Skin fragility syndrome in a cat with feline infectious peritonitis and hepatic lipidosis

A 6-year-old spayed female domestic shorthair cat with a 3-week history of inappetence, weight loss, and hiding was examined. A palpable abdominal fluid wave, dehydration, and a small tear on the left flank were noted during initial examination. When the cat was gently restrained for blood sampling, the skin on the dorsal neck tore, leaving a 15 cm x 7 cm flap of skin. Clinicopathological abnormalities included nonregenerative anaemia, hypoalbuminaemia, increased globulin concentration, and mildly elevated aspartate aminotransferase and alkaline phosphatase activities. Abdominal fluid was viscous and had a total protein of 5.3 g dL(-1) with 316 cells microL(-1), consistent with a modified transudate. Cytology of the abdominal fluid revealed 86% nondegenerate neutrophils, 13% macrophages, and 1% small lymphocytes. Histopathological evaluation and indirect immunohistochemistry confirmed a diagnosis of feline infectious peritonitis, hepatic lipidosis and feline skin fragility syndrome. Feline skin fragility syndrome has not previously been reported in association with feline infectious peritonitis (FIP). Its inclusion as a clinical sign associated with FIP may facilitate a diagnosis.     

Staining abnormalities of dermal collagen in cats with cutaneous asthenia or acquired skin fragility as demonstrated with Masson's trichrome stain

This retrospective study compared the Masson's trichrome staining properties of collagen in the skin of normal cats and cats with cutaneous asthenia or acquired skin fragility. A Masson's trichrome staining abnormality was seen in all ( n = 8) cats with cutaneous asthenia, three of four cats with acquired skin fragility, and none ( n = 10) of the normal cats. A grading system developed to classify the intensity and distribution of abnormally stained collagen fibres indicated that cats with cutaneous asthenia had higher scores ( P < 0.001) than normal cats. Cats with acquired skin fragility had intermediate scores that were not significantly different from either of the other two groups.     

Loss of retinoblastoma protein, but not p53, is associated with the presence of papillomaviral DNA in feline viral plaques, Bowenoid in situ carcinomas, and squamous cell carcinomas

Although papillomaviral (PV) DNA is frequently present in feline cutaneous squamous cell carcinomas (SCCs), a causative association cannot be proven. Oncogenic human PVs cause neoplastic transformation by inhibiting retinoblastoma (pRb) and p53 activity. Therefore, absence of pRb and p53 immunostaining, along with increased p16 immunostaining, indicates a PV cause in some human SCCs. If PVs cause cutaneous feline SCCs, it was hypothesized that a similar immunohistochemistry profile, along with PV DNA, would be detectable. This was investigated using 5 feline viral plaques, 10 Bowenoid in situ carcinomas, 19 SCCs from ultraviolet-exposed (UV-exposed) skin, and 11 SCCs from UV-protected skin. Papillomaviral DNA was amplified by polymerase chain reaction from 30 of 45 lesions. Reduced pRb immunostaining was present in 26 of 45; increased p16 immunostaining was in 30; and p53 immunostaining was in 19. Both reduced pRb immunostaining and increased p16 immunostaining were more frequent in lesions containing PV DNA. In contrast, no association was observed between p53 immunostaining and the presence of PV DNA. SCCs from UV-protected skin more frequently contained PV DNA, reduced pRb, and increased p16 than UV-exposed SCCs. UV exposure was not associated with p53 immunostaining within the SCCs. These results suggest that feline PVs alter cell regulation by degrading pRb. Unlike oncogenic human PVs, there was no evidence that feline PVs degrade p53. These results provide further evidence that PVs may cause feline cutaneous SCCs, especially those in UV-protected skin, and they suggest a possible mechanism of this oncogenic action.     

Feline immunodeficiency virus: a brief review.

Feline immunodeficiency virus (FIV), previously known as feline T-lymphotropic lentivirus (FTLV), was first described by Pedersen et al. (1987) who isolated the virus from cats with a variety of clinical signs suggestive of immunodeficiency. Since then FIV has become one of the most studied feline viruses, not least because of its similarity to human immunodeficiency viruses (HIV) which cause acquired immunodeficiency syndrome (AIDS) in man.     

Feline pituitary-dependent hyperadrenocorticism and insulin resistance due to a plurihormonal adenoma

A 12-year-old female spayed domestic short-haired cat presented for lethargy, poor hair coat, alopecia, difficulty walking, and mild polyuria/polydipsia. The cat's skin tore easily in the neck area during routine restraint for blood draw. Physical examination, blood analysis, and ultrasound imaging were all consistent with pituitary-dependent hyperadrenocorticism (PDH) with secondary insulin-resistant diabetes mellitus, which was nonketotic. Insulin therapy, fluids, and diet change were initiated for the diabetes mellitus and the owner reported improvement in clinical signs although the blood glucose measurements remained elevated. Surgical repair of the torn skin was successful. Although a guarded prognosis was given to the owner because of an advanced stage of hyperadrenocorticism, and the limited treatment options currently available for feline PDH, trilostane was agreed on as an initial therapeutic option. The day trilostane was to be initiated, the cat presented with dyspnea and the owner chose to euthanize. Because of the rarity of hyperadrenocorticism disease in the cat, permission was obtained by the owner for a necropsy to confirm suspected PDH as the underlying cause for insulin resistance and skin fragility syndrome.     

猫牛痘病毒感染研究进展

猫牛痘病毒感染是由牛痘病毒引起的猫及其他猫科动物的病毒性传染病,可引起猫的皮肤结块、口腔溃疡、系统性疾病或坏死性肺炎,偶尔还可引起人的皮肤损伤和淋巴炎。文章就猫牛痘病毒感染的病原学、流行病学、临床症状、诊断和治疗作一综述,以期为该病的研究和防制提供资料。     

Measurement of serum immunoglobulin E (IgE) specific for house dust mite antigens in normal cats and cats with allergic skin disease

The purpose of this study was to determine whether cats with allergic skin disease have significant concentrations of serum Immunoglobulin E (IgE) specific for antigens derived from the house dust mites (HDM) Dermatophagoides farinae (DF) and Dermatophagoides pteronyssinus (DP). Enzyme-linked immunosorbent assays (ELISA) were developed for this purpose. Binding of serum allergen-specific IgE was detected via the use of biotinylated Fc-epsilon receptor alpha chain protein (FcvarepsilonRIalpha). Following optimisation of the assay, serum samples from 59 cats with allergic skin disease and 54 clinically normal cats were screened. Results were expressed as ELISA units per ml (EU/ml) compared to a standard curve. Serological findings were correlated with the clinical presentation of affected cats. Cats with symptoms of feline allergic skin disease were grouped as follows: self-induced alopecia without lesions (group 1), papulocrusting dermatitis (group 2), eosinophilic granuloma complex (group 3), papular/ulcerative dermatitis of head and neck/facial dermatitis (group 4), and a combination of symptoms (group 5). Control normal cats comprised the final group (group 6). The Kruskal-Wallis test was used for statistical analysis. There was no significant difference between groups for DF- and DP-specific IgE concentrations with a p-value of 0.875 and 0.705, respectively. Although the FcvarepsilonRIalpha-based ELISA was able to detect house dust mite-specific feline IgE, the presence of this allergen-specific IgE correlates poorly with the presence of clinical manifestations of allergic skin disease. The results of this study question the clinical relevance of house dust mite-specific IgE in feline allergic skin disease.     

Papillomaviral DNA and increased p16CDKN2A protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet-protected skin

Squamous cell carcinomas (SCCs) are common feline skin tumours. While exposure to ultraviolet (UV) light causes some SCCs, a subset develop in UV-protected skin. In cats, papillomaviruses (PVs) cause viral plaques and Bowenoid in situ carcinomas (BISCs). As both may progress to SCC, it was hypothesized that SCCs in UV-protected skin may represent neoplastic transformation of a PV-induced lesion. To investigate this hypothesis, PCR was used to amplify PV DNA from 25 UV-protected and 45 UV-exposed SCCs. Oncogenic human PVs cause neoplasia by mechanisms that also increase p16(CDKN2A) protein (p16). As increased p16 is present in feline viral plaques and BISCs, immunohistochemistry was used to detect p16 within the SCCs. Papillomaviral DNA was amplified from 76% of UV-protected SCCs, but only 42% of UV-exposed SCCs. Increased p16 was present in 84% of UV-protected SCCs, but only 40% of UV-exposed SCCs. The more frequent detection of PV DNA and increased p16 within UV-protected SCCs supports the hypothesis that some develop from a PV-induced plaque or BISC. Felis domesticus PV-2 is thought to cause viral plaques and BISCs. This PV was detected most frequently within the UV-protected SCCs, supporting development from a PV-induced lesion. Increased p16 and PV DNA were less frequent within UV-exposed SCCs, presumably because these developed from actinic keratosis rather than a PV-induced lesion. The results support the hypothesis that some feline cutaneous SCCs are caused by PV infection and suggest that PVs may cause neoplasia by mechanisms that also increase p16.     

Idiopathic sterile pyogranuloma in three domestic cats

Pyogranulomatous inflammation has been extensively described in cats, in particular in cases of feline infectious peritonitis and also associated with Mycobacteria, Actinomyces, Nocardia, Rhodococcus and fungal infections. Idiopathic sterile pyogranulomatous dermatitis has also been described. In this case series we describe the clinical presentation, histopathology and outcome of three cases of feline idiopathic sterile steroid-responsive pyogranuloma with different presentation and different locations of the lesion, but with the common feature of having a mass with no superficial skin involvement.     

Cutaneous sarcoids in captive African lions associated with feline sarcoid-associated papillomavirus infection

Solitary and multiple cutaneous and mucocutaneous masses were identified in 5 of 24 captive African lions (Panthera leo) over a 6-month-period. All masses were surgically excised, and all were histologically similar to equine and feline sarcoids. DNA was extracted from formalin-fixed, paraffin-embedded tissue. Polymerase chain reaction amplified DNA sequences that had been previously detected in feline sarcoids and clinically normal bovine skin. All lions had been fed a diet that included bovine carcasses that had not been skinned. Since the cessation of feeding bovine carcasses with cutaneous lesions, no additional skin lesions have been observed within any of the lions. Herein is described the clinical, gross, and histopathological findings of sarcoids in 5 captive lions. As the causative papillomavirus most likely has a bovine definitive host, it is hypothesized that the lions were exposed to the virus by feeding on bovine carcasses with skin still attached.     

Evaluation of feline oral squamous cell carcinomas for p16 protein immunoreactivity and the presence of papillomaviral DNA

Oral squamous cell carcinomas (OSCCs) develop commonly in cats. While the cause of the feline neoplasms is unknown, a quarter of human OSCCs are caused by papillomavirus (PV) infection. As PV DNA has been previously detected in a feline OSCC, it was hypothesised that PV infection could be a significant cause of feline OSCCs. Human OSCCs that are caused by PVs contain increased p16^CDKN2A protein (p16), which can be detected using immunohistochemistry. In cats, increased p16 immunoreactivity has been reported within PV-associated skin lesions. This study evaluated p16 immunoreactivity within 30 feline OSCCs. Additionally, PCR was used to amplify PV DNA from the OSCCs. Increased p16 immunoreactivity was present within 2 OSCCs. However, as PV DNA was not amplified from any OSCC in this study, it cannot be confirmed that the increased p16 was caused by PV infection. Therefore, these results do not support the hypothesis that PVs are a significant cause of OSCCs in cats. Loss of p16 expression is considered an important process in the development of human non-PV-induced OSCCs. In contrast, loss of p16 immunoreactivity was only present in 2 feline OSCCs. This suggests that human and feline OSCCs develop due to different molecular mechanisms.     

In vitro evaluation of canine and feline calcium oxalate urolith fragility via shock wave lithotripsy

OBJECTIVE: To test the hypothesis that feline calcium oxalate uroliths are intrinsically more resistant to comminution via shock wave lithotripsy (SWL) than canine calcium oxalate uroliths through comparison of the fragility of canine and feline uroliths in a quantitative in vitro test system. SAMPLE POPULATION: Calcium oxalate uroliths (previously obtained from dogs and cats) were matched by size and mineral composition to create 7 pairs of uroliths (1 canine and 1 feline urolith/pair). PROCEDURE: Uroliths were treated in vitro with 100 shock waves (20 kV; 1 Hz) by use of an electrohydraulic lithotripter. Urolith fragmentation was quantitatively assessed via determination of the percentage increase in projected area (calculated from the digital image area of each urolith before and after SWL). RESULTS: After SWL, canine uroliths (n = 7) fragmented to produce a mean +/- SD increase in image area of 238 +/- 104%, whereas feline uroliths (7) underwent significantly less fragmentation (mean image area increase of 78 +/- 97%). The post-SWL increase in fragment image area in 4 of 7 feline uroliths was < 50%, whereas it was > 150% in 6 of 7 canine uroliths. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that feline calcium oxalate uroliths are less susceptible to fragmentation via SWL than canine calcium oxalate uroliths. In some cats, SWL may not be efficacious for fragmentation of calcium oxalate nephroliths or ureteroliths because the high numbers of shock waves required to adequately fragment the uroliths may cause renal injury.     

Clinical aspects of feline immunodeficiency and feline leukemia virus infection

Feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) are retroviruses with a global impact on the health of domestic cats. The two viruses differ in their potential to cause disease. FIV can cause an acquired immunodeficiency syndrome that increases the risk of developing opportunistic infections, neurological diseases, and tumors. In most naturally infected cats, however, FIV itself does not cause severe clinical signs, and FIV-infected cats may live many years without any health problems. FeLV is more pathogenic, and was long considered to be responsible for more clinical syndromes than any other agent in cats. FeLV can cause tumors (mainly lymphoma), bone marrow suppression syndromes (mainly anemia) and lead to secondary infectious diseases caused by suppressive effects of the virus on bone marrow and the immune system. Today, FeLV is less important as a deadly infectious agent as in the last 20 years prevalence has been decreasing in most countries.     

Thrombocytosis in cats: a retrospective study of 51 cases (2000-2005)

Feline haematology profiles of patients presented to the University of Bristol Small Animal Hospital from January 2000 to October 2005 were evaluated for thrombocytosis (defined as a platelets count of >700x10(9)/l and confirmed on smear evaluation). Thrombocytosis was found in 79 cats (4.64% of the hospital feline population), with values ranging from 703 to 1895x10(9)/l. Signalment, clinical presentation, concurrence of other haematological abnormalities, diagnoses and outcome were evaluated in 51 cases in which complete medical records were available. Other variables (feline immunodeficiency virus/feline leukaemia virus status, thyroxine level, haemoplasma PCR, toxoplasma antibody titres) were also evaluated. No association was found between the presence of thrombocytosis and breed or gender. Gastrointestinal signs were the most common clinical presentation. Lymphopenia was the most common concurrent haematological abnormality. Based on final diagnosis reached, cats were grouped both according to the DAMNITV classification and according to the body system affected. Amongst the DAMNITV classification, inflammatory/infectious conditions were most commonly associated with thrombocytosis. According to body systems, gastrointestinal involvement was most represented, followed by endocrine cases. No association was found between the severity of thrombocytosis and outcome.     

Amplification of papillomaviral DNA sequences from a high proportion of feline cutaneous in situ and invasive squamous cell carcinomas using a nested polymerase chain reaction

Squamous cell carcinomas (SCCs) are common skin tumours of cats. Previous studies have suggested that papillomaviral (PV) DNA is detectible within some feline SCCs. A PV DNA sequence has been previously amplified from five feline bowenoid in situ carcinomas (BISCs). Primers specific for this sequence were used in a nested polymerase chain reaction to compare PV detection rates in SCCs to rates within non-SCC skin lesions. Papillomaviral DNA was amplified from 20 of 20 BISC, 17 of 20 invasive SCC and 3 of 17 non-SCC controls. The rate of PV amplification from feline cutaneous SCCs was significantly higher than from non-SCC lesions. These results confirm that feline cutaneous SCCs are associated with PV infection. In humans, there is evidence that PVs promote SCC development within sun-exposed skin. The demonstrated association between PVs and feline cutaneous SCCs suggests, but does not prove, that PVs may also promote feline SCC development. If PVs are oncogenic in cats, prevention of PV infection may reduce feline cutaneous SCC development. To the authors' knowledge, this is the first time that PV DNA has been amplified from a non-SCC sample of feline skin.     

ESTIMATION OF FELINE RENAL VOLUME USING COMPUTED TOMOGRAPHY AND ULTRASOUND

Renal volume estimation is an important parameter for clinical evaluation of kidneys and research applications. A time efficient, repeatable, and accurate method for volume estimation is required. The purpose of this study was to describe the accuracy of ultrasound and computed tomography (CT) for estimating feline renal volume. Standardized ultrasound and CT scans were acquired for kidneys of 12 cadaver cats, in situ. Ultrasound and CT multiplanar reconstructions were used to record renal length measurements that were then used to calculate volume using the prolate ellipsoid formula for volume estimation. In addition, CT studies were reconstructed at 1 mm, 5 mm, and 1 cm, and transferred to a workstation where the renal volume was calculated using the voxel count method (hand drawn regions of interest). The reference standard kidney volume was then determined ex vivo using water displacement with the Archimedes’ principle. Ultrasound measurement of renal length accounted for approximately 87% of the variability in renal volume for the study population. The prolate ellipsoid formula exhibited proportional bias and underestimated renal volume by a median of 18.9%. Computed tomography volume estimates using the voxel count method with hand‐traced regions of interest provided the most accurate results, with increasing accuracy for smaller voxel sizes in grossly normal kidneys (–10.1 to 0.6%). Findings from this study supported the use of CT and the voxel count method for estimating feline renal volume in future clinical and research studies.     

Lack of circulating thyroid stimulating immunoglobulins in cats with hyperthyroidism

Although feline hyperthyroidism has become a commonly diagnosed disorder of older cats, the underlying etiology remains unknown. Pathological findings of adenomatous hyperplasia involving both thyroid lobes in most hyperthyroid cats suggests the possibility that feline hyperthyroidism may be similar to human Graves' disease, which results from high circulating levels of thyroid stimulating immunoglobulins (TSIs). To exclude high circulating levels of TSIs as the cause of feline hyperthyroidism, we measured intracellular concentrations of cyclic adenosine monophosphate (cAMP) in functioning rat thyroid cells (FRTL-5) incubated with IgG extracted from hyperthyroid cat serum. Since TSIs stimulate thyroid hormone secretion through activation of cAMP, their presence can be evidenced in vitro by generation of high cAMP concentrations in cultured thyroid cells. No significant difference was found in intracellular cAMP concentrations in FRTL-5 cells incubated with IgG from normal versus hyperthyroid cats. In contrast, IgG from a human patient with Graves' disease caused substantially more cAMP generation than either normal human IgG or IgG from the cats of this study. These results indicate that feline hyperthyroidism does not result from high circulating concentrations of TSI and, in that respect, is not analogous to Graves' disease.     

Clinical and immunological responses of cats to feline herpesvirus type 1 infection

Cats which were challenged with feline herpesvirus type 1 developed clinical signs typical of feline viral rhinotracheitis whether or not they had been vaccinated against the disease. However, the clinical disease was less severe and of shorter duration in the vaccinated cats. After challenge, feline herpesvirus type 1 was recovered from the nostrils, oropharynx and peripheral blood leucocytes. Leucocytosis, primarily a neutrophilia, occurred initially in all the cats and was followed after clinical recovery by a mild lymphocytosis. Intradermal skin testing with feline herpesvirus type 1 and cell control antigens produced a positive delayed type skin reaction. Histology of the affected skin 72 hours after injection showed cellular infiltration, predominantly with eosinophils and neutrophils. The severity of the reaction was greater and more prolonged in the skin of the ear than in the skin of the abdomen.     

Clinical outcome,PDGFRβ and KIT expression in feline histiocytic disorders: a multicentre study

Information about histiocytic disease in cats is limited. The aim of this study was to document clinical findings and outcome in feline histiocytic disorders, and characterize the expression of PDGFRβ and KIT in order to identify potential treatment targets. Morphologically diagnosed feline histiocytic tumours were reviewed and characterized by immunohistochemistry (IHC). Five cases of feline progressive histiocytosis (FPH), eight histiocytic sarcomas (HS) and two haemophagocytic histiocytic sarcomas (HaeHS) were confirmed. PDGFRβ was variably positive in most histiocytic cases, while KIT was negative in all. Clinical presentation, treatment and outcome were also evaluated. Partial responses were recorded in measurable disease with tyrosine kinase inhibitors and lomustine, and radiotherapy achieved long‐term control in some cases. Survival times were shortest in HaeHS and disseminated disease. PDGFRβ, but not KIT, may represent a therapeutic target in feline histiocytic disorders but more studies are needed to investigate other potential treatment targets.