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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.
Neonatal mercury poisoning, especially that due to merbromin ingestion, is uncommon. We describe the case of a 10 day old newborn infant who was given mercurochrome orally for 7 days due to misunderstanding of medical instructions. Initial symptoms included loss of appetite and low weight increase. Elevated blood mercury concentrations were found. Chelating therapy with dimercaprol was initiated and the patient's evolution was good. We discuss the potential toxicity of mercury and emphasise the importance of the transmission of information by physicians, especially to the immigrant population.
Two new extemporaneous negative-staining methods are proposed to detect Cryptosporidium oocysts in stools, using light-green and merbromine in 1% and 2% aqueous solution, respectively. A Ziehl-Neelsen stain as modified by Henriksen and Polhenz was used as a reference technique. A comparison between these two new stains and the reference, a modified Ziehl-Neelsen mod. method gave almost identical sensitivity and specificity. We propose their use in routine diagnosis for enteric cryptosporidiosis.
The mercurial compounds are known to be a common cause of allergic contact dermatitis. Immediate hypersensitivity is rarely induced by mercurial organic derivatives. However, none of the published cases showed both immediate and delayed hypersensitivity as was the case of one of our two patients. A boy and a woman experienced urticaria and anaphylaxis, respectively after topical application of Merchromine (Merbromine). We were able to demonstrate immediate hypersensitivity in both patients to mercuric fluorescein compounds by skin test and histamine liberation. In addition, the child but not the woman, showed delayed hypersensitivity to mercurial compounds.
Interaction of methylmercury (MM), an environmental and industrial toxicant, with selenium is well known but incompletely understood. Therefore, the effects of MM (10 micromol/kg i.v.) on the disposition of exogenous selenium were compared with those of other organic mercurials (merbromine, mercuribenzene sulfonic acid, and mercuribenzoic acid) in anesthetized bile duct-cannulated rats injected with sodium [(75)Se]selenite (10 micromol/kg i.v.). The mercurial organic acids (10 micromol/kg i.v.) differed strikingly from MM in their influence on selenium disposition. They promoted renal and hepatic accumulation as well as biliary excretion of selenium but decreased distribution to the muscle, testis, and brain as well as the pulmonary excretion of selenium. In contrast, MM altered selenium distribution in an opposite fashion: it diminished the biliary output of selenium and enhanced selenium exhalation. GC-MS analysis verified that this latter paradoxical effect resulted from increased exhalation of dimethyl selenide. Further studies indicated that the MM-induced increase in pulmonary excretion of dimethyl selenide cannot be due to a diminished conversion of this volatile selenium compound to trimethylselenonium ion (TMSe(+)), because MM influenced neither the urinary excretion nor the hepatic and renal concentration of TMSe(+) in selenite-injected rats. Compared to the selenite-exposed rats, the selenite plus MM-injected animals exhibited a significant rise in the hepatic level of S-adenosylmethionine (SAME), the endogenous methyl donor in selenium methylation, and the ratio of SAME to S-adenosylhomocysteine. Based on these and others' observations, it is hypothesized that MM may increase hepatic availability of SAME in selenite-dosed rats by counteracting selenite-induced inactivation of SAME synthetase, thereby facilitating SAME synthesis, and/or by acting as a methyl donor in formation of dimethyl selenide, thereby sparing SAME. In summary, the toxicologically and ecologically relevant interaction of MM and selenite is not mimicked by organic acid mercurials, possibly because it results in formation of lipophilic Hg- and Se-containing common compound(s) and because it also appears to involve methyl transfer from MM to selenium.
The Ti/TiO2/Au junction forms the basis of a promising new type of photovoltaic cell, provided that a light-harvesting antenna layer can be deposited on the thin gold film. We report that the electrical diode characteristics of the TiO2/Au Schottky barrier deteriorate by deposition of a hydrophobic quantum dot film, Merbromin dye adsorption, or electron-hole photogeneration in TiO2 under inert conditions. In the presence of oxygen and water vapor, the Schottky barrier characteristics and high photovoltage are recovered. The strong influence of the TiO2 surface chemistry on the (photo)electrical characteristics of the solar cell is discussed on the basis of an existing microscopic model.
The frequency of resistance to Hg2+ in 1980 to 1981 collections from Barnes Hospital, St. Louis, Mo., was only 2% for Staphylococcus aureus and 9% for Escherichia coli. The frequency of Hg2+ resistance in E. coli isolates from Jikei University Hospital, Tokyo, Japan, was 57% during 1972 to 1977 and decreased to 29% in 1979 to 1982; for S. aureus the frequency of Hg2+ resistance dropped from 36% in 1972 to 1977 to 10% in 1979 to 1982. Frequencies of resistances to cadmium (S. aureus) and arsenic (S. aureus and E. coli) remained approximately constant during this time. The decrease in frequency of mercurial resistance is attributed to the termination of the use of organomercurials (largely phenylmercury and thimerosal) in hospital liquid detergents and disinfectants. It is proposed that selection for mercurial resistance occurred within the hospital setting when there was widespread use of mercurials. The resistance patterns and phage types for each of four new mercurial-resistant S. aureus isolates from St. Louis were distinct, indicating that no single type of "hospital staph" predominates. Furthermore, resistance to thimerosal, merbromin, and methylmercury and the ability to volatilize 14C from [14C]methylmercury were found with the new isolates and never with previously known mercurial resistance plasmids in S. aureus.
Staphylococcus aureus was found to have a higher resistance to merbromin and mercuric chloride in the presence of Escherichia coli. The protective effect of the gram-negative organism on S. aureus was due to the production of extracellular glutathione and hydrogen sulfide and to an unequal distribution of the inhibitor between the two species. S. aureus did not significantly influence the resistance of E. coli to mercurials.
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.
Biophysical and genetic properties of six independently isolated plasmids encoding the degradation of the herbicides 2,4-dichlorophenoxyacetic acid and 4-chloro-2-methylphenoxyacetic acid are described. Four of the plasmids, pJP3, pJP4, pJP5, and pJP7, had molecular masses of 51 megadaltons, belonged to the IncP1 incompatibility group, and transferred freely to strains of Escherichia coli, Rhodopseudomonas sphaeroides, Rhizobium sp., Agrobacterium tumefaciens, Pseudomonas putida, Pseudomonas fluorescens, and Acinetobacter calcoaceticus. In addition, these four plasmids conferred resistance to merbromin, phenylmercury acetate, and mercuric ions, had almost identical restriction endonuclease cleavage patterns, and encoded degradation of m-chlorobenzoate. The two other plasmids, pJP2 and pJP9, did not belong to the IncP1 incompatibility group, had molecular masses of 37 megadaltons, encoded the degradation of phenoxyacetic acid, and possessed identical restriction endonuclease cleavage patterns.
Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes, and the effects of such exposure depend upon both the type of mercury to which exposed and the magnitude of the exposure. In general, the effects of exposure to organic mercury are primarily neurologic, while a host of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal. While the primary source of exposure to organic mercury for most populations is the consumption of methylmercury-contaminated fish and shellfish, there are a number of other organomercurials to which humans might be exposed. The antibacterial and antifungal properties of organomercurials have resulted in their long use as topical disinfectants (thimerosal and merbromin) and preservatives in medical preparations (thimerosal) and grain products (both methyl and ethyl mercurials). Phenylmercury has been used in the past in paints, and dialkyl mercurials are still used in some industrial processes and in the calibration of certain analytical laboratory equipment. The effects of exposure to different organic mercurials by different routes of exposure are summarized in this article.
A retrospective study about 80 cases of exomphalos treated in the digestive unit of the paediatric surgery department in Abidjan teaching hospital--Côte d'Ivoire had been performed to analyse the result of this malformation treatment during 8 years. Prenatal diagnosis was made in two cases on six antenatal ultrasounds. Prematurity involved 7% of newborn and their birth weight ranged from 2500 to 4000 grams in 70% of cases. Treatment began in 64% at birth, conservative treatment with merbromine tannage was systematic on the non disrupted exomphalos. Surgery was indicated in the disrupted exomphalos and in the complicated cases of conservative treatment. Intestinal occlusion was the main fatal complication observed in both treatments but most of the time it occurred with surgical closure. Total lethality reached 30%, influenced by exomphalos super infection and by neonatal resuscitation insufficient means. Authors think exomphalos lethality reduction implies antenatal ultrasonographic for early diagnosis which could indicate a possible caesarian section in case of the voluminous exomphalos in order to prevent disruption and neonatal resuscitation operation.
First isolation of a mercury-resistant strain of Yersinia enterocolitica is reported. This strain, named 138-A14, is resistant to mercuric chloride and merbromin, but sensitive to phenylmercuric borate and sodium merthiolate. The mercury resistance of 138-A14 is not transferable spontaneously to Escherichia coli K12 by conjugation.
We present the results of a study, spread over a 12-year period, concerning the frequency of skin sensitization to mercury and some of its compounds in a Spanish community. Among 2,592 subjects suspected of allergic contact dermatitis, 3.5 p. 100 had a positive test to metallic mercury 0.5 p. 100 in petroleum jelly. The pertinence of the test was regarded as "present" or "fast" in 63.9 p. 100 of the cases, and the dermatitis was found to be related to antiseptic Mercurochrome (merbromin) solutions, cosmetics containing ammoniated mercury and inhalation of mercury after breaking of thermometers. We consider that in children metallic mercury should be tested at a concentration not exceeding 0.1 p. 100. Among 2,154 subjects suspected of allergic contact dermatitis, 109 (5 p. 100) had a positive test to thiomersal 0.1 p. 100 in petroleum jelly. The pertinence of the test was regarded as "present" or "past" in 53.8 p. 100 of the cases, and the dermatitis was attributed to antiseptic solutions, eye drops, cosmetics and shoes. There was no cross-reaction between thiomersal and mercury, except in those cases where mercury chloride was the allergic determinant responsible for sensitization to thiomersal (39.4 p. 100 of the cases). Fifteen patients consulted for photoallergy to piroxicam, and all had a positive test to thiosalicylic acid which is the compound most frequently responsible for sensitization to thiomersal (51.6 p. 100 of our cases) and for cross-reaction between thiomersal and piroxicam.
Metastatic calcinosis is a common feature of chronic renal failure. Its first manifestations are bone demineralization and non-visceral and/or visceral calcification with mostly mural deposits in arteries and arterioles. It is initially characterized by hyperphosphataemia followed by secondary or tertiary hyperparathyroidism. Cutaneous involvement is a rare complication. Histologically, the lesions show vascular calcification with ischaemic skin necrosis. Extreme cases may produce calcinosis cutis (calciphylaxis), i.e. disseminated calcification of the subcutaneous tissue and dermis in the form of hard painful cutaneous nodules and plaques with subsequent ulceration. Metastatic calcinosis is a disease affecting adults, while the dystrophic or idiopathic type can develop in children. We present the case of a 6-year-old boy with end-stage renal disease, attributed to congenital renal hypoplasia, and accompanied by secondary hyperparathyroidism. He developed fulminant tertiary hyperparathyroidism and metastatic calcinosis of the lungs, as well as cutaneous necrosis of the buttocks and legs, subsequent to calcification of arteries and arterioles. A maternal renal transplant failed to function. The serum parathormone, calcium and phosphate levels could not be controlled by maintenance dialysis, phosphate binders and calcitriol. Total parathyroidectomy without autotransplantation of parathyroid tissue rapidly returned the serum parathormone, calcium and phosphate levels to normal. In addition, topical treatment using merbromine solution and hydrocolloid dressings, healed the ulcers with significant scar formation, within 2.5 months after parathyroidectomy. A renewed increase of the calcium x phosphate product, 2 months after parathyroidectomy, was attributed to mobilization of calcium compounds from the viscera, as confirmed by a chest X-ray.
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.
A total of 110 patients of symptomatic otomycosis was investigated, prospectively. Aural swabs were collected on 1st, 7th and 14th day and examined by direct microscopy and culture for fungi. Of these, 80 patients found to be having pure fungal infection, were taken up for mycological and therapeutic study. Fungi belonging to genus Aspergillus were isolated in 76 (95.0%) patients of which Aspergillus niger was the commonest isolate in 46 (57.5%), followed by A. flavus in 27 (33.7%), A. fumigatus in 3 (3.7%), Candida species in 3 (3.7%) and Mucor in 1 (1.2%). The patients were of all age groups but majority were between 21 and 30 years and the male-female ratio was equal. Of the total of 40 male patients, twenty-one were Sikhs using turban. Before developing the symptoms, forty five patients used oil, mixture of oil and garlic juice, antibiotics, steroids, antiseptics or wax solvent as ear drops. Only two patients were diabetic. No patient had fungal infection elsewhere in the body. The patients were called for regular follow-up for three weeks. In forty cases mercurochrome was applied as the antifungal agent after cleaning the external auditory canal, in twenty-three clotrimazole and in rest of the seventeen patients miconazole was used. On 7th day, only 11 (13.7%) patients grew different fungi in culture. They became symptom-free on 14th day and no fungal material could be seen on otoscopy, direct microscopy or culture. Mercurochrome was found to be most effective in these patients.
Dibrommercuryfluoresceine (DBMF) reacts stoichiometrically and quantitatively with the thiol group of cysteine, glutathione and thioglycolic acid respectively, at pH 7.0. Polarographical and spectrometrical titrations clearly show that in the spectra of the investigated mercaptides the wave length of the first absorption maximum of DMBF (507 nm) remains unchanged but the molar extinction coefficient increases by approximately 20%. Serum albumin, ovalbumin, beta-lactoglobulin and glyceraldehydephosphatedihydrogenase, after incubation with DBMF, form adducts with the dye from which the pure mercaptide complexes were separated by means of column chromatogrphy. These complexes were separated by means of column chromatography. These complexes show a bathochromic shift (520 nm) of the dye band which is decreased now by 50%. The molar extinction coefficient epsilon 520 has been determined from 32,000 to 33,850. On the basis of these values SH-contents of the four proteins were obtained which are in good accordance with data previously published in the literature. No selective reaction, f.i. with more accessible or/and reactive SH-groups was observed. After 30 min incubation with DBMF and washing with isotonic phosphate buffer, native animal tumor cells show in the main absorption band the bathochromically shifted dye maximum. A first temptative estimation of the protein SH-groups yielded 1.7-2.1 X 10(-14) mole SH/single cell. This result lies between the SH-content determined microspectrometrically on cells stained with DDD-Fast Blue B (1.1-1.55 X 10(-14)) and macroscopically on cell homogenates with DTNB (3.1 X 10(-14)). Up to now, no certain information can be given whether or to what extent unspecific absorption effects possibly might be involved in the data obtained with DBMF treated cells, but interaction with nucleic acids can be excluded with certainty on the basis of relevant model experiments.