Evaluation of three commercially available rotavirus detection methods for neonatal specimens.

Commercially available assay kits have now made detection of rotavirus in stool specimens possible as a routine laboratory test. One such kit, Rotazyme II (Abbott Laboratories, North Chicago, IL) has been reported to give a higher incidence of false positive results with neonatal stool than with stool from older patients. One hundred stool specimens from asymptomatic neonates (age range, two to five days) were tested by two ELISA methods and one latex agglutination method in order to evaluate the rate of false positivity in this group of patients. Negative staining electron microscopy was used as the reference method. The two ELISA methods were Rotazyme II and Rotavirus EIA (International Diagnostic Laboratories, St. Louis, MO), and the latex agglutination method was Meritec-Rotavirus (Meridian Diagnostics, Inc., Cincinnati, OH). The Rotavirus EIA and Meritec-Rotavirus tests gave 0% and 1% false positive results, respectively, while the Rotazyme II test gave a 4% false positive rate with an additional 19% equivocal results. This extensive comparative analysis of commercially available assays for detection of rotavirus in neonatal stool specimens suggests a false positive or equivocal rate with the Rotazyme II test that impairs clinical utility.

Pulmonary meningioma. A light- and electron-microscopic study.

A solitary subpleural lung tumor having the light- and electron-microscopic appearance of a typical meningioma is described. Its benign appearance and presence for 3 years without clinical or radiologic evidence of central nervous system tumor favor the lung as the primary site. Histogenesis is discussed and support for a subpleural origin is presented.

Melanotic adenocarcinoma of the anorectum.

Epithelial cells of an otherwise typical anorectal mucinous adenocarcinoma contained melanin pigment. Ultrastructurally, three cell populations were present. The largest population contained membrane-bound compound melanosomes in cells having glandular epithelial characteristics including surface specializations, microvilli, and mucin. Additionally, occasional melanocytes were intermixed with the tumor cells and finally very rare cells having both mucin and isolated melanosomes were present. We believe that this phenomenon is better explained by phagocytosis or transfer of melanin from melanocytes to neoplastic cells, rather than by melanin synthesis in adenocarcinoma.

Passive immune complex glomerulonephritis in mice: models for various lesions found in human disease. I. High avidity complexes and mesangiopathic glomerulonephritis.

Intravenous injection of mice with soluble complexes of highly avid rabbit antibody to egg albumin, prepared by dissolution of equivalence precipitates in large quantities of antigen, resulted in a purely mesangial localization of the complexes. When animals received three injections of complexes per day for 1 day it was noted that precipitates dissolved in 80 times the equivalence amount of antigen produced slight mesangial changes. When such complexes were injected for 2 or 3 days, outright mesangiopathic glomerulonephritis was observed in an increasing proportion of the animals. Equivalent amounts of antigen alone did not produce lesions.

Passive immune complex glomerulonephritis in mice: models for various lesions found in human disease. II. Low avidity complexes and diffuse proliferative glomerulonephritis with subepithelial deposits.

Intravenous injections of mice three times a day for 3 days with soluble complexes of 3 mg. of moderately avid rabbit antibody to chicken egg albumin prepared by dissolution of equivalence precipitates in 80 times the equivalence amount of antigen resulted in a combined mesangial and loop localization of immune complexes. With complexes formed from antibody of low avidity, injected four times a day for 3 days, a predominately subepithelial loop deposition of complexes was observed. Complexes formed from moderately avid antibody gave rise to a mainly mesangiopathic glomerulonephritis, whereas low avidity complexes were associated with a diffuse glomerulonephritis. These results, in combination with those of the previous paper, successfully reproduce the basic form of the lesions seen in active immune complex disease by passive means and suggest that antibody avidity is a major determinant of the site of localization of immune complexes and therefore of the morphologic form of the resulting glomerulonephritis. The importance of these observations for our understanding of the pathogenesis of human immune complex disease is considered.

Immune complex disease. VII. Experimental mesangiopathic glomerulonephritis produced by chronic immunization with thyroglobulin.

Immunohistologic and electron microscipic studies were performed on the kidneys of rabbits given daily intravenous injections of porcine thyroglobulin in amounts adjusted to the immune response of the individual rabbits. Glomerular lesions were restricted to the mesangium, were characterized by varying degrees of proliferation of mesangial cells and increase of mesangial matrix, and were accompanied by accumulations of rabbit immunoglobulins, C3, and porcine thyroglobulin. Electron-dense deposits were localized to the mesangium and the adjacent subendothelial space. Less than 10 per cent of the animals with mesangila lesions developed obvious impairment of glomerular function. Thyroglobulin-containing immune complexes were found to be rapidly removed from the mesangium, so that overloading of the mesangium and consequent accumulation of complexes in the adjacent capillary loops could not occur. Thus, the results provide further evidence that when immune complex deposition is restricted to the mesangium, relatively little interference with glomerular function results. This situation is paralleled in man by the lesions of subclinical lupus nephritis, chance proteinuria and hematuria, and the early lesions of Berger's disease.