Because of prevalence, breeding PKD positive cats to negative cats may be necessary for a while to prevent gene pool diversity loss. Blood type before transfusions or mating are recommended.
- Breed name synonyms: Himalayan, Himalayan-Persian, Longhair, Longhaired Exotic, Khmer (historical, Europe), British Longhair
- Registries: FIFE, TICA (separate from Himalayan here), CFA, *ACFA (separate from Himalayan), *CFF (separate from Himalayan here; chocolate and lavender are known as Kashmir). GCCF (division includes colourpoint, exotic SH), ACF (includes colourpoints), WCF (provisional Persian/Himalayan category), NZCF (colourpoints in here), CCA (Himalayan separate)
*CFF and ACFA distinguish between Peke-faced and standard Persian.
- Breed resources: The Atlantic Himalayan Club: himalayan.org/links.htm
CFA Persian Breed Council: persianbc.org
The Feline PKD Homepage: felinepkd.com/
United Silver and Golden Fanciers Online: unitedsilverandgoldenfanciers.com/
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