PUSTULAR DERMATITIS CAUSED BY IMPETIGO IN RED-TAILED MONKEYS ( CERCOPITHECUS ASCANIUS).

Impetigo is a bacterial infection of the superficial layer of the epidermis with crusting or bullae caused by Streptococcus spp., Staphylococcus spp., or both. A 14-yr-old red-tailed monkey ( Cercopithecus ascanius) presented with recurrent scabbing and ulceration under the nares over an 8-yr period. Repeated cultures and biopsy samples led to a presumptive diagnosis of impetigo, later confirmed on necropsy. Multiple antibiotic regimens were employed with varying success during multiple episodes, while lesions resolved on their own at other times. This condition has not been previously reported in a nonhuman primate, although it is not uncommon in humans.

The molecular logic of pemphigus and impetigo: the desmoglein story.

Desmosomes are intercellular adhesive junctions of epithelial cells that contain two major transmembrane components, desmogleins (Dsg) and desmocollins; these are both cadherin-type cell-cell adhesion molecules. Pemphigus is an autoimmune blistering disease caused by IgG autoantibodies that target Dsg1 and Dsg3 in pemphigus foliaceus and pemphigus vulgaris respectively. Bullous impetigo is a common and highly contagious superficial skin infection caused by Staphylococcus aureus. Staphylococcal scalded skin syndrome (SSSS) is a generalized form of bullous impetigo. The blisters in bullous impetigo and SSSS are induced by exfoliative toxin that specifically cleaves Dsg1. Clinical and microscopic localization of blisters in pemphigus, bullous impetigo and SSSS are logically explained at the molecular level by the desmoglein compensation theory; the similarity of lesions among these diseases is underscored by a similar pathogenesis.

[Bacterial skin infections in the dog (author's transl)]. / Bacteriële huidinfecties bij de hond.

The most common bacterial skin conditions in dogs are reviewed in the present paper. An introductory part on the pathogenesis of pyoderma and some universal morphological dermatological concepts is followed by a systematic study of superficial and deep forms of pyoderma. In addition to the bacterial diagnosis, the results of bacteriological examination of fifty-three dogs with pyoderma submitted to the University Clinic of small animal medicine are reported. Moreover, a guide to the institution of adequate therapy is suggested.

Identification of a novel Staphylococcus pseudintermedius exfoliative toxin gene and its prevalence in isolates from canines with pyoderma and healthy dogs.

Staphylococcal exfoliative toxins are involved in some cutaneous infections in mammals by targeting desmoglein 1 (Dsg1), a desmosomal cell-cell adhesion molecule. Recently, an exfoliative toxin gene (exi) was identified in Staphylococcus pseudintermedius isolated from canine pyoderma. The aim of this study was to identify novel exfoliative toxin genes in S. pseudintermedius. Here, we describe a novel orf in the genome of S. pseudintermedius isolated from canine impetigo, whose deduced amino acid sequence was homologous to that of the SHETB exfoliative toxin from Staphylococcus hyicus (70.4%). The ORF recombinant protein caused skin exfoliation and abolished cell surface staining of Dsg1 in canine skin. Moreover, the ORF protein degraded the recombinant extracellular domains of canine Dsg1, but not Dsg3, in vitro. PCR analysis revealed that the orf was present in 23.2% (23/99) of S. pseudintermedius isolates from dogs with superficial pyoderma exhibiting various clinical phenotypes, while the occurrence in S. pseudintermedius isolates from healthy dogs was 6.1% (3/49). In summary, this newly found orf in S. pseudintermedius encodes a novel exfoliative toxin, which targets a cell-cell adhesion molecule in canine epidermis and might be involved in a broad spectrum of canine pyoderma.

The comparative pathology of non-viral bullous skin diseases in domestic animals.

In a review of non-viral bullous skin diseases of domestic animals and a 4-year study of cases presented to the New York State College of Veterinary Medicine, we found 15 diseases: pemphigus vulgaris, pemphigus vegetans, pemphigus foliaceus, pemphigus erythematosus, bullous pemphigoid, systemic lupus erythematosus, dermatitis herpetiformis, toxic epidermal necrolysis, drug eruption, epidermolysis bullosa, epidermolysis bullosa simplex, familial acantholysis, bovine congenital porphyria, impetigo and subcorneal pustular dermatosis. The 15 diseases were placed in five categories: autoimmune, immune-mediated, hereditary, bacterial and idiopathic. A histologic classification of these disorders based on the site of blister formation and other important clinicopathologic, histologic and immunopathologic findings was developed.