Delayed presentation of amniotic fluid embolism: lessons from a case diagnosed at autopsy

Amniotic fluid embolism (AFE) syndrome, a catastrophic cause of respiratory failure typically occurs during labour, or soon after delivery. Systemic hypotension is the most prominent haemodynamic alteration documented in patients with AFE, a consequence principally of severe left-sided heart failure. A 22-year-old female was admitted to the respiratory intensive care unit with severe eclampsia and acute respiratory failure 4 h following delivery. Her blood pressure was elevated (systolic 150-180 mm Hg, diastolic 90-110 mm Hg) throughout the admission. She succumbed in spite of therapy for eclampsia and mechanical ventilation. Autopsy revealed large numbers of polygonal, anucleate foetal squames and mucin in the pulmonary vasculature typical of AFE while changes of eclampsia were found in the liver and kidneys. It appears that AFE syndrome can have a delayed presentation, as late as 4 h after delivery and haemodynamic collapse may not be mandatory if the patient has coexisting systemic hypertension secondary to severe eclampsia.     

Subcellular Distribution of Monoclonal Antibody Defined Epitopes on Immunodominant Mycobacterium tuberculosis Proteins in the 30-kDa Region: Identification and Localization of 29/33-kDa Doublet Proteins on Mycobacterial Cell Wall

Two different groups of monoclonal antibodies (MAbs) directed to different epitopes on 30-kDa region proteins of Mycobacterium tuberculosis were isolated; MAbs 5F9, 5D5 and 5D2 reacted with a single 33-kDa protein band, whereas MAb 3A8 reacted with a distinct 29/33-kDa doublet when analysed by immunoblotting. The present paper describes the distribution of MAbs defined epitopes in the 29-33-kDa region proteins in well-characterized subcellular fractions: cytosol, plasma membrane, cell wall as well as culture filtrate of M. tuberculosis. MAbs 5F9, 5D5 and 5D2 reactive epitopes were found in cytosol, whereas 3A8 epitope is distributed in all cellular compartments of the mycobacterium as well as in the culture filtrate. Localization of these epitopes by indirect immunofluorescence and immunogold-labelling demonstrated that only 3A8 epitope is present on the cell surface of the mycobacterium. Both immunoblotting and ELISA showed that only MAb 3A8, and not 5F9, 5D5 and 5D2, reacted with secreted BCG 85 antigen complex of Mycobacterium bovis BCG. Furthermore, using an MAb 3A8-coupled affinity column, we purified antigen 3A8 from the cytosol fraction of M. tuberculosis. All these MAbs reacted with antigen 3A8 with varying degrees of intensity, thus suggesting that they are directed to a single protein. Absence of 5F9, 5D5 and 5D2 epitopes in the cell wall, culture filtrate and to a single protein. Absence of 5F9, 5D5 and 5D2 epitopes in the cell wall, culture filtrate and BCG-85 complex suggests that these epitopes might have been lost during the processing of the same 33-kDa protein on its way out from cytosol to the cell wall or when the protein is secreted out into the culture filtrate. Our results demonstrate, for the first time, direct evidence of the presence of a 30-kDa region protein not only in secreted antigens but also in the cell wall and on the cell surface of the mycobacterium.