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Purpose of review The causes of exudative pleural effusions are diverse and frequently remain unclear despite exhaustive examinations. Recently recognized IgG4-related disease (IgG4-RD) is a fibroinflammatory disorder that can affect nearly any organ including the lungs. This review will focus on the involvement of IgG4 in exudative pleural effusion of unknown cause. Recent findings IgG4 is found to be involved in a proportion of patients with undiagnosed pleural effusions. Pleural involvement in IgG4-RD can be seen in isolation or association with other organ disease. Pleural thickening and/or effusion are common clinical features of IgG4-related pleural lesions, and this condition is histologically characterized by a lymphoplasmacytic infiltrate enriched in IgG4-positive plasma cells in the pleura. Although the pathogenesis of IgG4-RD is poorly understood, there is a growing body of evidence that indicates an antigen-driven process requiring T-cell and B-cell interaction in which autoantibodies, plasmablasts, follicular helper T cells and CD4+ cytotoxic T lymphocytes participate. Summary The possibility of IgG4-related pleural lesion should be considered in patients with pleural effusion of unexplained cause when lymphoplasmacytic infiltration is seen in a pleural biopsy specimen. This condition is responsive to systemic steroid therapy.

Background Up to 20% of pleural effusions in CCF patients could be exudative. Differentiating a transudate from exudate is crucial, in order to rule out malignancy. Diuretics increase fluid protein and can misclassify effusions as exudative. Aim We aimed to study causes and outcomes of exudates secondary to CCF. Methods Retrospective analysis of consecutive patients with suspected CCF (n=204), presenting to pleural clinic at our institution from 24/10/17 – 24/12/18. Electronic patient records from pleural clinics and in-patient episodes were reviewed, up to 12 months after initial presentation. Results 68/204 patients with suspected CCF had pleural effusion aspirated; 41 (20%) were frank exudates(pleural fluid protein > 35 g/dl). 6 aspirates (9%) were marked as traumatic. 50 patients (74%) had unilateral right sided effusion. Histopathology analysis revealed only 24% to be lymphocyte rich. 51 patients (75%) had evidence of cardiac dysfunction on echocardiogram within the last 6 months. 46 patients (68%) were on a minimum dose of 40 mg frusemide at the time of pleural aspiration – no correlation was observed between diuretics dose and fluid protein (CORRELL -0.08). 24/41 exudates (59%) had alternate pathology accounting for high fluid protein including 5 malignant, 8 parapneumonic, 2 recent MI, 4 recent cardiac surgery and 5 with combination of above. 5/17 remaining patients needed a pleural biopsy on clinical grounds which showed fibrinous pleuritis in all five cases. Rest of the patients were observed for a period of 12 months and none turned malignant. Conclusion Most exudative pleural effusions in CCF can be explained by alternative diagnoses, diuretic therapy or traumatic tap. Pleural biopsy in such cases should only be resorted to if suspicion of malignancy is high as most effusions resolve with medical therapy on subsequent follow up.

portuguesDescreve-se os aspectos epidemiologicos, clinicos, patologicos e bacteriologicos da pleuropneumonia por Mannheimia haemolytica em caprinos, apos transporte prolongado. Quarenta caprinos transportados da regiao Nordeste para a regiao Sul do Brasil morreram durante a viagem ou 2-3 dias apos o desembarque. Clinicamente, observou-se dispneia, secrecao nasal mucopurulenta e tosse. Na necropsia foram coletados multiplos fragmentos de orgaos para analises histopatologicas e identificacao do agente envolvido. Todos os pulmoes apresentaram consolidacao pulmonar predominantemente em regiao cranioventral, associada a deposicao acentuada de fibrina, espessamento e aderencia pleurais em 90% dos casos. Histologicamente, havia pleuropneumonia fibrinossupurativa caracterizada por infiltrado neutrofilico difuso associado a fibrina. Colonias nao hemoliticas [85% (34/40)] e hemoliticas [15% (6/40)] foram obtidas pelo isolamento bacteriologico. Mannheimia spp. foi isolada em 26 amostras, os quais posteriormente foram confirmados como Mannheimia haemolytica (99% de identidade), pela amplificacao e sequenciamento parcial do gene 16S rDNA. O estresse pode favorecer o desenvolvimento de pleuropneumonia bacteriana em caprinos, e cepas nao hemoliticas de M. haemolytica podem causar doenca em animais com imunodepressao acentuada. Palavras-chave: doencas de caprinos; doencas respiratorias; patologia; PCR EnglishThis study described the epidemiological, clinical, pathological and bacteriological aspects of Mannheimia haemolytica pleuropneumonia in goats associated with shipping stress. Forty goats transported from the Northeast to the Southern region of Brazil died during shipment, or 2-3 days after unloading. Clinical signs included dyspnea, mucopurulent nasal discharge, and coughing. All goats were necropsied, and multiple tissues were collected for histopathological analysis and involved agent identifications. All lungs showed pulmonary consolidation, predominantly affecting the cranioventral lobes, in addition to the marked fibrinous pleuritis, pleural thickening, and pleural adhesions, that affected 90% of the goats. Histologically, there was fibrino-suppurative pleuropneumonia characterized by a diffuse neutrophilic infiltrate admixed with fibrin. Non-hemolytic [85% (34/40)] and hemolytic [15% (6/40)] species were obtained in bacteriological culture. Fir Mannheimia spp. was reported in 26 isolates and subsequently confirmed as M. haemolytica (99% identity), after amplification and partial sequencing of the 16S rDNA gene. Stress may trigger the development of bacterial pleuropneumonia in goats, and non-hemolytic strains of M. haemolytica may cause this condition in goats with severe immunosuppression. Key words: goat diseases; respiratory diseases; pathology; PCR

A pleuropneumonia suína, causada por Actinobacillus pleuropneumoniae, é uma doença caracterizada pela apresentação fibrino-hemorrágica com pleurite adesiva. A enfermidade está presente em todos os países produtores de suínos, sendo responsável por prejuízos econômicos elevados. No Brasil e no mundo, diversos grupos vêm conduzindo estudos na busca por um melhor entendimento da doença e de sua epidemiologia. Avanços importantes foram obtidos, entre os quais a caracterização dos fatores de virulência, implicados na apresentação clínica da enfermidade; e a aplicação de novos métodos de diagnóstico. A difusão das técnicas de biologia molecular como ferramenta diagnóstica em Medicina Veterinária tem contribuindo para a identificação de Actinobacillus pleuropneumoniae. Nesta revisão, são abordados os aspectos mais recentes sobre a patogênese e o diagnóstico deste importante patógeno.

Patient initials or identifier number N/A ### Relevant clinical history and physical exam Degos Disease, also known as malignant atrophic papulosis, is a very rare, genetic disease with an unclear etiology. It is a distinctive vasculopathy syndrome characterized by a thrombotic diathesis

A five-membered radiographic constellation is characteristic of S.L.E.: (1) minimal bilateral fibrinous pleuritis; (2) ill-defined patches or linear bands or plaques in the lung bases; (3) fluctuation in the size and configuration of the heart; (4) slight enlargement of the spleen; (5) conspicuous lack of irreversible structural damage to the joints. The first four can be seen frequently on serial chest roentgenograms. Table IV is a statistical summary of these findings. IV . Organ or tissue involved Usual manifestation Per cent of patients found positive Pleura Pleuritis 74 Lung Pneumonitis 50 Heart Carditis 53 Spleen Slight enlargement 34 Joint Minimal osteoporosis 26

Sixty-one of 68 sets of bovine lungs from which only Haemophilus somnus was isolated had microscopic lesions of purulent bronchiolitis and bronchopneumonia. In 37 of 61 lungs, the bronchiolar exudates were markedly necrotic with accompanying necrosis of the adjacent bronchiolar epithelium. Bronchiolitis obliterans was prominent in 23 of 28 lungs affected with chronic lesions with abscesses present in seven. Alveolar filling with inflammatory cells (neutrophils with fewer macrophages) was limited to peribronchiolar alveoli in 25 of 61 lungs and was multifocal to diffuse in the other 36. Lesions in the remaining lungs (7 of 68) were classified as fibrinous pneumonia with bronchiolitis (2), fibrinous pleuritis (2), suppurative interstitial pneumonia with vasculitis (2), and diffuse congestion (1).

Heavily infected lungs are focally to diffusely consolidated but never involve an entire lobe. The alveoli are filled with grayish material, between which the pinkish alveolar walls can be seen with a hand lens (Fig. 264). If tissue necrosis or abscesses are present, another organism should also be looked for. In contrast to consolidated lungs, the lungs are not hyperemic and are less voluminous. No fibrinous pleuritis occurs unless bacterial or fungal pneumonia is present.

FIBRINOUS pericarditis is a well known feature of the uremic state. However, fibrinous pleuritis with pleural pain and friction rub in uremia has received little recognition. During the past 18 months, 20 clearly audible episodes of pleural rub were observed in 11 azotemic subjects. These patients, who had no evidence of pneumonia, pulmonary embolization or systemic disease as causes of the pleuritis, ranged in age from 23 to 76 years, and 10 were male (presumably reflecting the sex distribution in a Veterans Administration hospital). Seven patients had chronic proliferative glomerulonephritis, one membranous glomerulonephritis, one arteriolonephrosclerosis, one vasculitis with acute renal . . .