Tuesday 6 December 2016

Dermatološki dan 2016

Dermatološki dan je za nami. Za vse ki ste se udeležili ali pa se na žalost niste mogli, objavljamljo tukaj še enkrat program in prilagamo linke za pdf dokumente (kliknite na naslov), če si želite kaj prebrati naknadno.   
  1. Srbež – diagnostični in terapevtski izziv
  2. Allergen specific immunotherapy: definitely worth a try!
  3. New methods of desensitisation for Canine atopic dermatitis
  4. Food allergy - an update!
Tukaj pa še nekaj informacij o glavni predavateljici Dr. Nini Fischer.

Nina je diplomirala na veterinarski fakulteti LMU v Münchnu 2007.  Veterinarsko diplomo je pripravljala v Severni Karolini v ZDA pri Prof. Thierry Olivry-ju, na področju autoimunih obolenj od 2008 do 2009. Svoj internship in specializacijo iz veterinarske dermatologije je absolvirala na Kliniki za male živali v Zürichu in prejela naziv diplomata 2014. Nina je trenutno zaposlena na veterinarski fakulteti v Zürichu kot klinik in docentka na oddelku za dermatologijo ter pripravlja svojo habilitacijo na področju alergologije. Publicirala je več člankov s področja alergologije, papilloma virusnih infekcij in pemphigoidnega kompleksa. Nina je od 2015 tudi blagajnik v Švicarski Dermatološki Sekciji.

Friday 18 November 2016

Dermatološki dan 2016



Dragi člani Dermatološke sekcije in vsi kolegi, ki vas zanima dermatologija malih živali.
Vabimo vas na dermatološki dan, kjer bodo predstavljene najnovejše metode
diagnostike in zdravljenja s področja alergij in srbeža ter novosti s svetovnega
dermatološkega kongresa. Na koncu predavanj ste dobrodošli predstaviti tudi svoje

KJE:               Grand Hotel Bernardin, Portorož
KDAJ:            sobota 3.12. 2016 s pričetkom ob 9 uri do kosila
KDO:             Nina Fischer, dr.vet.med. dipl. ECVD
Ana Rostaher, dr.vet.med. dipl. ECVD

Več informacij na: http://vetkongres.si/

Kotizacija za soboto znaša za člane Dermatološke sekcije 70€

Članarino lahko poravnate na: SZVMŽ, Cesta v Mestni Log 47, 1000 Ljubljana Številka tekočega računa: IBAN: SI56 0310 7100 0013 109.


1.     Srbež – diagnostični in terapevtski izziv
2.     Nove metode specifične imunoterapije (SIT): subkutano, oralno ali intralimfatično?–
3.     Diagnostika alergije na hrano: kje smo in kam gremo?
4.     Diskusija primerov, novosti iz svetovnega dermatološkega kongresa
5.     Letna skupščina Dermatološke sekcije (20 min)
*Popoldan po želji neformalna diskusija o dermatoloških primerih članov

Monday 13 April 2015

Mystery case answer

This is Arwen, a 3,5 years old, spayed Viszla. Her skin lesions started soon after developing diarrhea and vomiting. She was treated with immuno-suppressive doses of glucocorticoids and recovered very slowly.
Main important question was: asking for medications, food history and possible insect bites
We found out that Arwen was eating often walnuts and that day more then 100g.
What is your problem list? Urticaria and erythematous patches, vomiting and diarrhea
What are your main differentials?  Urticaria, urticarial vasculitis
What tests would you like to perform? Checking clinical signs of anaphylaxis (inlcuding blood preassure), hematology, biochemistry, abdominal ultrasound, skin biopsy, intradermal testing and western blot for walnuts 

Saturday 21 March 2015

Cytological evaluation of inflammatory and neoplastic skin disease PART 1

Inflammatory cells are usually neutrophils, eosinophils, macrophages, lymphocytes, plasma cells.


Eosinophilic plaque in a cat
Interdigital granuloma in a dog

Non-inflammatory cells:
- Epithelial cells: tend to exfoliate in high numbers are often present in cohesive clusters and sheets. Individual cells are round, cuboidal or polygonal. Most epithelial cells have well-defined cell borders. We see them on a regular basis in the inflammatory preparations, where they are admixed with bacteria, fungi and inflammatory cells. In non-neoplastic tumours we find them often in inclusion type cysts or cystic epithelial tumours. They should be evaluated for criteria of malignancy. 

Normal epidermal cells by layers
Squamous cell carcinoma
Basal cell tumor

- Mesenchymal cells (spindle cells):  Tissue cells tend to exfoliate in low numbers and are present in loose aggregates or groups. The cells are usually spindle shaped but can appear more ovoid and plump.  If these cells are contained in an inflammatory exudate they can become reactive and can mimic pleomorph neoplastic cells. Usually this is seen in granulation tissue. However, a high number of spindle-shaped cells are indicative of neoplasia. The origin is very difficult to detect, they can arise form adipose, fibrous, vessel, neural etc. tissue.
Spindle cell tumor of soft tissue origin

- Round-cells: Round-cell lesions tend to exfoliate readily, although cells can be fragile, requiring gentle preparation for cytology. Cells are discrete with well-defined cell borders. Common cells of this category include lymphocytes, histiocytes, mast cells, and plasma cells, as well as cells of transmissible venereal tumors.      

Mast cell tumor


Sunday 1 February 2015

Primary cornification disorders

The cornification process represents morphologic changes in the whole life span of the keratinocytes. It starts already in the basal cell layer keratinocytes and ends with the final differentiated corneocytes of the ‘strong and compact’ stratum corneum. The main functions of this layer are the toxin/microbe/trauma/UV light protection and prevention of fluid loss (skin hydration). Four key steps are included in these processes:
1.     Formation of the protein core (aggregation of keratins, with the help of fillagrin)
2.     Formation of the protein envelope (replacement of the previous cell membrane with a ‘stronger’ one consisting of small peptides)
3.     Formation of the lipid lamellar bilayers (consisting of cholesterol, long-chain fatty acids, and ceramides, important role of lamellar bodies)
4.     Desquamation (corneodesmosomes are cleaved by proteases, the corneocytes are shed into the environment)

Cornification disorders arise when there is a problem in establishing a normal stratum corneum. They are usually secondary, to an allergic, parasitic, metabolic, (para)neoplastic or endocrine disease. Primary cornification disorders, the so-called ichthyoses are due to a genetic defect somewhere in the cornification process or elements: structural proteins, lipid metabolism, enzymes. Some investigators include abnormalities in sebaceous gland function (eg, sebaceous adenitis, sebaceous gland dysplasia) as primary cornification disorders as well. The diagnostic approach involves thorough clinical assessment and ruling out secondary causes. Skin biopsies and genetic test are usually inevitable to make a final diagnosis.

Icthyosis resembles primary cornification disorders is at present subdivided into epidermolytic and non-epidermolytic forms on the basis of light microscopy.

1. Epidermolytic ichthyosis in the Norfolk terrier is autosomal recessive and caused by a mutation in epidermal keratin 10. It was also described in some other breeds (Rhodesian ridgeback). These dogs have multifocal areas of hyperpigmented hyperkeratosis (intertriginous areas) and dark scaling. The skin is sensitive to mechanical trauma (erosions).

2. Non-epidermolytic

This group is corresponding to the autosomal recessive congenital ichthyosis (ARCI) in humans, which is the official classification for a heterogeneous group of disorders with overlapping phenotypes (e.g. lamellar ichthyosis, congenital ichthyosiform erythroderma). A variety of mutations affecting lipids and structural proteins cause similar phenotypes and light microscopic changes. In humans, there are currently 8 known mutations, in comparison researchers characterized 3 in veterinary medicine. The current nomenclature used by pathologists in veterinary medicine is to label these ARCI disorders by the breed predilection, as described bellow. We will se if this will change in the future.

Golden retriever ichthyosis
Golden retrievers may presents with usually mild-moderate non-pruritic generalised scaling (mild to moderate) disorder, in the age from 3 weeks to 3 years (85% before 1 year of age). In France a high prevalence (50%) was shown in this breed. The causing gene is now known to be PNPLA1 (belonging to the patatin-like phospholipase family). It is coding for a protein responsible for lipolytic and/or lipogenic activity of neutral lipids (not triglycerides). These studies in dogs helped to reveal the cause also in human patients with ARCI. In non-breeding animals a diagnosis based on clinical and histopathological findings is sufficient. Performing a genetic test (www.antagen.com) in breeding animals to assess carrier state is recommended.

American Bullterier ichthyosis
American bulldogs typically have a more severe phenotype (then Golden retrievers) with lesions evident before weaning (sometimes shortly after birth). The scaling is generalized (also in the coat) with large, light brown adherent scale on the ventral thorax and abdomen, the skin is often erythematous. The abdominal skin of adult dogs may be reddish-brown. The animals may show otitis, pododermatitis and intertrigo. Secondary Malassezia infections may develop and be associated with a significant pruritus. Pedigree analyses are highly suggestive of an autosomal recessive trait and the responsible gene is coding for the protein ICHTHYN. The test can be performed at The University of Pennsylvania USA (dogderm@vet.upenn.edu)

Jack (Parson) Russel Icthyosis
The clinical lesions are characterized by thick, adherent scales (0,5 -2 cm large) predominantly on ventral skin areas (abdomen, ventral neck). The skin of the food pads and nose may be thickened and greasy. The dogs may develop severe secondary yeast and/or bacterial infections with corresponding inflammation and pruritus. Nonepidermolytic ichthyosis in Jack Russell terriers (JRT) is caused by a loss of function mutation in transglutaminase 1 (TGM1). TGM1 mediates calcium dependent cross-linking of peptides (e.g. involucrin, loricrin) to form the cornified envelope- the strong exterior of the corneocyte.

Non-determined cornification disorders
Some other breeds are described with clinical signs of ichthyosis, but the molecular characterization is not available yet. The following breeds are mentioned: Cavalier King Charles spaniel dogs (keratoconjunctivitis starting from eyelid opening age, a roughened/curly haircoat, scaling with abdominal hyperpigmentation, footpad hyperkeratosis, and nail dystrophy), West Highland White terriers, soft-coated Wheaton terrier.

Unconfirmed cornification disorders
For some diseases, there is lack of sufficient evidence that they are a primary cornification disorders. Vitamin A – responsive dermatosis, generalized sebaceous gland hyperplasia and primary seborrhea are in this moment controversial diseases.

- Barnhart KF et al. A heritable keratinization defect of the superficial epidermis in norfolk terriers. J Comp Pathol. 2004 May;130(4):246-54.
- Credille KM. Transglutaminase 1-deficient recessive lamellar ichthyosis associated with a LINE-1 insertion in Jack Russell terrier dogs. Br J Dermatol. 2009;161(2):265-72.
- Credille KM et al.  Mild recessive epidermolytic hyperkeratosis associated with a novel keratin 10 donor splice-site mutation in a family of Norfolk terrier dogs. Br J Dermatol. 2005 Jul;153(1):51-8.
- Grall A et al. PNPLA1 mutations cause autosomal recessive congenital ichthyosis in golden retriever dogs and humans. Nat Genet. 2012;44(2):140-7
- Guaguere E et al. Clinical, histopathological and genetic data of ichthyosis in the golden retriever: a prospective study. J Small Anim Pract. 2009;50(5):227-35
- Lewis et al. Characterization and management of a Jack Russell terrier with congenital ichthyosis. Vet Dermatol
1998; 9(2) pages 111–118.
- Mauldin E. Proceedings of the 27th Annual congress of the ESVD-ECVD 2014, p.124-127
- Mauldin EA. Canine ichthyosis and related disorders of cornification. Vet Clin North Am Small Anim Pract. 2013 ;43(1):89-97
- Mauldin EA et al.
The clinical and morphologic features of nonepidermolytic ichthyosis in the golden retriever. Vet Pathol. 2008;45(2):174-80.

Sunday 25 January 2015

NOVOST Journal club za člane - Februar 2015

Dragi člani, se želite udeležiti interaktivne diskusije preko skypa?

Kdaj: Februar 2015: torek, sreda ali četrtek 10., 11 ali 12. ob 20h
: max. 1,5h
Tema: Spodnji članki, vaši klinični primeri, razna dermatološka vprašanja
(članke ste dobili po emajlu, ali pa predstavite članek po vašem okusu).
Potrditev udeležbe: na elektronsko doodle anketo (vpišite kar svoje skype ime)
ali pa na emajl : ana_rostaher@yahoo.com

Lista člankov
1. Urticarial vasculitis in a French bulldog. Declercq J Vet Dermatol. 2015 Feb;26(1):72-3.
2. Feline leishmaniosis: a case with a high parasitic burden. Migliazzo A et al.
Vet Dermatol. 2015 Feb;26(1):69-70.
3. Concurrent Bartonella henselae infection in a dog with panniculitis and owner with ulcerated nodular skin lesions. Rossi MA et al. Vet Dermatol. 2015 Feb;26(1):60-e22
5. Efficacy of oclacitinib (Apoquel) compared with prednisolone for the control of pruritus and clinical signs associated with allergic dermatitis in client-owned dogs in Australia
Caroline Gadeyne et al Vet Dermatol. 2014 Dec;25(6):512-8,
6. Deslorelin for the treatment of hair cycle arrest in intact male dogs. Albanese et al. Vet Dermatol. 2014 Dec;25(6):519-22

Kratka navodila

Predstavitev publikacije naj obsega sledeče:
-       Povzetek v 1 stavku - bistvena ugotovitev članka
-       Namen raziskave ali oziroma zakaj je bil klinični primer predstavljen
-       Opis kliničnega primera oz. materialov in metod
-       Rezultati, če je študija oz. kaj se je dogajalo s kliničnim primerom
-       Diskusija (bistvene ugotovitve)
-       Kritična ocena članka (pozitivna in negativna)

Približno 10 minut, nato še diskusija.