Investigating the depth of thermal burns in elephants

Histological examination of burn injuries in elephants revealed that the depth was not as severe as expected from clinical observation. Although the actual burn depth was deep, the thickness of elephant skin, especially the dermis, resulted in the lesions being classified as less severe than expected. Examination of skin samples from selected areas showed that most lesions were either superficial (1st degree) or superficial partial-thickness (superficial 2nd degree) burns with the occasional deep partial thickness (deep 2nd degree) wound. These lesions however, resulted in severe complications that eventually led to the death of a number of the elephants.     

Full-thickness cutaneous burn in black-haired skin on the dorsum of the body of a Dalmatian puppy

A 10-week-old Dalmatian puppy was presented for evaluation of plaques and eschars limited to the black-haired markings on the dorsum of the body. The plaques and eschars were of acute onset. Histopathologic evaluation revealed epidermal, adnexal, and vascular necrosis, and subepidermal vesiculation consistent with a full-thickness burn. Because of the history of exposure to direct sunlight, limitation of plaques and eschars to black-haired dorsal skin, histopathology, and lack of another identifying cause, the lesions were attributed to a thermal burn from sunlight.     

Thermal Burns in Four Dogs during Anesthesia

Thermal burns occurred in four anesthetized dogs as a result of using latex surgical gloves filled with warm water to treat hypothermia. The burns were on relatively hairless skin that had been in contact with the gloves. Small containers full of warm water are a relatively inefficient source of heat, but if the temperature of the water exceeds 45 degrees C and the container contacts the animal's skin, thermal injury can result.     

Transpupillary diode laser retinopexy in dogs: ophthalmoscopic,fluorescein angiographic and histopathologic study

Objective To evaluate the ophthalmoscopic, fluorescein angiographic and light microscopic effects of diode laser retinopexy application in the tapetal and nontapetal fundus in the dog, and to ascertain appropriate laser power settings for production of photocoagulative lesions in these two regions. Animals studied Three adult female Beagle dogs. Procedures Laser burns were applied to selected areas in the fundus with an indirect headset delivery system using settings varying from 100 to 200 milliWatts (mW) and from 100 to 600 milliSeconds (mS) with total delivered energy ranging between 15 and 100 milliJoules (mJ). The dogs were then monitored by ophthalmoscopic examination and fluorescein angiography at regular intervals for 7–28 days. Histopathologic studies were performed at 7, 14 and 28 days after laser application. Results The diode laser produced ophthalmoscopically visible lesions in the nontapetal fundus with all laser settings used, and the appearance of these lesions corresponded to the energy levels used, and degree of pigment in the lased region. Gray‐white colored lesions with minimal subsensory retinal edema were seen with settings as low as 100 mWatts/150 mSeconds. In the tapetal fundus, laser burns were more difficult to produce, less repeatable, and required higher energy levels. Laser burns appeared as bronze, dark green or black discolorations of the tapetum with varying degrees of subsensory retinal edema. Lesions were more reproducible and were achieved with lower settings in the tapetal area of the tapetal/nontapetal junction. Ophthalmoscopically, depigmentation and repigmentation of the RPE (nontapetal fundus) and degenerative changes in the overlying retina (tapetal fundus) developed in the laser burns over the 28‐day study period. Fluorescein angiographic studies showed disruption of the blood–retinal barrier at the level of the RPE and fluorescein leakage into the subsensory retinal space was seen in most lesions at 24 h, was minimal at 3 days, and had resolved by 7 days. Histologically, grayish‐white lesions in the nontapetal fundus, and bronze to small black lesions in the tapetal fundus were typically characterized by outer retinal necrosis and RPE migration. Gliosis was considered minimal, was confined to the retina, and no inflammatory cells were seen. Peripheral intense white lesions (nontapetum) and lesions with a black center (tapetal fundus) were characterized by more extensive panretinal and choroidal necrosis. Most of the nontapetal lesions and a few in the tapetal fundus showed the formation of a central retinal detachment. Conclusions The diode laser effectively produces lesions suitable for retinopexy in both the nontapetal, pigmented fundus and the tapetal fundus, although variably so in the latter region. Initial laser settings of 100–150 mW/200 mS for the pigmented fundus, and 150 mW/200–300 mS for the peripheral tapetal fundus are recommended, and the clinician should gradually increase time interval settings to achieve a grayish‐white lesion in the nontapetum, and a bronze to slightly black lesion in the tapetal fundus. If possible, retinopexy should be applied to the peripheral tapetal area or tapetal/nontapetal junction.     

无菌大鼠深二度烫伤感染模型机体炎性反应的研究

为探究无菌大鼠深二度烫伤感染模型机体炎性反应，试验利用无菌大鼠分别建立深二度烫伤损伤模型和烫伤后绿脓杆菌感染模型，比较这两种模型和SPF级大鼠深二度烫伤模型在愈合过程、炎性反应及病理变化等方面的异同。20只6周龄雌性Wistar无菌大鼠，在超净工作台内采用恒温恒压烫伤仪94℃作用8 s造成大鼠深二度烫伤，随机分为2组，一组伤口感染浓度为1×10⁵ CFU/mL绿脓杆菌菌液0.5 mL，一组不做处理，创面保持无菌状态，SPF级Wistar大鼠在同样条件下烫伤，创面不做处理。分别观察3组大鼠的伤口结痂时间、脱痂时间和愈合时间，并在烫伤前（0 h），烫伤后24 h、3 d和7 d时，取血清，检测炎性因子肿瘤坏死因子-α（TNF-α）、白细胞介素1α（IL-1α）、粒细胞-巨噬细胞刺激因子（GM-CSF）的变化。结果显示，感染绿脓杆菌大鼠组开始结痂所需时间显著长于SPF级大鼠组和无菌大鼠组（P<0.05）；而脱痂及愈合所需时间显著变短（P<0.05）；感染绿脓杆菌组大鼠烫伤24 h时，皮下组织中可见淋巴细胞，有慢性炎性反应；3 d时，真皮深层有化脓性感染，横纹肌周围可见大量炎细胞，烫伤7 d时，皮下组织中有轻微血管扩张充血，化脓性感染减轻，无菌烫伤大鼠与SPF级烫伤大鼠皮肤在烫伤后一周内有轻度炎性反应。3组大鼠烫伤后，血清GM-CSF、IL-1α及TNF-α水平均较烫伤前显著升高（P<0.05）；烫伤24 h时，感染绿脓杆菌大鼠组和无菌大鼠组血清IL-1α水平显著高于SPF级大鼠组（P<0.05）；无菌大鼠组血清GM-CSF水平显著高于SPF级大鼠组和感染绿脓杆菌大鼠组（P<0.05）；烫伤3 d时，染绿脓杆菌大鼠组和无菌大鼠组血清IL-1α水平显著高于SPF大鼠组（P<0.05），无菌大鼠组血清GM-CSF水平显著高于染绿脓杆菌大鼠组（P<0.05）。综上所述，无菌大鼠对烫伤刺激反应迅速强烈，血清中炎性因子迅速升高，SPF级大鼠深二度烫伤后炎性反应缓慢；无菌大鼠深二度烫伤伤口感染1×10⁵ CFU/mL绿脓杆菌，脱痂时间和愈合时间反而缩短。     

Comparison of clinical history and dermatologic findings in 29 dogs with severe eosinophilic dermatitis: a retrospective analysis

The medical records and histopathological sections of 29 dogs diagnosed with a unique eosinophilic dermatitis resembling Wells' syndrome were reviewed in an attempt to elucidate the pathogenesis of this syndrome. The medical records were reviewed for information on dermatological lesion appearance, systemic signs in other organ systems, clinical analyte abnormalities, and drug therapy. Histological sections of dogs with moderate to severe eosinophilic dermatitis without folliculitis and furunculosis were reviewed and evaluated for the presence of collagen flame figures. Three categories of patients were found. Category 1 consisted of 17 dogs treated for vomiting and/or diarrhoea (often haematochezia or haematemesis) prior (mean: 4.6 days) to the onset of skin lesions. Fourteen category 1 dogs had erythematous lesions (macules, papules or plaques) that were most pronounced on the abdomen. Sixteen of the 17 dogs received multiple classes of drugs, and 59% were hypoalbuminemic. Category 2 consisted of five dogs that had skin lesions and gastrointestinal signs at presentation and four of these dogs were hypoalbuminemic. Category 3 included seven dogs without enteric illness. A positive drug score was found in six category 1 dogs and one each from categories 2 and 3. Eighteen cases had eosinophilic dermatitis without flame figures, seven cases had early flame figures and four had well-developed flame figures. These changes did not correlate with the categories of clinical presentation. More than 50% of the dogs developed eosinophilic dermatitis following treatment for severe gastrointestinal disease. The authors propose that this represents a unique syndrome that may have causal drug association.     

Photodynamic hyperthermal chemotherapy with indocyanine green: a novel cancer therapy for 16 cases of malignant soft tissue sarcoma

Sixteen cases of malignant soft tissue sarcoma (STS; 10 canines and six felines) were treated with a novel triple therapy that combined photodynamic therapy, hyperthermia using indocyanine green with a broadband light source, and local chemotherapy after surgical tumor resection. This triple therapy was called photodynamic hyperthermal chemotherapy (PHCT). In all cases, the surgical margin was insufficient. In one feline case, PHCT was performed without surgical resection. PHCT was performed over an interval of 1 to 2 weeks and was repeated three to 21 times. No severe side effects, including severe skin burns, necrosis, or skin suture rupture, were observed in any of the animals. No disease recurrence was observed in seven out of 10 (70.0%) dogs and three out of six (50.0%) cats over the follow-up periods ranging from 238 to 1901 days. These results suggest that PHCT decreases the risk of STS recurrence. PHCT should therefore be considered an adjuvant therapy for treating companion animals with STS in veterinary medicine.     

The effects of low voltage current on healing of thermal third degree wounds.

Bilateral third degree burns were created on the flanks of eight miniature swine. Each animal had one side treated daily with low intensity direct (LIDC) of 400 microamperes (muA) by contact electrode for 2 hours morning and afternoon until healing occurred. The polarity of the electrode was negative in 4 pigs and positive in 4 pigs. One group of 4 pigs had the eschar surgically removed 24 hours post burn. Weekly biopsies and cultures were taken of treated and control wounds. Results indicated: local treatment of 400 muA LIDC did not hasten or delay healing of thermal third degree burns; escharectomy hastened wound healing by 10 days, and superficial proteus infection occurred in 80% of all wounds.     

Acute febrile neutrophilic vasculitis of the skin of young Shar-Pei dogs

Three young Shar-Pei dogs were presented for signs of an acute widespread dermatopathy associated with fever and malaise. Cutaneous lesions initially consisted of multifocal areas of skin discolouration (haemorrhagic papules, macules or plaques) or oedema, preferentially affecting the head and limbs. In some locations, pus-filled bullae were evident also. Cutaneous lesions exuded seropurulent liquid and, in time, usually progressed to full thickness necrosis and ulceration. Lesions were so widespread and severe that one of the dogs was euthanased because its owners could not afford the reconstructive surgery required to close the skin deficits left at the completion of otherwise successful therapy. Histological examination of representative biopsies showed neutrophilic dermatitis and vasculitis, which ultimately resulted in ischaemic necrosis of skin. Therapy with immunosuppressive doses of corticosteroids, and in one case cyclophosphamide, resulted in prompt amelioration of the underlying inflammatory process, although regions of skin deprived of their blood supply eventually became necrotic and sloughed. Healing occurred through granulation, contraction and epithelialisation. The physical findings in these three dogs were so similar that it is likely all suffered from the same breed-related syndrome, an immune-mediated vasculitis precipitated by some event, such as vaccination or an undetected infection. Whatever the inciting cause, it was most likely a one-off event, as the two surviving dogs were readily weaned off immunosuppressive medication without relapse.     

Subepidermal bullous dermatosis due to topical corticosteroid therapy in dogs

Six adult dogs were presented with an unusual bullous dermatosis affecting the glabrous skin of the ventral abdomen and medial thighs. Clinically, flaccid bullae were accompanied by erythema, ulceration, haemorrhage and hyperpigmentation in four of six dogs; the remaining two dogs had thin skin without grossly apparent bullae. Histologically, subepidermal bullae and clefting, vascular proliferation and dilatation (phlebectasia), and alteration in the density and staining of superficial dermal collagen were seen in all dogs. In all cases, corticosteroid-containing topical products had been applied to the affected areas prior to the development of the dermatosis; skin lesions resolved when topical corticosteroids were withdrawn. Follow-up biopsy of three dogs showed resolution of the previously abnormal collagen and subepidermal clefting. Residual lesions included phlebectasia, comedones and hyperpigmentation. The authors postulate that subepidermal clefting was due to local, corticosteroid-induced skin fragility. This is the first report, to our knowledge, of bullous skin disease in dogs resulting from topical corticosteroid therapy.     

Epidemiology, clinical signs, histopathology and molecular characterization of canine leproid granuloma: a retrospective study of cases from Brazil

Thirty-eight cases of canine leproid granuloma were diagnosed between 2000 and 2008. Diagnosis was based upon clinical and histopathological findings and the presence of acid-fast bacilli in skin sections. The clinical lesions were localized predominantly on the pinnae and included papules, plaques and nodules, with or without ulceration. Boxer dogs were the breed most affected. Histopathological findings included nodular to diffuse pyogranulomatous, lymphoplasmocytic inflammatory infiltrates, with or without necrosis, localized in the dermis or subcutaneous tissue. The bacillary loading and morphology were variable among the lesions analysed. There was no significant correlation between bacterial load and histopathological pattern, dominant type of inflammatory infiltration or the amount of necrosis or giant cells. No correlation was observed between giant cells and histopathological pattern. In the majority of cases where a PCR-based assay was done, a novel mycobacterium species as the main aetiological agent was identified, as reported in previous studies.     

Cutaneous asthenia in the dog. A report of two cases

Two cases of cutaneous asthenia in Danish dogs are described. Case 1 was a Weimeraner; case 2 a Golden Retriever. In both instances the dogs had acquired numerous lesions of the skin within the first half year of their lives. The wounds exhibited good healing but led to broad, thin and pliable scars. Both dogs had in several instances received attention to gaping wounds, characterized by little tendency of bleeding. The clinical examination reveiled that the skin was hyperextensible and possessed pendulous folds, particularly behind the elbows. The degree of hyperextensibility was evaluated by means of a skin extensibility index. Furthermore, it was possible to manipulate the digital cushion in an unphysiological manner. One of the dogs were euthanised, and in case 2 the clinical diagnosis was confirmed by histopathological examination. No conclusion could be drawn regarding the mode of inheritance in the two cases, but existing literature strongly suggests the existence of a genetic disposition and thus, elimination of the disease related gene from any breeding program is of great importance.     

Battered pets'': non-accidental physical injuries found in dogs and cats

Records of 243 cases of non-accidental injury (NAI) in dogs, and 182 cases in cats, submitted by a sample of small animal practitioners in the UK, revealed a wide range of injuries. These included bruises, fractures, repetitive injuries, burns and scalds, stab and incised wounds, poisoning, asphyxiation and drowning (which showed remarkable similarities to NAI in children), as well as sexual abuse and injuries specifically caused by firearms. Traumatic skeletal injuries in the dogs were more commonly found in the anterior part of the skeleton, in comparison with those resulting from road traffic accidents. Young male dogs and young cats were particularly at risk of NAI. A moderately increased risk was identified in the Staffordshire bull terrier, cross-breed dogs and the domestic shorthaired cat, whereas the Labrador retriever showed a decreased risk. No single injury or group of injuries, when divorced from the circumstances surrounding a suspect case, could be considered to indicate, conclusively, NAI. Repetitive injuries, however, were highly suggestive of NAI.     

Complications and outcome after thoracodorsal axial pattern flap reconstruction of forelimb skin defects in 10 dogs, 1989-2001

OBJECTIVE: To determine (1) the frequency and extent of complications associated with thoracodorsal axial pattern flap reconstruction of forelimb skin defects in dogs and (2) outcome after treatment of such complications. STUDY DESIGN: Retrospective clinical study. SAMPLE POPULATION: Ten dogs. METHODS: Medical records for 10 dogs that had a thoracodorsal axial pattern skin flap reconstruction of a forelimb skin defect were reviewed. RESULTS: Three dogs had complete flap survival. Partial necrosis of the distal flap, ranging from an estimated 2% to 53% (mean, 21%) of the flap surface area, occurred in 7 dogs. Six dogs required surgical management of the skin necrosis, resulting in successful resolution in 5 dogs, whereas, in 2 dogs, the wound healed by second intention. Positive bacterial cultures were obtained from 3 dogs with distal flap necrosis. Seroma formation was noted in 2 dogs; the entire flap survived in 1 dog, whereas the second dog developed distal flap necrosis. Edema and bruising of the distal portion of the flap were noted in 8 dogs; distal flap necrosis subsequently developed in 7 dogs. Partial incisional dehiscence, which healed by second intention, occurred in 2 dogs. Of 6 owners available for follow-up, all were satisfied with the functional outcome, but 1 owner was not satisfied with the cosmetic appearance. CONCLUSIONS: Partial flap necrosis was a frequent complication of thoracodorsal axial pattern flap reconstruction of forelimb skin defects and required additional wound care or surgical intervention to achieve healing. CLINICAL RELEVANCE: Thoracodorsal axial pattern flaps can provide full-thickness skin coverage of extensive skin defects of the forelimb, but owners should be aware of the likelihood of local wound complications.     

Histological and ultrastructural studies of renal lesions in Babesia canis infected dogs treated with imidocarb

Histological and electron microscopic examinations of the kidneys of 8 dogs suffering from fatal, naturally acquired Babesia canis infection and nephropathy are presented. Seven animals were treated with imidocarb dipropionate on average 4.5 days prior to death. Severe anaemia was present only in 2 cases. Degenerative histological changes observed mostly in the proximal convoluted tubules included vacuolar-hydropic degeneration, necrosis and detachment of renal tubular epithelial (RTE) cells from the basement membrane. Necrotic debris occasionally formed acidophilic casts within the tubules. In some cases, necrosis of the whole tubule was observed. Haemoglobin casts in the tubules and haemoglobin droplets in RTE cells seldom appeared. No significant histological changes were seen in the glomeruli. Ultrastructural lesions in RTE cells included nuclear membrane hyperchromatosis, karyopyknosis, karyolysis, swelling or collapse of mitochondria with fragmentation of cristae and vacuolar-hydropic degeneration in the endoplasmic reticulum and microvilli. Nuclear oedema was also observed. Many RTE cells exhibiting necrosis collapsed. Vacuolar-hydropic degeneration and necrosis were also observed in the glomerular and interstitial capillary endothelium. The severe acute tubular necrosis described in this study is probably the result of hypoxic renal injury. Systemic hypotension leading to vasoconstriction in the kidneys might be the most important cause of renal hypoxia in B. canis infections, but anaemia may also contribute to inadequate oxygenation. Imidocarb should be applied with caution in patients with possible renal involvement until further data become available on its potential nephrotoxicity in dogs.     

Thermal burns of the spectacle associated with supplementary heating in native New Zealand geckos

ABSTRACT

Case history: Gradual onset of ocular opacity was observed in three gold-striped geckos (Woodworthia chrysosiretica), and five Pacific geckos (Dactylocnemis pacificus) held in two adjacent terrariums in a zoological institution located in the North Island of New Zealand. Ultraviolet light and heat had been provided for the previous 3–4 years by a fluorescent bulb, but in the last 4 weeks of winter a ceramic heat bulb had been added, situated 10?cm above the upper mesh of the cage

Clinical findings: All eight geckos presented with mostly bilateral lesions of varying severity confined to the central or upper quadrant of the spectacles. These lesions ranged from variable areas of opacity within the stroma of the spectacle to similarly distributed ulcers of the surface epithelium of both spectacles. The spectacle lesions in the Pacific geckos responded well to treatment with topical combined antimicrobial therapy, within 18–29 days. The gold-striped geckos suffered complications including dysecdysis, severe spectacle ulceration and perforation, mycotic spectaculitis, and widespread mycotic dermatitis resulting in death or leading to euthanasia.

Pathological findings: In the three gold-striped geckos, there were extensive areas of deep ulceration and replacement of the spectacle with a thick serocellular crust containing large numbers of fungal elements. The affected areas of the stroma were expanded by large deposits of proteinaceous and mucinous material, pyknotic cellular debris and moderate numbers of heterophils and macrophages as well as infiltrating fungal hyphae.

Diagnosis: Mycotic spectaculitis with ulceration and perforation, and disseminated mycotic dermatitis likely secondary to thermal burns.

Clinical relevance: This is the first report of thermal burns of the spectacle in any reptile. There was species variation in the burn severity with gold-striped geckos showing more severe lesions, possibly due to a mix of behavioural and anatomical factors. The thermal burns to the spectacles in three cases were complicated by delayed healing, perforation, dysecdysis and severe mycotic infection.     

Evaluation of papillomaviruses associated with cyclosporine-induced hyperplastic verrucous lesions in dogs

OBJECTIVE: To determine whether cyclosporine A-induced hyperplastic skin lesions of dogs were associated with papillomavirus infections. ANIMALS: 9 dogs that were treated with cyclosporine A and developed hyperplastic skin lesions. PROCEDURE: History and clinical and histopathologic data were collected. Paraffin-embedded skin biopsy specimens from hyperplastic skin lesions were immunostained for common papillomavirus genus-specific structural antigens by use of a polyclonal rabbit anti-bovine papillomavirus type 1 antiserum. Sections from each tissue block underwent DNA extraction, and polymerase chain reaction (PCR) assays were performed with several sets of primers to amplify a wide range of papillomavirus DNA from humans and other animals. RESULTS: In 7 of 9 dogs, there were more than 10 hyperplastic skin lesions that microscopically resembled those of psoriasiform lichenoid dermatosis. In those dogs, results of testing for papillomavirus via immunohistochemical analyses and PCR assays were negative. In the other 2 dogs, there were only 1 and 3 verrucous lesions, and in those dogs, histologic evaluation revealed koilocytes and nuclear viral inclusions that were immunoreactive for papillomavirus antigens. Papillomavirus DNA was amplified from both dogs. One of the sequences was characteristic for the canine oral papillomavirus, whereas the other had similarities with the recently described canine papillomavirus 2. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs, hyperplastic skin lesions occasionally develop during treatment with cyclosporine A. Most of the lesions resemble those of psoriasiform lichenoid dermatosis, although papillomavirus can be detected in some instances.     

Pulmonary Lymphomatoid Granulomatosis in Seven Dogs (1976–1987)

Seven dogs with pulmonary lymphomatoid granulomatosis were reviewed. The disease occurred in six large-breed and one small-breed dogs. The dogs were five to 14 years old (mean, 8.4; median, 7), and four of seven dogs were males. Three dogs had been previously treated with adulticide therapy for canine dirofilariasis. Clinical histories included a progressive respiratory disease characterized by varying degrees of cough, dyspnea, exercise intolerance, and weight loss. Thoracic radiographic features included hilar lymphadenopathy, pulmonary masses of varying sizes, and mixed pulmonary patterns of lobar consolidation with ill-defined interstitial and alveolar pulmonary infiltrates. Cardiovascular changes compatible with chronic dirofilariasis were present in three dogs. The clinical course was usually progressive and fatal. The survival time ranged from six days to four years (mean, 12.5 mos; median, 3 mos). Gross and histologic features included mass lesions with areas of necrosis that replaced normal pulmonary architecture. Cytologically, these lesions were characterized by infiltration with pleomorphic, angioinvasive mononuclear cells that often resulted in vascular obliteration. The infiltrating cells resembled large lymphoid cells that possessed large hyperchromatic nuclei and small amounts of cytoplasm. Systemic lymphoid neoplasia with peripheral lymphadenopathy was diagnosed in two dogs. In both cases, lymph-node cytology was similar to the cellular infiltrates found in the lungs and consistent with a diagnosis of lymphomatoid granulomatosis. These features are compared with previously reported cases of canine lymphomatoid granulomatosis and those features identified in a similar disease described in man.     

Dermal necrosis caused by Pasteurella multocida infection in turkeys

Severe dermal necrosis caused by Pasteurella multocida Serotype 1 was diagnosed in three dressed turkey carcasses and two live turkeys from a commercial flock. The dressed carcasses were among several condemned at a processing plant. The isolate, P. multocida Serotype 1, produced progressive dermal necrosis when experimentally inoculated into injured skin of turkeys. The organism was reisolated from the dermal lesions. The turkey houses were found to be infested by mice; the skin injury and infection with P. multocida probably originated from mouse bites.