Severe Ulcerative Dermatitis Research Articles

Successful Treatment of Severe Ulcerative Dermatitis in an Aubry's Flapshell Turtle (Cycloderma aubryi )

An adult, wild-caught, intact female Aubry’s flapshell turtle (Cycloderma aubryi) that had been in the collection for 21 months, presented with rapid onset of multifocal, tan-white, 1.5 cm and smaller, crateriform, ulcerated lesions on the carapace and plastron. Empirical antibiotic therapy, initiated on the suspicion of an infectious etiology, yielded no clinical improvement and the disease progressed. Multifocal osteomyelitis was visible deep to the dermatological lesions on the carapace and plastron on computed tomographic (CT) imaging, and culture results included Stenotrophomonas maltophilia and Achromobacter (Alcaligenes) xylosoxidans. Two months after surgical debridement and ostectomy, healing of lesions was incomplete and slow to progress. Photobiomodulation (PBM) was initiated on some of the lesions, and the treated lesions showed grossly visible indications of progressive healing after 17 days; there were no indications of healing in the untreated lesions. All lesions were subsequently treated with PBM, and the patient made a full recovery. This case report describes successful treatment of severe ulcerative dermatitis in a softshell turtle using advanced imaging (CT), surgical debridement and ostectomy, supportive care, husbandry modifications, and PBM. This report highlights that PBM can be a valuable therapeutic tool that should be considered for treatment of ulcerative dermatitis in softshell turtles, especially in patients with delayed wound healing or chronic dermatologic lesions.

An IL17RA frameshift variant in a Holstein cattle family with psoriasis-like skin alterations and immunodeficiency

BackgroundSkin lesions and dermatoses in cattle are often associated with infections due to bacteria, fungi or environmental risk factors. Dermatoses with genetic etiology have been described in cattle. Among these rare disorders, there are primary congenital dermatoses that are associated with inherited nutritional deficiencies, such as bovine hereditary zinc deficiency or zinc deficiency-like syndrome. This study presents three cases of Holstein cattle with congenital skin lesions observed on a single farm that resemble zinc deficiency-like syndrome. Close clinical and pathological examinations took place in two cases. Pedigree analysis indicated autosomal recessive inheritance and whole-genome sequencing of both affected calves was performed.ResultsThe two calves showed retarded growth and suffered from severe ulcerative dermatitis with hyperkeratosis, alopecia furunculosis and subcutaneous abscess formation. Blood analysis showed correspondent leukocytosis with neutrophilia whereas minerals, macro- and micronutrients were within the reference ranges. Variant calling and filtering against the 1000 Bull Genomes variant catalogue resulted in the detection of a single homozygous protein-changing variant exclusively present in both sequenced genomes. This single-nucleotide deletion in exon 3 of IL17RA on bovine chromosome 5 was predicted to have a deleterious impact on the encoded protein due to a frameshift leading to a truncated gene product. Genotyping of the affected cattle family confirmed recessive inheritance.ConclusionsA loss-of-function mutation of the IL17RA transmembrane protein could be identified as most likely pathogenic variant for the psoriasis-like skin alterations observed in the two affected Holstein calves. In man, rare recessive diseases associated with IL17RA include immunodeficiency 51 and chronic mucocutaneous candidiasis. This supports the observed immunodeficiency of the presented cases. This study reports the first naturally occurring IL17RA-associated animal model.

Subacute dermal toxicity of perfluoroalkyl carboxylic acids: comparison with different carbon-chain lengths in human skin equivalents and systemic effects of perfluoroheptanoic acid in Sprague Dawley rats

Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are used in various fields but raise concerns regarding human health and environmental consequences. Among PFASs, perfluorooctanoic acid (PFOA) and short-chain perfluoroalkyl carboxylic acids (SC PFCAs) are detectable in skin-contact consumer products and have dermal absorption potential. Here, we investigated the effects of dermal exposure to PFOA and SC PFCAs using in vitro and in vivo models. Human skin equivalents were topically treated with 0.25mM and 2.5mM PFOA and SC PFCAs (perfluoropentanoic acid, PFPeA; perfluorohexanoic acid, PFHxA; and perfluoroheptanoic acid, PFHpA) for 6days, and cell viability, interleukin (IL)-1α, oxidative stress markers (malondialdehyde, MDA; and 8-hydroxydeoxyguanosine, 8-OHdG), and histopathology were examined. MDA levels were significantly higher in the PFASs groups than in controls. Compared with SC PFCAs, 2.5mM PFOA caused more IL-1α (p < 0.001) release, decreased skin thickness and microscopic abnormalities. To evaluate systemic effects, Sprague Dawley (SD) rats were dermally treated with 250 and 1000mg/kg PFHpA for 2weeks and clinical and anatomic pathology were assessed. At 1000mg/kg, 83% of the rats died, with severe ulcerative dermatitis at the application site. Adverse PFHpA-treated systemic changes were observed in the kidney, liver and testes, and histopathologic lesions such as renal tubular necrosis, hepatocellular necrosis, and germ cell degeneration were seen at 250 and 1000mg/kg. Our study suggests that SC PFCAs have fewer effects on the skin than PFOA, but SC PFCAs can have adverse effects on major organs with systemic exposure at high concentrations.

Laboratory investigation into the role of largemouth bass virus (Ranavirus, Iridoviridae) in smallmouth bass mortality events in Pennsylvania rivers

BackgroundMortality episodes have affected young-of-year smallmouth bass (Micropterus dolomieu) in several river systems in Pennsylvania since 2005. A series of laboratory experiments were performed to determine the potential role of largemouth bass virus (Ranavirus, Iridoviridae) in causing these events.ResultsJuvenile smallmouth bass experimentally infected with the largemouth bass virus exhibited internal and external clinical signs and mortality consistent with those observed during die-offs. Microscopically, infected fish developed multifocal necrosis in the mesenteric fat, liver, spleen and kidneys. Fish challenged by immersion also developed severe ulcerative dermatitis and necrotizing myositis and rarely panuveitis and keratitis. Largemouth bass virus-challenged smallmouth bass experienced greater mortality at 28 °C than at 23 or 11 °C. Co-infection with Flavobacterium columnare at 28 °C resulted in significant increase in mortality of smallmouth bass previously infected with largemouth bass virus. Aeromonas salmonicida seems to be very pathogenic to fish at water temperatures < 23 °C. While co-infection of smallmouth bass by both A. salmonicida and largemouth bass virus can be devastating to juvenile smallmouth bass, the optimal temperatures of each pathogen are 7–10 °C apart, making their synergistic effects highly unlikely under field conditions.ConclusionsThe sum of our data generated in this study suggests that largemouth bass virus can be the causative agent of young-of-year smallmouth bass mortality episodes observed at relatively high water temperature.

Ulcerative pododermatitis and disseminated erosive lesions associated with cowpox virus infection in a domestic cat

The authors report on a case of feline cowpox virus infection associated with severe ulcerative dermatitis of a paw and disseminated erosive lesions. While the anamnesis of the cat being...

Ulcerative Dermatitis and Valvular Endocarditis Associated withStaphylococcus aureusin a Hyacinth Macaw (Anadorhynchus hyacinthinus)

An 18-yr-old male hyacinth macaw (Anadorhynchus hyacinthinus) was found dead in his aviary with no preexisting signs. The bird had a chronic history of feather damaging behavior, with severe ulcerative dermatitis. Pathologic findings revealed a vegetative valvular endocarditis, myocarditis, septicemia, chronic severe glomerulonephritis, and thyroid dysplasia. Staphylococcus aureus was isolated from the valve, the liver, and the skin. Repeated trauma and low-rate bacteriemia may have contributed to the development of endocarditis. Translocation of S. aureus skin infection in the bloodstream may lead to subacute endocarditis in humans and such mechanism is suspected in this case. This case suggests that endocarditis associated with S. aureus septicemia is a potential complication of feather damaging behavior. This case also reports a systemic complication of ulcerative dermatitis secondary to feather damaging behavior. Endocarditis has been poorly reported in psittacine species, and such medical complication of feather damaging behavior has never been reported to our knowledge. Furthermore, S. aureus is a bacteria of public health concern and should be integrated into the differential when pet parrots with dermatitis are in proximity to owners.

Do‐it‐yourself cement work: the main cause of severe irritant contact dermatitis requiring hospitalization

There are myriads of potentially irritant agents causing acute irritant contact dermatitis. In the large majority of cases, dermatitis is mild to moderate, and patients do not need hospitalization. However, some agents or special circumstances may cause severe dermatitis requiring more intensive therapy. The aim of this study was to evaluate causative agents of severe acute irritant contact dermatitis requiring hospitalization. In this single-centre observational cohort study, we included 54 consecutive patients presenting with signs and symptoms of acute irritant contact dermatitis for which hospitalization was necessary. The severity of dermatitis was graded (grade I-IV) according to intensity, and details related to the skin irritation (irritant agent, area of exposure, time interval to onset of symptoms, and duration of hospitalization) were determined. All cases with severe ulcerative dermatitis (grade IV) were caused by wet cement, owing to prolonged skin contact. These cement burns are clearly associated with amateur work, younger age, male preponderance, and leg localization. The study data provide clear-cut evidence that wet cement is a severely irritant substance that regularly causes the most severe form of acute irritant contact dermatitis. The main causative prerequisite for these cement burns is do-it-yourself work with poor protective measures.

T cell requirement for development of chronic ulcerative dermatitis in E- and P-selectin-deficient mice.

C57BL/6 mice deficient in E- and P-selectin (E(-/-)P(-/-)) kept under specific pathogen-free barrier conditions have high circulating neutrophil counts and develop hypercellular cervical lymph nodes with substantial plasma cell infiltrates, severe ulcerative dermatitis, conjunctivitis, and lung pathology, which eventually lead to premature death. To test the hypothesis that the pathology in E(-/-)P(-/-) mice may be caused by dysfunctional lymphocyte activity, we crossed E(-/-)P(-/-) mice with recombination activation gene (Rag)-1(-/-) mice to generate E(-/-)P(-/-)Rag-1(-/-) mice lacking mature T and B lymphocytes. E(-/-)P(-/-)Rag-1(-/-) mice had circulating neutrophil counts and plasma G-CSF levels similar to E(-/-)P(-/-) mice. Remarkably, none of the E(-/-)P(-/-)Rag-1(-/-) mice developed conjunctivitis or ulcerative dermatitis typical of E(-/-)P(-/-) mice. These mice were overall healthier in appearance than E(-/-)P(-/-) mice, and histopathologic changes in the lung were reduced. Cervical lymph nodes in E(-/-)P(-/-)Rag-1(-/-) mice were much smaller than those of E(-/-)P(-/-) mice, containing few mononuclear cells and no plasma cells. These data show that the severe disease phenotype of E(-/-)P(-/-) mice depends on lymphocyte function. We conclude that a dysregulated immune response in E(-/-)P(-/-) mice causes disease development, but is not necessary for elevated neutrophil counts.

Dermal dysplasia, hypotrichosis, and dorsal skin ulcers in adult NMRI-mice after X-irradiation in utero.

Prenatal X-irradiation in mice leads to a marked incidence of hypotrichosis and alopecia in offspring, when irradiation occurs during the stage of late organogenesis (day 11-13 p.c.). In addition, severe ulcerative dermatitis occurs in offspring starting at 2 months of age, with marked preference for those animals, which have been irradiated at least during days 11-13 p.c. This occurs without any dose dependence; application of doses between 2.4 Gy and 7.2 Gy results in approximately similar incidence rates of skin ulcers (range between 39.1 and 48.0%). There is no sex preference and no dependence on housing. At autopsy no special abnormalities were found in the internal organs with the exception of frequent signs of amyloidosis. This disease pattern could also be produced in germ-free animals. The intracutanous administration of skin extracts from affected animals into unirradiated mice leads to a marked infiltration of leukocytes. It is therefore suggested that prenatal X-irradiation induces a distinct dysplasia of the epidermis, which is followed by an endogenous leukotactic activity.

Effects of Mutant Steel Alleles on Leukemogenesis and Life-Span in the Mouse2

Mutant alleles at the steel locus produce the pleiotropic effects of congenital anemia, sterility, and lack of hair pigmentation. Strain (WC/Re X C57BL/6)F1 Sl/Sld mice lived only half as long as heterozygotes and homozygous normal controls, differing only at the steel locus. Lymphocytic leukemia developed spontaneously in 37% of mice of the Sl/Sld genotype at an average age of 370 +/- 25 days and in 5% of heterozygotes and homozygous normal controls at 965 +/- 41 days. Severe ulcerative dermatitis occurred in 56% of Sl/Sld mice at an average age o4f 441 +/- 21 days and in 20% of heterozygotes and homozygous normal controls at 722 +/- 50 days. The mutant steel alleles provided an opportunity for study of the role of chronic anemia in life shortening and of a mechanism of gene action in spontaneous leukemogenesis.

Canary pox in sparrows and canaries (Fringillidae and in weavers (Ploceidae). Pathology and host specificity of the virus.

An epornitie of canary pox occurred in white-crowned sparrows ( Zonotrichia leucophrys gambelli), golden-crowned sparrows ( Zonotrichia atricapilla), and house sparrows ( Passer domesticus), which had been caught in the wild and were being studied in laboratories. Of 900 exposed birds, 100 died naturally with the disease and 200 with clinical signs, and their 600 cage mates were killed. The earliest lesion was proliferative dermatitis around the eyes and beak. Next, severe ulcerative dermatitis, often with secondary bacterial and mycotic infections, developed under the wing; rhinitis, pneumonia, pleuritis, and peritonitis occurred in advanced cases. Histologically, there were eosinophilic, sudanophilic, cytoplasmic inclusions in epithelial cells and in subepidermal lymphoreticular cells. The isolated virus produced 100% mortality when inoculated into white-crowned sparrows, house sparrows, and canaries but only local cutaneous reactions in pigeons, turkeys, and chickens.