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Mycobacterial nodular granulomas affecting the subcutis and skin of dogs (canine leproid granuloma syndrome).

OBJECTIVE: To obtain a better understanding of a disease affecting dogs in which nodular mycobacterial granulomas are present in the subcutis or skin. DESIGN: Retrospective survey PROCEDURE: A diagnosis of an unidentified mycobacterial infection was made in 45 dogs following detection of acid-fast bacilli surrounded by granulomatous or pyogranulomatous inflammation in tissue sections. Eight cases were identified from the records of our diagnostic laboratory. In all cases culture for mycobacteria was unsuccessful. Another 37 cases were identified by practitioners and veterinary pathologists in response to a survey mailed to veterinary clinics throughout Australia. Data from these 45 cases were entered into a data base. The data set was incomplete, as some respondents did not answer all questions. RESULTS: Over 90% of affected dogs had short coats and about half were Boxers or Boxer-cross dogs. A weak seasonal trend for the development of primary lesions in autumn and winter was identified. Cases were recorded from New South Wales (35 dogs), Western Australia (4), Queensland (4), Tasmania (1) and New Zealand (1). The subcutis and skin of the ears and head (including the ears) were involved in 64% and 85% of cases, respectively, for which lesion site was recorded. Culture was attempted but was unsuccessful in 19 cases, including 11 cases where material was submitted to our laboratory and/or a Mycobacteria Reference Laboratory. Lymph node enlargement, internal organ involvement or constitutional signs were not a feature of the syndrome, and most lesions did not worry the dogs. Although many practitioners recorded a favourable response to therapy with doxycycline (response rate 57%) or amoxycillin-clavulanate (63%), spontaneous resolution of infection was thought to have occurred in six of seven dogs (86%) not given systemic antimicrobials, and three dogs where antimicrobials had failed previously. A minority of cases failed to respond to antimicrobial therapy and continued to have chronic lesions. There was no discernible trend for dogs of a particular age or sex to be affected. CONCLUSION: This syndrome is caused by saprophytic mycobacteria of limited pathogenicity that give rise to lesions restricted principally but not exclusively to the subcutis and skin of body extremities. Fastidious growth requirements have prevented their isolation on synthetic media used for culture of mycobacteria. Organisms presumably enter the subcutis following a breach in integrity of the epidermal barrier and produce self-limiting disease in immunocompetent dogs. Lesions tend to resolve spontaneously. The possibility of a public health threat from affected dogs is highly unlikely.

Animals↗

Deficiency of interleukin-2 production upon addition of soluble egg antigen to cultures of isolated hepatic granulomas or hepatic granuloma cells from mice infected with Schistosoma japonicum.

Schistosoma japonicum-infected C57BL/6 mice show similar dynamics of hepatic granulomatous inflammation and delayed hypersensitivity elicited by soluble egg antigens (SEA) which reach peak levels at 9 weeks of infection and then spontaneously regress. In an attempt to link the level of interleukin 2 (IL-2) production to the spontaneous regression of hepatic granulomatous inflammation, the study determined the dynamics of IL-2 production by SEA-challenged isolated hepatic granulomas (HG) and cells isolated enzymatically from the HG. The production of IL-2 by SEA-stimulated HG or HG cells reached its peak when these preparations from 9-week-infected mice were stimulated and fell thereafter. Some possible mechanisms that might explain the IL-2 deficiency were examined. This deficiency is not due to the in vitro binding of IL-2 by the HG cells of infected mice and is, therefore, due rather to underproduction of IL-2. The deficiency was also not explained by reduced numbers of antigen-presenting cells (macrophages or B cells) or of L3T4+ T lymphocytes. In vitro SEA-induced IL-2 production by HG cells from acutely infected mice was suppressed consistently by Lyt-2+ T cells from the spleens and in the majority of our experiments by Lyt-2+ T cells from the HG of mice infected for 10 weeks. These findings are consistent with the main features of our working hypothesis, but it remains to be proven that in vivo deficiency of lymphokine(s) such as IL-2 is responsible for the spontaneous decrease in granulomatous inflammation and that this lymphokine deficiency is a result of suppression.

Animals↗

[Do the eosinophilic granulomas observed in Brittany represent a form of anisakiasis? The larvae of Thynnascaris aduncum do not produce these granulomas experimentally].

To explain the enigmatical origin of gastric eosinophilic granulomas prevailing among patients in Brittany (France), we have tried to experiment with the larvae of Thynnascaris (Thynnascaris aduncum (Rud.)), a Nematode found in the sardine (Sardina pilchardus (Walbaum)), a fish sometimes eaten raw in our country. In a preliminary experiment, larvae of Thynnascaris were observed to penetrate the mucosa of the rabbit stomach in vitro at room temperature. But in vivo, whatever the means, the ways and the experimented mammals of our study, we have failed to experimentally reproduce such tumours. We think that this result belongs to the fact that the larvae of Thynnascaris in the conditions of our experimentation could not perform an evolution in homeothermal animals.

Animals↗

Review of diseases presenting as "midline granuloma". Clinical implications for the appropriate workup of patients with midline granuloma syndrome with emphasis on recent diagnostic advances in lymphoid neoplasms that present as midline destructive lesions.

Midline destructive disorders (so-called 'midline granuloma') comprise a wide variety of diseases that present as destructive lesions in the upper airways. These diverse diseases include infectious, immune and neoplastic disorders, each of which obviously requires a differing therapy. The clinician must have an appreciation of these diseases in order to make a rational approach to diagnosis. Because of recent advances in immunohistochemical techniques, cell typing will necessitate certain changes in the manner in which biopsy material is initially handled. This paper discusses the differential diagnosis of midline destructive disease, the pathologic techniques necessary to diagnose them and recent ideas concerning the pathogenesis of the malignant lymphoid processes which cause some of these diseases.

Biopsy↗

[Granuloma disseminatum partim anulare partim papulosum. Clinical variant of granuloma anulare disseminatum--therapeutic trial with etretinate].

We report on a clinically and morphologically interesting case of generalized granuloma anulare showing disseminated lichenoid papules as well as anulare formations. Histopathology confirmed the clinical diagnosis. Under oral application of etretinate, the lesions decreased significantly within 3 weeks; complete remission was noticed after 5 months.

Drug Administration Schedule↗

[The role of radiotherapy in the treatment of granuloma gangraenescens (lethal midline granuloma].

The granuloma gangraenescens in the oral, maxillary and facial region is a rare disease. It is a destroying process in the region of palate, nose, paranasal sinuses, cheeks and orbit with characteristic signs of granulomatosis, infection and malignancy. The disease shows often a lethal development with cachexia or sepsis. Besides local inflammations and tumors, the granulomatosis of Wegener, and the so-called necrotizing sialometaplasia are above all to be excluded by differential diagnosis. Five cases are presented in order to describe the diagnostic and therapeutic problems. In literature, the greatest efficacy is attributed to radiotherapy, however, a detailed definition of the most efficient irradiation conditions cannot be given yet because of the small number of cases. Good long-term results or recoveries can be achieved in 75 to 80% of cases by a relatively high radiation dose of 40 to 50 Gy administered within four to five weeks. During the observation time of two to six years, no one of the five patients treated here only by megavoltage therapy showed a recurrence.

Adult↗