Pulmonary histopathology in dalmatians with familial acute respiratory distress syndrome (ARDS).

The histopathological changes in the lungs of 12 related Dalmatians with idiopathic acute respiratory distress syndrome (ARDS) are described. Affected dogs had multiple foci of marked atypical hyperplasia and squamous metaplasia of the bronchiolar epithelium, patchy ongoing fibrosis with myofibroblastic metaplasia, smooth muscle hyperplasia and occasional honeycombing of alveolar walls, and hyperplasia of atypical type II pneumocytes. There was an abrupt transition between these proliferative lesions and areas of acute alveolar oedema with hyaline membranes in partially normal lung. Diseased areas were associated with moderate lymphohistiocytic interstitial inflammation. Immunohistochemical labelling for cytokeratin expression indicated that the metaplastic epithelium was of bronchiolar origin and that it extended into peribronchiolar alveolar spaces. Some of the bronchiolar lesions were pre-neoplastic and one adult dog suffered from bronchoalveolar carcinoma. These lesions are compared with the two forms of idiopathic interstitial pneumonia reported as causes of ARDS in man: acute interstitial pneumonia (AIP) and acute exacerbation of idiopathic pulmonary fibrosis (IPF). The observed lesions in the Dalmatians are distinct from the diffuse alveolar damage that characterizes AIP, but show some histological similarities to the usual interstitial pneumonia (UIP) that occurs in IPF with acute exacerbation in man. UIP has not previously been described in the dog.

Macroscopical and histopathological changes in regressing primary and recurrent equine sarcoids during active specific bio-immunotherapy.

Healing sarcoids were followed in 18 horses which had taken part in previous clinical studies on a total of 29 horses suffering from either primary or recurrent sarcoids, treated with bio-immunotherapy. In the present study, attention was paid to changes observed in these fibroblastic skin tumours during their regression. The tumours were surgically debulked leaving the base in the skin. The horses were immunized according to bio-immunotherapy at 2- to 4-week intervals with an autogenous vaccine made from the excised part of the tumour until the base had visibly regressed. Healing was followed by inspections and serial biopsies from the base, studied under light microscope. Visibly normal epithelisation developed first at the margin of the base, progressing gradually to the centre. The mean rate of epithelisation was approximately equal to normal horse skin. Most of the histopathological features typical of equine sarcoid diminished significantly in the follow-up biopsies, when the first signs of visibly normal epithelisation were observed. The changes were more evident among the primary than the recurrent tumours. No leucocyte infiltration, lysis or apoptosis were found during the regression. Bio-immunotherapy seems to simulate a spontaneous healing process.

Treatment of acute Chlamydia pneumoniae infection with telithromycin in C57BL/6J mice.

OBJECTIVES: The efficacy of telithromycin, a new ketolide antibiotic, was investigated in the treatment of acute Chlamydia pneumoniae infection in a mouse model. METHODS: C57BL/6J mice were inoculated intranasally, and the effects of three different doses of telithromycin (25, 50 and 100 mg/kg) were assessed after 5 and 10 days of treatment. Lungs for culture, PCR, histopathology, and blood for serum samples were collected immediately after each treatment period and at 3 weeks post-inoculation. C. pneumoniae-specific antibodies were analysed, and the effect of treatment was assessed by culture, detection of C. pneumoniae DNA and determination of histopathological inflammatory changes in mouse lungs. RESULTS: Culture negativity in the lungs was achieved with the higher doses, 50 and 100 mg/kg, after 10 days of treatment. C. pneumoniae DNA was not totally eradicated with the treatments, but the groups treated with 50 and 100 mg/kg doses for 10 days had the lowest DNA positivity rates (10%) 3 weeks after the inoculation. In lung histopathology, the efficacy of telithromycin on inflammatory changes was also dose-dependent: higher doses were more effective in reducing the inflammatory reaction. Overall, the 25 mg/kg dose had a weaker effect compared with the others. CONCLUSIONS: Telithromycin had both time- and dose-dependent effects on the eradication of chlamydia and on reducing infection-induced inflammatory changes in mouse lungs.

Lung injury leading to respiratory distress syndrome in young Dalmatian dogs.

A progressive pulmonary disease resulting in severe respiratory failure and death in an average of 3 weeks was diagnosed in 11 young Dalmatian dogs. The dogs were from 4 litters, all genetically related by a common ancestor. The initial clinical signs were tachypnea and noisy respiration. Respiratory distress developed shortly before death and was characterized by strenuous and rapid respirations, along with cyanosis and vomiting. On blood gas analysis, there were severe arterial hypoxemia, hypercapnia, and marked alveolar-arterial oxygen difference. Radiographically, a diffuse pattern of alveolar, interstitial, and peribronchial densities was observed in the lungs. Most dogs developed pneumomediastinum and gastroesophageal intussusception in the terminal phase of the disease. There was no response to treatment with antibiotics, corticosteroids, diuretics, or oxygen. At necropsy, the lungs were wet, heavy, and relatively airless. Absence of 1 kidney in 2 dogs and severe internal hydrocephalus in 2 dogs were additional necropsy findings. Pulmonary histopathology included metaplasia and atypia of the alveolar and bronchiolar epithelium, a nonpurulent inflammatory reaction characterized mainly by mononuclear cells and macrophages, eosinophilic hyaline membrane formation, and focal pulmonary fibrosis. The histological manifestations were typical of acute lung injury. Clinically, the findings were consistent with adult respiratory distress syndrome (ARDS), except for the relatively long course. No known risk factors for ARDS, such as trauma, toxin exposure, infection, or endotoxemia could be identified. The relationship of the other abnormalities (ie, renal aplasia, hydrocephalus) to the pulmonary disease also remains obscure. An inherited defect is suspected, because segregation analysis of the 4 litters suggests autosomal recessive inheritance.