Lipoid (lipid) pneumonia

Lipoid pneumonia is an unusual form of lung disease resulting from the accumulation of lipids in the alveoli, where they provoke a foreign body reaction with associated inflammation and sometimes local fibrosis. The lipids may be endogenous or exogenous in origin, and the clinical mechanisms and circumstances differ accordingly. Exogenous lipoid pneumonia occurs when animal, vegetable, or mineral oils are aspirated or inhaled into the lungs, provoking a foreign body reaction with chronic inflammation. Typical symptoms are cough and breathlessness. The chest radiograph and CT may show interstitial thickening, with areas of consolidation that may coalesce into a mass (paraffinoma) which simulates carcinoma. Bronchoalveolar lavage and biopsy show lipid-laden macrophages. In endogenous lipoid pneumonia the lipids are derived from surfactant and cholesterol released from decaying cells distal to bronchial obstruction.

Dystrophic mineralisation in chronic exogenous lipid pneumonia in cats

Case series summary Exogenous lipid pneumonia with mineralisation of the lung parenchyma was diagnosed in three cats with radiographs, CT and/or bronchoalveolar lavage cytological findings. All three cats had a common clinical history of chronic constipation and long-term forced oral administration of mineral oil. All three cases showed radiographic findings compatible with aspiration pneumonia, with an alveolar pattern in the ventral part of the middle and/or cranial lung lobes. Minor improvement of the radiographic lung pattern in the follow-up studies was seen in two cats, and a miliary ‘sponge-like’ mineralised pattern appeared in the previously affected lung lobes months to years after the diagnosis. In one cat, patchy fat-attenuating areas in the consolidated lung lobes were present on thoracic CT. Cases 1 and 2 showed respiratory signs at the initial presentation, while in case 3 the radiographic findings were incidental and the cat had never exhibited respiratory signs. Relevance and novel information This is the first report to describe dystrophic mineralisation of the lung in exogenous lipid pneumonia and also the first to describe the CT features in cats. Exogenous lipid pneumonia should be included in the differential diagnosis in cases of miliary ‘sponge-like’ mineral opacities in the dependent part of the lung lobes on thoracic radiographs or CT in cats, especially in cases of chronic constipation, previously exposed to mineral oil.

Lipid-Related Lesions in Quaker Parrots (Myiopsitta monachus)

The Quaker parrot has been used as a psittacine model to study clinical lipidology and lipid-related disorders. However, while Quaker parrots appear to be anecdotally susceptible to a variety of spontaneous dyslipidemic disorders and lesions caused by excess lipid accumulation, epidemiologic data are lacking. A multicenter retrospective study on 652 pathology submissions (411 necropsies and 243 biopsies) from Quaker parrots was performed by recording the final pathological diagnoses, age, and sex for each bird. The prevalence of lesions associated with lipid metabolism, such as hepatic lipidosis, atherosclerosis, xanthomas, adipose tumors, coelomic steatitis/steatonecrosis, endogenous lipid pneumonia, and acute pancreatic necrosis/pancreatitis, was reported. Multiple logistic regression models were used to characterize the effects of sex and age on these lesions, and the prevalence of hepatic lipidosis and atherosclerosis was compared to those in a random sample of control psittacine birds. The raw prevalence of atherosclerosis and hepatic lipidosis was 5.6% (95% confidence interval [CI], 3.4%–7.8%) and 21.2% (95% CI, 17.2%–25.1%), respectively. While the prevalence of atherosclerosis was similar to other psittacine species, hepatic lipidosis was more common in Quaker parrots. Quaker parrots also showed a unique susceptibility to acute pancreatic necrosis with a prevalence of 12.9% (95% CI, 9.7%–16.1%). Male parrots were found to be more susceptible than females to lipid accumulation lesions ( P = .0024), including atherosclerosis ( P = .018) and hepatic lipidosis ( P < .001). This retrospective study confirms the high susceptibility of Quaker parrots to lipid-related disorders and presents epidemiological data that may be useful to avian clinicians, pathologists, and researchers using Quaker parrots.

Morbillivirus-associated lipid pneumonia in Arctic foxes

We describe lipid pneumonia in 5 of 24 Arctic foxes ( Vulpes lagopus) in association with morbillivirus infection, and lymphoid depletion in 3 of these 5 foxes. Canine distemper virus (CDV) immunohistochemistry yielded positive staining in lung, lymph nodes, spleen, adipose tissue, and renal pelvic urothelial cells in 5 cases. Liver and bone marrow samples collected from these cases tested positive for morbillivirus by reverse-transcription PCR assay. Strains belonged to the CDV Arctic lineage based on sequencing of the hemagglutinin gene followed by phylogenetic analysis. Phylogenetic analysis of the phosphoprotein gene showed that the identified CDV strains were not closely related to any previously documented strains responsible for outbreaks in different animals in other parts of the world.

Immunopathology of Postprimary Tuberculosis: Increased T-Regulatory Cells and DEC-205-Positive Foamy Macrophages in Cavitary Lesions

Postprimary tuberculosis occurs in immunocompetent people infected withMycobacterium tuberculosis. It is restricted to the lung and accounts for 80% of cases and nearly 100% of transmission. Little is known about the immunopathology of postprimary tuberculosis due to limited availability of specimens. Tissues from 30 autopsy cases of pulmonary tuberculosis were located. Sections of characteristic lesions of caseating granulomas, lipid pneumonia, and cavitary stages of postprimary disease were selected for immunohistochemical studies of macrophages, lymphocytes, endothelial cells, and mycobacterial antigens. A higher percentage of cells in lipid pneumonia (36.1%) and cavitary lesions (27.8%) were positive for the dendritic cell marker DEC-205, compared to granulomas (9.0%,P<.05). Cavities contained significantly more T-regulatory cells (14.8%) than found in lipid pneumonia (5.2%) or granulomas (4.8%). Distribution of the immune cell types may contribute to the inability of the immune system to eradicate tuberculosis.