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A patient is described who appeared to be suffering from mercury intoxication caused by local application of merbromin to an operation wound and who developed aplastic anemia, which we ascribed to merbromin.
Mercury and organomercurial resistance determined by genes on ten Pseudomonas aeruginosa plasmids and one Pseudomonas putida plasmid have been studied with regard to the range of substrates and the range of inducers. The plasmidless strains were sensitive to growth inhibition by Hg(2+) and did not volatilize Hg(0) from Hg(2+). A strain with plasmid RP1 (which does not confer resistance to Hg(2+)) similarly did not volatilize mercury. All 10 plasmids determine mercury resistance by way of an inducible enzyme system. Hg(2+) was reduced to Hg(0), which is insoluble in water and rapidly volatilizes from the growth medium. Plasmids pMG1, pMG2, R26, R933, R93-1, and pVS1 in P. aeruginosa and MER in P. putida conferred resistance to and the ability to volatilize mercury from Hg(2+), but strains with these plasmids were sensitive to and could not volatilize mercury from the organomercurials methylmercury, ethylmercury, phenylmercury, and thimerosal. These plasmids, in addition, conferred resistance to the organomercurials merbromin, p-hydroxymercuribenzoate, and fluorescein mercuric acetate. The other plasmids, FP2, R38, R3108, and pVS2, determined resistance to and decomposition of a range of organomercurials, including methylmercury, ethylmercury, phenylmercury, and thimerosal. These plasmids also conferred resistance to the organomercurials merbromin, p-hydroxymercuribenzoate, and fluorescein mercuric acetate by a mechanism not involving degradation. In all cases, organomercurial decomposition and mercury volatilization were induced by exposure to Hg(2+) or organomercurials. The plasmids differed in the relative efficacy of inducers. Hg(2+) resistance with strains that are organomercurial sensitive appeared to be induced preferentially by Hg(2+) and only poorly by organomercurials to which the cells are sensitive. However, the organomercurials p-hydroxymercuribenzoate, merbromin, and fluorescein mercuric acetate were strong gratuitous inducers but not substrates for the Hg(2+) volatilization system. With strains resistant to phenylmercury and thimerosal, these organomercurials were both inducers and substrates.
The region of plasmid NR1 concerned with resistance to Hg2+ and organomercurials consists of sequences found on restriction endonuclease fragments EcoRI-H and EcoRI-I. When both fragments were cloned together into a derivative of plasmid ColE1, the hybrid plasmid conferred properties indistinguishable from those of the parental plasmid, NR1: resistance to Hg2+ and to the organomercurials merbromin and fluoresceinmercuric acetate and the inducible synthesis of the enzyme mercuric reductase. When fragment EcoRI-I was cloned into plasmid ColE1, cells containing the plasmid was as sensitive to Hg2+ and organomercurials as plasmidless strains. When fragment EcoRI-H was cloned into ColE1, cells with the hybrid plasmid were hypersensitive to Hg2+ and organomercurials. This hypersensitivity was inducible by prior exposure to low, subtoxic Hg2+ or merbromin levels. It was associated with an inducible hyperbinding activity attributed to a gene governing Hg2+ uptake and found on fragment EcoRI-H (which contains the proximal portion of a mercuric resistance [mer] operon).
We report on two outbreaks of Mycobacterium chelonei subsp. abscessus cutaneous infections, which occurred between June 1974 and April 1975 in a series of 24 patients (15 studied bacteriologically) subjected to venous stripping for varicose veins. The source of infection was the aqueous solution of merbromin used in presurgical care.
A neonate with an infected omphalocele was treated locally with merbromin (mercurochrome) for five days. Extensive skin peeling with bullous lesions, edema, and fever developed three days after mercurochrome therapy. The infant died on the ninth day. Autopsy revealed evidence of heavy metal poisoning of the kidney, excessive mercury levels in the blood, and in tissues of the brain, kidney, and liver.
Penicillinase plasmids of Staphylococcus aureus often contain genes conferring resistance to inorganic mercury (Hg(2+)) and the organomercurial phenylmercury acetate. The mechanism of resistance was found to be the enzymatic hydrolysis of the organomercurial phenylmercury to benzene plus inorganic ionic mercury, which was then enzymatically reduced to metallic mercury (Hg(0)). The Hg(0) was rapidly volatilized from the medium into the atmosphere. After the mercurial was degraded and the mercury was volatilized, the resistant cells were able to grow. These plasmids also conferred the ability to volatilize mercury from thimerosal, although the plasmid-bearing strains were equally as thimerosal sensitive as the S. aureus without plasmids. None of the plasmids conferred the ability to volatilize mercury from several other organomercurials, however: methylmercury, ethylmercury, p-hydroxymercuribenzoate, merbromin, and fluorescein mercuric acetate. (Organomercurial resistance-conferring plasmids of Escherichia coli and Pseudomonas aeruginosa that we have been studying confer the ability to degrade two or three of these organomercurials.) Although mercury was not volatilized from p-hydroxymercuribenzoate or fluorescein mercuric acetate, the plasmid-bearing strains were resistant to these organomercurials. The ability to volatilize mercury from Hg(2+) and phenylmercury was inducible. The range of inducers included Hg(2+), phenylmercury, and several organomercurials that were not substrates for the degradation system. Mercury-sensitive mutants have been isolated from the parental plasmids pI258 and pII147. Thirty-one such mercury-sensitive strains fall into three classes: (i) mercury-sensitive strains totally devoid of the phenylmercury hydrolase and Hg(2+) reductase activities; (ii) mutants with normal hydrolase levels and no detectable reductase; and (iii) mutants with essentially normal hydrolase levels and low and variable (5 to 25%) levels of reductase activities. The mercury-sensitive strains were also sensitive to phenylmercury, including those with the potential for hydrolase activity.
Ninety-six cases of exomphalos or gastroschisis managed at The children's Hospital, Sheffield, during the period 1964-74 are analysed. There were 306 cases with minor lesions, 30 with major lesions, 27 with a ruptured exomphalos and only 3 with gastroschisis. The overall mortality rate was 46-9 percent. Survival could be closely correlated with the birth weight, the nature of the primary lesion, the presence or absence of liver within the sac and the presence and severity of associated congenital anomalies. A "scoring system" based on these criteria is proposed to predict the prognosis of an infant with an exomphalos.
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Measurement of the important performance parameters shows that Kodak Kodirex film is more suitable than conventional ones for dark-field transmission electron microscopy of molecules at very high mignification. Results are cited for 120 kV; but the relation ship is valid up to 3 MV.
Mercurochrome strongly inhibits aspartate transaminase and 2,3-dicarboxyethylated aspartate transaminase. The native enzyme exhibits a biphasic time-course of inactivation by mercurochrome with second-order rate constants 1.62 x 10(4) M-1 - min-1 and 2.15 x 10(3) M-1 - min-1, whereas the modified enzyme is inactivated more slowly (second-order rate constant 6.1 x 10(2) M-1 - min-1) under the same conditions. The inhibitor inactivates native and modified enzyme in the absence as well as in the presence of substrates. Mercurochrome-transaminase interaction is accompanied by a red shift in the absorption maximum of the fluorochrome of about 10 nm. Difference spectra of the mercurochrome-enzyme system versus mercurochrome, compared with analogous spectra of mercurochrome-ethanol, revealed that the spectral shifts recorded during mercurochrome-transaminase interaction are similar to those that occur when mercurochrome is dissolved in non-polar solvents. Studies of mercurochrome complexes with native or modified transaminase, isolated by chromatography on Sephadex G-25, revealed that native transaminase is able to conjugate with four mercurochrome molecules per molecule, but the modified enzyme is able to conjugate with only two mercurochrome molecules per molecule.
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The rate of survival for infants with intact giant exomphatos has much improved during the last 20 years; this is partly due to better respiratory and nutritional support. The use of a staged operative closure using a sialon prosthesis has been advocated for 12 years, but our data do not show this to be superior to nonoperative management.
Local tissue effects caused by a selected group of topically applied ENT-drugs are analysed. By means of a testing system consisting of vital mircoscopy, infrared thermography and microangiography applied to hamsters and rabbits, an evaluation of the varying degree of tissue injury is made. According to the degree of tissue damage the tested substance could be graded in three groups (I-III). The drugs belonging to group I show fairly little microcirculatory disturbance, while those belonging to group III cause tissue necrosis. Our conclusion is that topically applied drugs should be used with caution, especially on previously injured tissues.
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Many well known histochemical techniques have been employed to study the neurosecretory products in invertebrates and vertebrates. Among these aldehyde-fuchsin (AF) has been one of the two specific stains to demonstrate the presence of neurosecretory cells. Various counterstains have been employed with AF. However, AF is also useful in demonstrating the presence of mucosubstances or elastin. A method is described here for a simultaneous demonstration of neurosecretory substances (NSS) and mucosubstances (MS) by mercurochrome counterstaining. For this method sections of material fixed in methanol-formaldehyde-acetic acid (MFA) or alcoholic Bouin's or Susa were oxidized in 0.3% permanganate with 0.3 ml concentrated H2SO4 for 1 to 2 minutes, decolorized in 1% oxalic acid, stained in 0.5% aqueous basic fuchsin containing 1 ml concentrated HCl and 1 ml paraldehyde for 10 min and counterstained with 0.5% aqueous mercurochrome. After mercurochrome counterstaining the characteristic AF staining (purple colour) of NSS is dramatically swamped (becoming brick red) but the purple developed by MS remains unaltered in vertebrate and invertebrate material. Eosin or other counterstains do not behave in this way.
Premature ventricular contractions are relatively often encountered in patients after surgical treatment of ischaemic heart disease. Mercurascan (MSC), given at 0.05 mg/kg of body weight, favourably affected both the incidence and duration of arrhythmia. Unlike other antiarrhythmics, MSC did not affect the heart rate nor blood pressure. Postoperative treatment of ventricular arrhythmia with MSC is a promising procedure and merits further clinical and experimental investigation.