Veterinary Dermatology 2005, 16, 401– 406
Case report
Blackwell Publishing, Ltd.
Generalized calcinosis cutis associated with probable leptospirosis in a dog JOHN S. MUNDAY*, DAVID J. BERGEN† and WENDI D. ROE* *New Zealand Veterinary Pathology Ltd. and Department of Pathobiology, Institute of Veterinary and Animal Biological Sciences, Massey University, Palmerston North, †Northern Waikato Veterinary Services, Huntly, New Zealand (Received 28 February 2005; accepted 19 July 2005)
Abstract A 6.5-year-old male German Shepherd acutely developed renal and hepatic disease. Serology revealed high concentrations of antibodies against Leptospira copenhageni, and a presumptive diagnosis of leptospirosis was made. The dog was successfully treated with antibiotics and supportive care over a 12-day period. Sixty-two days after the initial presentation, alopecia predominantly involving the dorsum and perineal areas developed. The skin lesions expanded over a 20-day period. Histology revealed generalized calcinosis cutis with follicular atrophy. An injection of 0.01 mg kg−1 dexamethasone suppressed serum cortisol concentrations. No treatment was given and lesions resolved over the following 30 days. This is the third case of generalized calcinosis cutis that has developed in an adult dog after severe systemic disease. Both previous cases developed calcinosis cutis in association with blastomycosis. To the authors’ knowledge, this is the first report of generalized calcinosis cutis in an adult dog in association with a presumptive bacterial infection.
IN TRO D U C T ION
C A S E R E P O RT
Calcinosis cutis is the deposition of calcium salts within the skin.1 It can be subclassified depending on the distribution and the cause of the calcium deposition.2 Localized calcinosis cutis is present at a single site, whereas lesions of generalized calcinosis cutis are widespread and multiple.3 Calcinosis cutis can develop as a result of four different processes.4,5 Dystrophic calcinosis cutis is the calcification of altered skin.3 Serum calcium and phosphorus concentrations are normal.3 Metastatic calcinosis cutis is the calcification of normal skin as a result of increased serum calcium and/or phosphorus concentrations.3 Idiopathic calcinosis cutis develops within undamaged skin without abnormal serum calcium or phosphorus concentrations.3 Finally, iatrogenic calcinosis cutis is caused by exposure to calcium-containing substances.6,7 This case report describes a dog that developed generalized calcinosis cutis approximately 2 months after severe systemic disease. The calcinosis cutis subsequently resolved without treatment.
A 6.5-year-old male German Shepherd presented to a veterinary clinic with a 2-day history of lethargy and anorexia. Clinical examination revealed marked icterus, and initial differential diagnoses included haemolytic anaemia, liver damage and bile duct blockage. Blood samples were taken and serum chemistry analysis revealed increased alanine aminotransferase and alkaline phosphatase concentrations (Table 1), consistent with hepatic necrosis and cholestasis. Blood urea nitrogen (BUN) and creatinine concentrations were also increased, suggesting concurrent kidney disease. Urinalysis revealed a specific gravity of 1.019, 2+ protein, 4+ blood and 3+ bilirubin. Leptospirosis was suspected because of the evidence of acute liver and kidney damage. The dog had not received vaccination against this disease. The dog was treated with subcutaneous 40 mg kg−1 procaine penicillin q 12 h (Bovicillin, Bomac Laboratories Ltd, Manukau City, New Zealand) and intravenous lactated Ringer’s solution (2.5 mL kg−1 h−1). The following day, serology revealed a titre of 1/400 against Leptospira copenhageni. Although a definitive diagnosis is not possible using a single antibody titre, the high level of antibodies detected in this dog, combined with the acute hepatic and kidney disease, strongly suggested a diagnosis of acute leptospirosis. On the third day of treatment, the dog started vomiting and developed diarrhoea that contained mucous and blood. Enrofloxacin 5 mg kg−1 q 12 h (Baytril, Bayer
Correspondence: J. S. Munday, Department of Pathobiology, Institute of Veterinary and Animal Biological Sciences, Massey University, Private Bag 11 222, Palmerston North, New Zealand. Tel.: 006463569099; Fax: 006463505636; E-mail:
[email protected] © 2005 European Society of Veterinary Dermatology
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Table 1. Haematological and biochemical data from a 6.5-year-old, male German Shepherd that developed generalized calcinosis cutis shortly after recovering from severe system disease. RBC, red blood cells. Reference ranges were provided by the diagnostic laboratory that performed the analyses
RBC (× 1012 L−1) Segmented neutrophils (× 109 L−1) Lymphocytes (× 109 L−1) Monocytes (× 109 L−1) Alkaline phosphatase (ALP) (IU L−1) Alanine aminotransferase (ALT) (IU L−1) Bilirubin (µmol L−1) Albumin (g L−1) Urea (mmol L−1) Creatinine (µmol L−1) Phosphorus (mmol L−1) Calcium (mmol L−1) Adjusted calcium (mmol L−1)23 Calcium–phosphorus index
0 day
3 days
7 days
12 days
69 days
6.5 15.5 1.7 1.9 676 332 270 31 40.3 655 3.73 2.58 2.68 10
6.0 35.8 0.9 7.0 621 220 457 32 37.8 324 2.43 2.56 2.63 6.4
6.6 27.6 0.7 5.0 1023 202 249
6.1 13.9 2.9 1.9 810 162 97
31 215
15.9 131
5.0 8.1 2.2 0.4 35 51 6 32 10.1 101 1.85 2.1 2.17 4.0
NZ Ltd, Auckland, New Zealand) was given subcutaneously to prevent secondary infection of the damaged gastrointestinal mucosa by gram-negative bacteria. Metoclopramide (Metaclopramide injection, Pharmacia (Perth) Pty Ltd, Bently, Australia) was administered intravenously at a dose of 0.33 mg kg−1 q 12 h to reduce vomiting. An additional blood sample was taken. The following day, haematemesis was observed and intravenous 0.66 mL kg−1 q 12 h ranitidine (Zantac injectable, GlaxoSmithKline, Parma, Italy) was administered. Seven days after initial presentation, the vomiting stopped and the antibiotic was changed to 20 mg kg−1 q 12 h oral amoxicillin/clavulanate (Augmentin, GlaxoSmithKline, Auckland, New Zealand). The antibiotic was changed at this time to avoid repeated subcutaneous injections. Additional blood tests revealed liver enzyme activities and bilirubin concentrations that were similar to those measured at first presentation. Serum BUN and creatinine concentrations were lower than at initial presentation, but still increased above reference ranges. The dog’s clinical attitude gradually improved over the following 4 days at which time intravenous therapy was discontinued. Blood taken 12 days after initial presentation suggested reduced hepatocyte necrosis and cholestasis as well as improved renal function. The dog was discharged the following day on oral doxycycline 3.3 mg kg−1 q 24 h (Vibravet, Pfizer, Auckland, New Zealand). A 14-day course of oral doxycycline is recommended to eliminate the renal carrier phase of leptospirosis.8 Sixty-two days after the disease onset, a small focus of partial alopecia was observed on the dorsal surface of the head. This area slowly expanded over the next week. At this time, the lesion was 12 × 5 mm, well demarcated and almost completely alopecic. Additionally, multiple, roughly circular up to 10 cm in diameter, poorly demarcated areas of partial alopecia were visible on the dorsolumbar region and perineum extending down the caudal aspect of the hind legs. The affected areas were not reddened or painful, and the owners had not noticed the dog excessively scratching. Skin scrapings and tapings were unremarkable. A blood sample did not reveal evidence
Reference ranges 5.5–8.5 3–11.5 1.0–4.8 0.2–1.4 0–185 0–75 0–6 26–44 2.6–10.2 45–135 1.0–3.0 2.2–3.0 2.2–3.0
of liver or kidney disease. Trichography revealed a predominance of telogen bulbs within hairs plucked from the affected areas. Telogen effluvium was suspected and no treatment was given. The dog was re-examined 7 days later (76 days after disease onset). The areas of partial alopecia had enlarged and involved approximately 40% of the dorsum and perineum. The alopecic areas appeared as multiple poorly defined patches that measured up to 15 cm in diameter. Affected skin was observed to be irregularly thickened but did not appear darkened or reddened. Occasional 1–2-mm white papules were visible within affected areas. Multiple skin biopsies were taken and fixed in 10% buffered formalin solution. Skin biopsies from affected skin on the head, shoulder, dorsal thorax, lateral thorax and perineum were examined histologically. Mineralization was visible within all samples but was most marked within samples from the head and perineum, of intermediate severity within samples from the shoulder, and only identifiable using von Kossa-stained sections within samples from the dorsal and lateral thorax. Calcification of the external follicular root sheath was visible multifocally throughout all the samples. Mineralization was also visible within the deep dermis in samples from the head and perineum and the superficial dermis within samples from the shoulder. The deep dermal mineralization appeared as up to 1-mm diameter foci of refractile darkly speckled material (Fig. 1). The material stained black using von Kossa stain, confirming calcification (Fig. 2). The foci of deep dermal calcification were surrounded by fibrosis and moderate numbers of macrophages. Osseous metaplasia was visible within some larger foci of calcification. Superficial dermal linear calcification appeared as narrow horizontal refractile basophilic bands interpreted as mineralized dermal fibres. Follicles within sections from the head, perineum and shoulders were smaller with follicular plugging and trichilemmal keratinization. Anagen hair follicles were not visible within samples from the head and perineum, and few anagen follicles were visible within biopsy samples from other locations. Dermal blood vessels throughout the sections appeared within normal
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hair loss was first noted and 124 days after initial disease development), the owners reported complete hair regrowth. No additional clinical disease has been observed in this dog 9 months after resolution of the skin lesions.
D IS C U S S IO N
Figure 1. Skin biopsy from the perineum of a 6.5-year-old male German Shepherd. The asterisk indicates focal dermal calcification. The calcification is surrounded by moderate fibrosis and granulomatous inflammation. H&E bar = 110 µm.
Figure 2. Skin biopsy from the perineum of a 6.5-year-old male German Shepherd dog. The arrowheads indicate dermal calcification. The asterisk indicates a hair follicle. von Kossa stain bar = 140 µm.
histological limits and no evidence of blood vessel mineralization was observed. Clinically normal skin was not biopsied, and it could not be determined whether calcification was also present in unaffected skin. The generalized calcinosis cutis and follicular atrophy were considered suggestive of hyperadrenocorticism. A low-dose dexamethasone suppression test was performed by administering 0.01 mg kg−1 IV dexamethasone (Dexadresson-V, Intervet Ltd., Auckland, New Zealand) followed by serum cortisol measurement 4 and 8 h later. Serum cortisol concentrations were markedly reduced throughout the 8-h time period, suggesting that an adrenal or pituitary neoplasm was not the cause of the skin lesions. A thyroid hormone assay was within normal limits. As no cause of the skin lesions could be determined, no treatment was given. Approximately 3 days later, hair loss ceased and hair regrowth was observed 15 days later. Thirty days later (62 days after
Calcinosis cutis can be categorized both on the distribution and the cause of the lesions. Dystrophic calcinosis cutis occurs as a result of alterations within the skin that promote calcification without concurrent changes in serum calcium or phosphorus concentrations.5 Generalized dystrophic calcinosis cutis is most commonly observed in veterinary medicine in dogs with hyperadrenocorticism.3 Approximately 40% of cushingoid dogs develop calcinosis cutis, and it is thought that excess cortisol alters the structure of proteins within collagen and elastin fibres, predisposing them to calcification.3 Generalized calcinosis cutis has been reported in farmed chinchillas in association with adrenocortical hyperplasia.9 The animals were suggested to have excessive endogenous glucocorticoid production as a result of chronic stress. 9 Calcinosis cutis does not develop secondary to hyperadrenocorticism in other animal species or humans.3,5 Generalized dystrophic calcinosis cutis occasionally develops in dogs as a result of diabetes mellitus.3 In humans, generalized dystrophic calcinosis cutis is observed most commonly as a result of dermatomyositis, systemic lupus erythematosus, systemic sclerosis and calcinosis Raynaud esophageal sclerodactyly telangiectasia syndrome.5 Localized dystrophic calcinosis cutis in animals and humans most commonly develops secondary to degeneration of a neoplasm (especially pilomatricoma or lipoma) or follicular cyst.3,5 It also rarely occurs as a result of trauma or an inflammatory process.3,5 Metastatic calcification is defined as the calcification of normal tissues caused by raised serum calcium and/ or phosphorus concentration.5 Alterations in extracellular calcium or phosphorus concentrations disrupt intracellular calcium regulation, resulting in tissue mineralization.5 The product of serum calcium and phosphorus concentrations is referred to as the calcium– phosphorus index. In dogs, a high calcium–phosphorus index most commonly causes calcification of the kidneys, gastric mucosa, lungs, systemic arteries and pulmonary veins.10 These tissues are thought to be predisposed to calcification as they secrete acid and thus have an internal alkaline compartment.11 As the skin does not have an alkaline environment, it is usually spared and metastatic calcinosis cutis is rare in dogs and cats.3 Lesions of metastatic calcinosis cutis in animals are usually confined to the foot pads;3,12–14 however, the formation of discrete nodular calcifying masses close to the scapula of a dog15 and on the chin of a cat14 has also been reported. Reduction of the calcium–phosphorus index can result in lesion resolution.12,14 Metastatic calcinosis cutis is a rare complication
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of hypercalcaemia and hyperphosphataemia in people.16 Calciphylaxis is a specific subset of metastatic calcinosis cutis that has been reported in people.5 This occurs in approximately 1% of human patients with end-stage renal disease and is characterized by calcification of superficial dermal blood vessels and subsequent dermal infarction and necrosis.5,17 Although the pathogenesis is poorly understood, most cases develop because of a combination of increased calcium–phosphorus index and a ‘challenging agent’ that can be as diverse as subcutaneous injections, coagulopathies, human immunodeficiency virus infection, Crohn’s disease or corticosteroid therapy.17 Idiopathic calcinosis cutis occurs without identifiable tissue alterations or abnormal serum calcium or phosphorus concentrations.3,5 Localized idiopathic calcinosis cutis (also called calcinosis circumscripta and tumoral calcinosis) occurs frequently in dogs and horses18 and rarely in cats3 and Mongolian gerbils.19 Generalized idiopathic calcinosis cutis has been observed in puppies after systemic illness.1 It has also been reported to develop, and then spontaneously resolve by 1 year of age, in healthy puppies.3 Two dogs were reported to develop generalized idiopathic calcinosis cutis in association with systemic blastomycosis.4 A third dog with blastomycosis was reported to develop localized lesions.4 Generalized idiopathic mineralization of the basement membrane zone of the hair follicle occurs as a senile change in miniature poodles.20 Iatrogenic calcinosis cutis has been reported as a consequence of subcutaneous injection of calciumcontaining solutions in a dog21 and a cat.7 Additionally, calcinosis cutis was observed after a dog contacted a calcium chloride-containing landscaping product.6 In humans, iatrogenic calcinosis cutis has been reported after extravasation of intravenous calcium solutions and after the use of calcium-containing solutions during electromyography or electroencephalography.22 The initial disease in this dog was considered to be leptospirosis as a result of the high antibody titre, suggestive clinical signs and the lack of vaccination. However, identification of bacteria using dark-field microscopy examination of urine, urine culture or tissue biopsies is necessary to confirm this diagnosis.8 Because of intermittent shedding of small numbers of bacteria, both urine examination and culture have poor sensitivity.8 In addition, the initiation of antimicrobial therapy prior to the serology findings would have further reduced the sensitivity of subsequent urine culture in this case. Leptospira interrogans serovar copenhageni is a common cause of canine leptospirosis in New Zealand. This serovar is closely related to Leptospira interrogans serovar icterohemorrhagica, and the two serovars are serologically and clinically indistinguishable (J. CollinsEmerson, pers. comm.). Infected dogs, as in the presently described case, become bacteraemic and typically show evidence of both kidney and liver disease.23 Although the precise pathogenesis of the generalized calcinosis cutis in this dog is uncertain, three mechanisms are considered most likely. First, hyperphosphataemia
as a result of reduced kidney function may have resulted in metastatic calcinosis cutis. Uraemia (indicative of reduced kidney function) was present in this dog until day 12, and the calcium–phosphorus index was, respectively, 10 and 6.4 on day 0 and day 3 after disease presentation. Metastatic calcification has been reported to develop at calcium–phosphorus indices above 5.7.4 However, previously reported lesions of metastatic calcification in dogs were restricted either to the foot pads3 or periarticular soft tissues15 rather than the generalized lesions observed in this present case. The second possible cause of the calcinosis cutis in this dog is dystrophic calcification as a result of alterations in the dermis. As leptospirosis causes bacteraemia and has been cultured from a skin lesion,24 it is possible that bacteria deposited in the skin caused direct dermal damage. However, this appears unlikely as other canine dermatitides rarely result in calcification. Additionally, bacterial damage to the dermal collagen is unlikely to have been restricted to the dorsum of this dog. Alternatively, it is possible that increased release of adrenal glucocorticoids caused by the stress of the disease could have altered the dermal collagen. The follicular atrophy visible histologically within samples taken from this dog was consistent with hyperadrenocorticism. The dorsal distribution of the calcinosis cutis visible in this dog was also similar to the dorsal lesion distribution seen in cushingoid dogs.3 Chronic stress has been reported to cause calcinosis cutis and follicular atrophy in chinchillas.9 However, most dogs that experience severe stress caused by systemic illness do not subsequently develop calcinosis cutis. Therefore, the third possible pathogenesis for the development of the calcinosis cutis in this dog is a combination of altered collagen (as a result of increased endogenous glucocorticoids or direct bacterial dermal damage) in the presence of an increased calcium– phosphorus index. Hypercalcaemia promotes dystrophic calcification in people.11 Although hypercalcaemia did not develop in this dog, it appears likely that increases in serum phosphorus could likewise promote dystrophic calcification. Interestingly, a similar mechanism may have resulted in the generalized calcinosis cutis that developed in two dogs in association with systemic blastomycosis.4 In both dogs, a transiently increased calcium-phosphorus index (presumably the result of granulomatous inflammation) and prolonged severe systemic disease were reported.4 Hyperphosphataemia is a common incidental finding in young dogs.25 The increased serum phosphorus concentrations may explain why young dogs appear to develop generalized calcinosis cutis after systemic illness more commonly than adult animals. Idiopathic calcinosis cutis in healthy dogs has been reported to resolve at 1 year of age. This may coincide with the decline in serum phosphorus concentrations that occurs at this age.25 To the authors’ knowledge, this is the third adult dog that has been reported to develop generalized calcinosis cutis in association with systemic disease. Leptospirosis was suspected as the cause of the systemic disease;
© 2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 401– 406
Canine calcinosis cutis due to Leptospirosis however, this was not definitively diagnosed. Regardless, the observations in this case suggest that the stress of severe systemic disease combined with impaired renal function can result in generalized calcinosis cutis. When the results of this case are considered along with the previously reported dogs that developed generalized calcinosis cutis after blastomycosis, it appears that the calcinosis cutis spontaneously regresses once the systemic illness is resolved.
REFEREN C E S 1. Gross TL, Ihrke PJ, Walder EJ. Veterinary Dermatopathology: a Macroscopic and Microscopic Evaluation of Canine and Feline Skin Disease. St. Louis, Missouri: Mosby Year Book, 1992: 223– 8. 2. Ogretmen Z, Akay A, Bicakci C et al. Calcinosis cutis universalis. Journal of the European Academy of Dermatology and Venereology 2002; 16: 621– 4. 3. Scott DW, Miller WH, Griffin CE. Muller and Kirk’s Small Animal Dermatology, 6th edn. Philadelphia: W.B. Saunders, 2001. 4. Gortel K, McKiernan BC, Johnson JK et al. Calcinosis cutis associated with systemic blastomycosis in three dogs. Journal of the American Animal Hospital Association 1999; 35: 368–74. 5. Walsh JS, Fairley JA. Calcifying disorders of the skin. Journal of the American Academy of Dermatology 1995; 33: 693–706. 6. Schick MP, Schick RO, Richardson JA. Calcinosis cutis secondary to percutaneous penetration of calcium chloride in dogs. Journal of the American Veterinary Medical Association 1987; 191: 207–11. 7. Ruopp JL. Primary hypoparathyroidism in a cat complicated by suspect iatrogenic calcinosis cutis. Journal of the American Animal Hospital Association 2001; 37: 370–3. 8. Nelson RW, Couto CG. Small Animal Internal Medicine, 2nd edn. St. Louis: Mosby, Inc., 1998: 1273–9. 9. Tisljar M, Janic D, Grabarevic Z et al. Stress-induced Cushing’s syndrome in fur-chewing chinchillas. Acta Veterinaria Hungarica 2002; 50: 133– 42. 10. Kruger JM, Osborne CA. Canine and feline hypercalcemic nephropathy. Part 1. Causes and consequences. Compendium on Continuing Education for the Practicing Veterinarian 1994; 16: 1299–316. 11. Kumar V, Abul KA, Fausto N. Cellular adaptations, cell injury, and cell death. In: Kumar V, Abul KA, Fausto N eds. Robins and Cotran Pathologic Basis of Disease, 7th edn. Philadelphia: Elsevier Saunders, 2005: 3– 46.
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12. Komori S, Washizu M. Metastatic calcinosis circumscripta treated with an oral charcoal absorbent in a dog. Journal of Veterinary Medical Science 2001; 63: 913–6. 13. Jackson HA, Barber PJ. Resolution of metastatic calcification in the paws of a cat with successful dietary management of renal hyperparathyroidism. Journal of Small Animal Practice 1998; 39: 495–7. 14. Declercq J, Bhatti S. Calcinosis involving multiple paws in a cat with chronic renal failure and in a cat with hyperthyroidism. Veterinary Dermatology 2005; 16: 74–8. 15. Spotswood TC. Tumoral calcinosis in a dog with chronic renal failure. Journal of the South African Veterinary Association 2003; 74: 29–32. 16. Tan HH, Cheong WK. Cutaneous gangrene secondary to metastatic calcification in end stage renal failure – a case report. Singapore Medical Journal 1996; 37: 438–40. 17. Hassaballa H, Luther MS, Bloom MK et al. Systemic calciphylaxis in a patient with end-stage renal disease and a normal parathyroid hormone level taking erythropoietin intramuscularly. Endocrine Practice 1999; 5: 46– 50. 18. Roudebush P, Maslin WR, Cooper RC. Canine tumoral calcinosis. Compendium on Continuing Education for the Practicing Veterinarian 1988; 10: 1162–5. 19. Vincent AL, Ash LR. Further observations on spontaneous neoplasms in the Mongolian gerbil, Meriones unguiculatus. Laboratory Animal Science 1978; 28: 297–300. 20. Seaman WJ, Chang SH. Dermal perifollicular mineralization of toy poodle bitches. Veterinary Pathology 1984; 21: 122–3. 21. Schaer M, Ginn PE, Fox LE et al. Severe calcinosis cutis associated with treatment of hypoparathyroidism in a dog. Journal of the American Animal Hospital Association 2001; 37: 364–9. 22. Kagen MH, Bansal MG, Grossman M. Calcinosis cutis following the administration of intravenous calcium therapy. Cutis 2000; 65: 193–4. 23. Prescott JF, McEwen B, Taylor J et al. Resurgence of leptospirosis in dogs in Ontario: recent findings. Canadian Veterinary Journal 2002; 43: 955–61. 24. Anderson JF, Miller DA, Post JE et al. Isolation of Leptospira interrogans serovar grippotyphosa from the skin of a dog. Journal of the American Veterinary Medical Association 1993; 203: 1550–1. 25. Nelson RW, Turnwald GH, Willard MD. Endocrine, metabolic, and lipid disorders. In: Willard MD, Tvedten H, Turnwald GH eds. Small Animal Clinical Diagnosis by Laboratory Methods, 3rd Edn. Philadelphia: W.B. Saunders Company, 1999: 136–71.
Résumé Un Berger allemand âgé de 6.5 ans a développé soudainement une maladie hépatique et rénale. La sérologie a montré des taux élevés d’anticorps dirigés contre Leptospira copenhageni et un diagnostic de leptospirose a été fait. Le chien a été traité avec succès avec des antibiotiques et une réanimation pendant 21 jours. 62 jours après la première consultation, une alopécie du dos et de la zone périanale est apparue. Les lésions se sont étendues en 20 jours. L’histologie a montré une calcinose généralisée avec atrophie folliculaire. Une injection de 0.01 mg/kg de dexaméthasone a freiné les concentrations de cortisol. Aucun traitement n’a été administré et les lésions ont disparu en 30 jours. Il s’agit du troisième cas de calcinose cutanée chez un chien adulte après une maladie systémique sévère. Les deux cas précédents étaient associés à une blastomycose. Il s’agit du premier cas décrit de calcinose cutanée en association avec une infection bactérienne. © 2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 401–406
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J S Munday, D J Bergen and W D Roe Resumen Un perro pastor alemán de 6.5 años de edad desarrolló una enfermedad renal y hepática de forma aguda. Mediante serología se observaron altas concentraciones de anticuerpos frente a Leptospira copenhageni, y dándose un diagnóstico presuntivo de leptopirosis. El perro fue tratado con éxito con antibióticos y cuidados de mantenimiento durante 12 días. Sesenta y dos días tras la presentación inicial observamos alopecia afectando principalmente el dorso y periné. Las lesiones de la piel crecieron en tamaño a lo largo de veinte días. El análisis histopatológico reveló calcinosis cutis generalizada con atrofia follicular. Una inyección de 0.01 mg/kg de dexametasona neutralizó la concentración de cortisol en suero. Sin otro tratamiento adicional las lesiones curaron durante los siguientes 30 días. Este es el tercer caso de calcinosis cutis generalizada observado en un perro adulto tras una severa enfermedad sistémica. Los casos previos desarrollaron calcinosis cutis asociada con blastomicosis. Según nuestras informaciones, este es el primer caso de calcinosis cutis generalizada en un perro adulto asociada con una presunta infección bacteriana. Zusammenfassung Ein 6.5 Jahre alter Deutscher Schäferhund entwickelte eine akute Nieren- und Lebererkrankung. Serologisch wurde ein hoher Titer an Leptospira copenhageni Antikörpern nachgewiesen und die Verdachtdiagnose einer Leptospirose gestellt. Über einen Zeitraum von 12 Tagen wurde der Hund mit Antibiotika und unterstützender Therapie erfolgreich behandelt. Zweiundsechzig Tage nach der Erstpräsentation entstand eine Alopezie, die in erster Linie den Rücken und die Perinealgegend betraf. Über einen Zeitraum von 20 Tagen wurden diese Hautläsionen größer. Histologisch wurde eine generalisierte Calcinosis cutis mit follikulärer Atrophie festgestellt. Eine Injektion von 0.01mg/kg Dexamethason unterdrückte die Kortisolkonzentration im Serum. Der Hund wurde nicht behandelt und die Veränderungen verschwanden innerhalb der nächsten 30 Tage. Es handelt sich hierbei um den 3. Fall von generalisierter Calcinosis cutis, die bei einem adulten Hund nach einer schweren systemischen Erkrankung entstand. Die beiden vorhergehenden Fälle entwickelten Calcinosis cutis im Zusammenhang mit einer Blastomykose. Soweit dem Autor bekannt, ist dies der erste Fallbericht einer generalisierten Calcinosis cutis, die bei einem erwachsenen Hund im Zusammenhang mit einer mutmaßlichen bakteriellen Infektion auftrat.
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