Idiopathic Lipoid Pneumonia: An incidental finding in autopsy specimen

Lipoid pneumonia is a rare form of pneumonia which was initially described to be caused by inhalation or aspiration of fatty substances. Certain autopsy studies have reported the incidence to be 1.0-2.5%. Based on the mode of lipid acquisition, it has been classified into endogenous, exogenous or idiopathic types. Almost 50% of the patients with lipoid pneumonia are asymptomatic, and may be discovered by chance during routine chest imaging. In symptomatic patients, the symptoms are non- specific. However, it can produce inflammatory pneumonitis that can progress to irreversible pulmonary fibrosis as seen in our case. We present a case of a 53-year-old deceased male. A piece of one of his lungs was received after autopsy, which appeared normal grossly. There was no history of any illness before death. Microscopy revealed interstitial fibrosis with collection of foamy macrophages in alveolar spaces and cholesterol crystals surrounded by inflammatory reaction including occasional giant cells. The clinical picture and radiologic changes in cases of lipoid pneumonia can mimic bacterial pneumonia and tuberculosis. The occupational history is of extreme importance and should always be investigated

Autopsy: a value to primordial and primary prevention for lung diseases

Background: Lung disorders spectrums include congestion, oedema, various inflammatory lesions, chronic obstructive pulmonary diseases and neoplastic lesions. The clinical and radiological findings in respiratory diseases are nonspecific and therefore a histopathological study is essential. Autopsies are necessary to establish cause of death of the person with help of antemortem history and investigations to rule out lung lesions. Aims and objectives were to identify the histopathological spectrum of lung disease and frequency of various lung pathologies in respect to age and sex.Methods: The retrospective study of 285 lung autopsy specimens received were fixed and processed. Routine paraffin sectioning was done followed by hematoxylene and eosin (H and E) staining. Relevant clinical and postmortem findings, gross and microscopic examination findings were recorded.Results: Most common lung pathology found was Edema and congestion in 149 cases (52.2%), pneumonia in 87 cases (30.5%) followed by tuberculosis in 33 cases (11.5%). Out of total 285 cases, 222 (77.9%) were males and 63 cases (22.2%) were females. The male to female ratio was 3.5:1. Maximum numbers of cases, in age group of 31-45 years were 108 cases (37.89%) followed by in age group 46-60 years were 90 cases (31.57%) followed by age group of 16-30 years 15.8%.Conclusions: Advances in diagnostic technology have not reduced the value of autopsy for the study and evaluation of the disease process. It has become crucial for adopting correct prophylactic actions for primordial and primary prevention of pulmonary dysfunctions

Knockout of angiotensin converting enzyme-2 receptor leads to morphological aberrations in rodent olfactory centers and dysfunctions associated with sense of smell

Neuronal morphological characterization and behavioral phenotyping in mouse models help dissecting neural mechanisms of brain disorders. Olfactory dysfunctions and other cognitive problems were widely reported in asymptomatic carriers and symptomatic patients infected with Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). This led us to generate the knockout mouse model for Angiotensin Converting Enzyme-2 (ACE2) receptor, one of the molecular factors mediating SARS-CoV-2 entry to the central nervous system, using CRISPR-Cas9 based genome editing tools. ACE2 receptors and Transmembrane Serine Protease-2 (TMPRSS2) are widely expressed in the supporting (sustentacular) cells of human and rodent olfactory epithelium, however, not in the olfactory sensory neurons (OSNs). Hence, acute inflammation induced changes due to viral infection in the olfactory epithelium may explain transient changes in olfactory detectabilities. As ACE2 receptors are expressed in different olfactory centers and higher brain areas, we studied the morphological changes in the olfactory epithelium (OE) and olfactory bulb (OB) of ACE2 KO mice in comparison with wild type animals. Our results showed reduced thickness of OSN layer in the OE, and a decrease in cross-sectional area of glomeruli in the OB. Aberrations in the olfactory circuits were revealed by lowered immunoreactivity toward microtubule associated protein 2 (MAP2) in the glomerular layer of ACE2 KO mice. Further, to understand if these morphological alterations lead to compromised sensory and cognitive abilities, we performed an array of behavioral assays probing their olfactory subsystems’ performances. ACE2 KO mice exhibited slower learning of odor discriminations at the threshold levels and novel odor identification impairments. Further, ACE2 KO mice failed to memorize the pheromonal locations while trained on a multimodal task implying the aberrations of neural circuits involved in higher cognitive functions. Our results thus provide the morphological basis for the sensory and cognitive disabilities caused by the deletion of ACE2 receptors and offer a potential experimental approach to study the neural circuit mechanisms of cognitive impairments observed in long COVID