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The present study was aimed at investigating the innate susceptibility of C57BL/6-Cftrunc/Cftrunc knockout [B6-Cftr (-/-)] mice to pulmonary infection with Pseudomonas aeruginosa. Our results indicate that 58.4% of B6-Cftr (-/-) mice died within 6 d following lung infection with 10(5) P. aeruginosa entrapped in agar beads, whereas only 12.1% of B6-Cftr (+/+) mice died over the same period of time. Moreover, the number of bacteria recovered from the lungs of B6-Cftr (-/-) mice 3 and 6 d after infection was significantly higher than that observed in their littermate controls. No correlation was found between the weight or age of the animals and the number of viable bacteria recovered from the lungs of mice. Histopathological examination of lung sections from P. aeruginosa-infected mice revealed that the infection results in a severe bronchopneumonia. Both B6-Cftr (-/-) knockout mice and their littermate controls developed similar lung pathology during the course of infection. Overall, results reported in the present study suggest that a defect at the Cftr locus leads to an exacerbation of P. aeruginosa lung infection resulting in a dramatically increased mortality rate and higher bacterial load.

A case of acquired idiopathic agammaglobulinaemia in a 23-yr-old woman is presented. The picture included frequent and recurrent lung, sinus and mastoid infections, and diarrhoea. The pathogenesis, radiological picture, and differential diagnosis of this immunological disorder are described.

Glomerular changes of 70 cases of pulmonary diseases and 25 control cases among 1100 consecutive autopsy cases were studied by light, immunofluorescence, and electron microscopy. These pulmonary diseases consisted of 11 cases of chronic obstructive bronchiolitis (COB), 15 cases of bronchopneumonia, 4 cases of acute interstitial pneumonia, 22 cases of idiopathic interstitial pneumonia (IIP), and 18 cases of lung cancer free from IIP. Bacteriological examination of the lung was performed in these cases including control cases on autopsy. Mesangial IgA deposition was predominant in 25 out of the 70 study cases (36%) frequently accompanied by C3, whereas slight mesangial IgA deposition was observed in one of the control cases. Incidence of IgA deposition was 64% in IIP, 54.5% in COB, 13.3% in bronchopneumonia, 16.7% in lung cancer and 25% in acute interstitial pneumonia. The results of the present study suggest that recurrence or persistence of inflammatory processes of the lung leads to IgA-mediated immune abnormalities and to mild mesangial changes with predominant IgA deposition, which are similar to the immunopathologic features of IgA nephropathy.

Autopsy records of 600 profoundly retarded and 405 less retarded were examined for a thirty-one-year period at Pacific State Hospital. The profoundly retarded were found to have more respiratory infections at autopsy, and more deaths of such infections. Profound retardation was a particularly outstanding risk when in combination with epilepsy, inability to ambulate, and developmental cranial anomalies. Non-infectious respiratory morbidity and mortality are more common in the less retarded, apparently because of their living longer to develop these complications.

Chronic bronchopneumonia associated with microlithiasis was diagnosed in a 9-year-old domestic shorthair cat with a 3-month history of coughing and dyspnea. Thoracic radiography revealed multifocal patchy alveolar infiltrates in all lung fields. Numerous acellular, concentrically laminated, periodic acid-Schiff-positive microliths were seen in mucus from tracheal washing. Microliths were composed primarily of calcium carbonate. A definite cause could not be identified. There was no response to treatment and the cat was euthanatized. Marked type-II alveolar cell proliferation, peribronchiolar smooth muscle proliferation, and alveolar microlithiasis were seen histologically. Microliths are rarely encountered in tracheal washings from companion animals. Their pathophysiologic properties and meaning remain to be established.