Erratum to "Measles outbreaks - potential threat for health care professionals" Infect Prev Pract, Volume 2, Issue 3, September 2020, 100074.

[This corrects the article DOI: 10.1016/j.infpip.2020.100074.].

What is the Preferred Screening Tool for COVID-19 in Asymptomatic Patients Undergoing a Surgical or Diagnostic Procedure?

INTRODUCTION: Since the outbreak of COVID-19, measures were taken to protect healthcare staff from infection, to prevent infection of patients admitted to the hospital and to distribute PPE according to need. To assure the proper protection without overuse of limited supply of these equipments, screening of patients before surgical or diagnostic procedure was implemented. This study evaluates the results of this screening. METHOD: All patients screened for COVID-19 before procedure warranting either general, locoregional anaesthesia or sedation were included. Screening included a symptom questionnaire by phone, PCR and HRCT chest testing. Surgical or procedural details were registered together with actions taken based on screening results. RESULTS: Three hundred ninety-eight screenings were performed on 386 patients. The symptom questionnaire was completed in 72% of screenings. In 371 screenings, PCR testing was performed and negative. HRCT chest found 18 cases where COVID-19 could not be excluded, with negative PCR testing. Three patients had their surgery postponed due to inconclusive screening, and additional measures were taken in three other patients. There were incidental findings in 14% of HRCT chest scans. DISCUSSION: Pre-operative screening will differentiate if PPE is needed for procedures and which patients can safely have elective surgery during this COVID-19 pandemic and in the times to come. HRCT chest has no additional value in the pre-operative screening of asymptomatic patients. Screening can be performed with a symptom questionnaire, and additional screening with PCR testing in high-risk patient groups should be considered.

Measles outbreaks - potential threat for health care professionals.

The ongoing spread of measles is a major concern for public health. Optimal vaccination coverage amongst health care professionals (HCP) is essential for individual protection. This is illustrated by our two cases of measles infection in HCP during the 2018 outbreak in Europe. We developed a questionnaire to assess protection against measles amongst HCP working in acute care of a tertiary hospital in The Netherlands. In total, 29% of these professionals were not protected against measles. During current worldwide measles outbreaks, it is paramount for employee health protection, patient protection and disease control to register and optimize employees' immunity.

New insights in diagnosing Schistosoma myelopathy.

At present non-invasive tests for diagnosing Schistosoma myelopathy are sub-optimal. We present a novel serological method, using paired liquor and serum samples, resulting in the diagnosis of Schistosoma myelopathy in a male patient with proximal muscle weakness. The patient recovered after praziquantel treatment.

[Optimalization of antibiotic policy in the Netherlands. VII. SWAB-guidelines for antimicrobial therapy in adults patients with infectious endocarditis]. / Optimaliseren van het antibioticabeleid in Nederland. VII. SWAB-richtlijnen voor antimicrobiële therapie bij volwassen patiënten met infectieuze endocarditis.

The Working Party on Antibiotic Policy (Dutch acronym: SWAB) has developed guidelines for in-hospital antimicrobial therapy of adult patients with infective endocarditis. The choice and the duration of antimicrobial therapy are determined by the infecting micro-organism, the sensitivity of this micro-organism to antimicrobial therapy, the location of the endocarditis (left- or right-sided) and the presence of intracardial prosthetic material. While waiting for the culture results, the antibiotic treatment of an infected native valve is benzylpenicillin (in cases which begin subacutely or have a long history) or flucloxacillin (cases which begin acutely, are fulminant or in i.v. drug users), and gentamicin. If a prosthetic valve is infected then treatment of choice is vancomycin and gentamicin. Further antibiotic treatment depends on the causative micro-organism. Streptococci, enterococci and staphylococci are the most frequently occurring of these.

Optimisation of the antibiotic guidelines in The Netherlands. VII. SWAB guidelines for antimicrobial therapy in adult patients with infectious endocarditis.

The Working Party on Antibiotic Policy (Dutch acronym is SWAB) is a Dutch organisation that develops guidelines for in-hospital antimicrobial therapy of bacterial infectious diseases. This present guideline describes the antimicrobial treatment for adult patients with infective endocarditis. The choice and duration of antimicrobial therapy is determined by the infecting micro-organism, sensitivity of this micro-organism for antimicrobial therapy, location of the endocarditis, left-sided or right-sided, and presence of intracardial prosthetic material. In this guideline, the empirical therapy for endocarditis is discussed as well as the therapy for the most frequent causative organisms: streptococci, enterococci, staphylococci and HACEK micro-organisms.

Papillary necrosis associated with the HIV protease inhibitor indinavir.

The HIV protease inhibitor indinavir may cause nephrolithiasis and interstitial nephritis. The renal consequences of indinavir-associated nephrotoxicity are uncertain. We report a case of papillary necrosis in a patient treated with indinavir. An asymptomatic HIV-infected woman experienced right-sided renal colicky pain during treatment with indinavir. She passed a non-solid stone and continued indinavir treatment. Intravenous pyelogram performed 20 months later following an episode of left-sided colicky pain showed right-sided papillary necrosis. Indinavir-associated nephrolithiasis and chronic interstitial nephritis were the only possible causes identified in this patient. Physicians should be aware that indinavir nephrolithiasis may cause papillary necrosis.

Lymphocyte homing and Ig secretion in the murine mammary gland.

In mice the majority of the immunoglobulins (Ig) in milk belongs to the IgA class. Prior to its transepithelial transportation into the milk, dimeric IgA (dIgA) is bound to the transmembrane form of the secretory component or polymeric Ig receptor (SC/pIgR). The latter is synthesized in the epithelial cells lining the ducts and alveoli of the mammary gland. A candidate for playing the role of adhesion molecule to primed lymphocytes present in the murine mammary gland might be the mucosal addressin cell adhesion molecule-1 (MAdCAM-1). We studied the correlation between the levels of IgA in colostrum and milk, the number of IgA producing plasma cells in the mammary gland and the expression of MAdCAM-1 in mammary gland endothelial cells during pregnancy and lactation. The relation between the IgA levels in the milk and the expression levels of pIgR in mammary gland epithelial cells was also investigated. We found that the expression of MAdCAM-1 and pIgR starts in early-mid pregnancy; the number of IgA-producing plasma cells and the IgA concentration in milk increase from early lactation onwards. The MAdCAM-1 expression declines during lactation whereas the pIgR levels and IgA-producing plasma cell numbers rise until the end of lactation. Because the MAdCAM-1 level starts to rise several days before the rise of the IgA-producing plasma cell level, MAdCAM-1 cannot be the rate determining factor governing extravasation of primed B cells to the mammary gland. We also conclude that the pIgR is present in sufficient amounts to enable increasing S-IgA secretion into the milk during lactation.

Strongyloides stercoralis infection: how to diagnose best?

Four patients are described with a Strongyloides stercoralis infection. Several techniques to diagnose this infection are discussed. The so-called Baermann method is emphasised. Especially in chronic infections the combination of serology and the Baermann method seems the best diagnostic approach. Treatment with albendazole or ivermectin are suggested treatments.

Two rapid complementary methods to detect progressive zidovudine resistance mutations in mononuclear cells of HIV-infected patients.

The objective of the study was to evaluate a rapid screening technique for the presence of mutations in the viral reverse transcriptase gene of HIV following prolonged therapy with zidovudine in patients with AIDS. Peripheral blood mononuclear cells (PBMCs) of 14 HIV-infected patients were analyzed by micro-titer point mutation assay (PMA) before therapy with zidovudine and after at least 10 months of treatment. In addition, five of these were analyzed longitudinally. Three nontreated HIV-seropositive individuals were tested as controls. To confirm the validity of the PMA, patients' material was also analyzed with the single strand conformational polymorphism (SSCP) assay. After 10-55 months of treatment, at codons 41, 70, and 215 a shift from predominantly wild type strains to a mixture of wild type and mutant strains (21%-100% mutant sequences) appeared in the majority of patients' PBMCs. At codons 67 and 219, the wild type strain persisted after therapy in all but 3 patients. Most mutations were detected by SSCP as well as by PMA, except for one mutation at codon 41 and one at codon 70. However, when the two mutations were both present, SSCP and PMA were both able to detect these mutations. In conclusion, both PMA and SSCP are rapid and simple methods for screening for mutations causing drug resistance in zidovudine-treated HIV-infected patients. Although PMA is more labor-extensive than SSCP, the advantage of PMA over SSCP is that it permits the quantitative detection of point mutations coding for zidovudine resistance. The application of these assays may improve procedures of monitoring and modifying antiretroviral therapy on an individual basis.

Safety, tolerance, and pharmacokinetics of atevirdine mesylate (U-87201E) in asymptomatic human immunodeficiency virus-infected patients.

Atevirdine mesylate (U-87201E) is a new nonnucleoside (bisheteroarylpiperazine) inhibitor of human immunodeficiency virus type 1 reverse transcriptase. In a double-blind, escalating single-dose study the safety, tolerance, and pharmacokinetics of atevirdine mesylate were investigated in 24 asymptomatic human immunodeficiency virus-seropositive male patients. Each patient received one single oral dose of atevirdine mesylate and placebo separated by an interval of 1 to 3 weeks. For each dose level (400, 800, 1,200, and 1,600 mg) six patients received drug and placebo on separate occasions. Blood samples were collected before dosing and at intervals afterward for safety evaluation and estimation of atevirdine and metabolite levels. The concentrations of atevirdine and its principal metabolite (U-89255) in serum were determined by high-performance liquid chromatography. The results of the study showed that atevirdine mesylate is well tolerated at all dose levels. No clinically significant effects on vital signs, electrocardiograms, or laboratory tests were observed. Occasional headache and nausea were reported both in the drug group and in the placebo group. The times to peak values were relatively short (0.5 to 1.0 h), suggesting a rapid absorption. The maximum concentrations of drug in serum were 1.4 microM (400 mg), 4.2 microM (800 mg), 7.3 microM (1,200 mg), and 5.8 microM (1,600 mg). The values of the pharmacokinetic parameters for atevirdine were found to have relatively large intersubject variabilities, and consequently, the study had little power to detect dose-dependent changes in the values of the pharmacokinetic parameters. The oral clearance of atevirdine tended to increase by 90% as the atevirdine mesylate doses increased from 400 to 1,600 mg, but this change in oral clearance was not statistically significant. The values of the pharmacokinetic parameters determined in the study were similar to those found in a previous single-dose study in healthy volunteers.

Non-radioactive PCR method for quantification of HIV-infected peripheral blood mononuclear cells in HIV-positive subjects.

A nested PCR method for quantification of HIV-infected peripheral blood mononuclear cells (PBMC) which does not use radioactivity nor plasmids is described. Quantification was achieved by means of limiting dilutions and an ACH2 cell standard. The method was used to study 23 HIV-infected patients. A significant correlation was seen between the stage of HIV disease, as classified by CDC criteria, and the number of infected PBMC. Although the CD4+ cell count also correlated well with the stage of HIV disease, there was only weak correlation between the result obtained by the PCR method and the CD4+ cell count.

Activation of the mas oncogene involves coupling to human alphoid sequences.

We have shown previously that mouse NIH3T3 cells transfected with DNA from a human ovarian carcinoma were rendered tumourigenic by an activated mas oncogene in four independent transfection experiments. In all cases the 5'-noncoding region was rearranged in comparison to the original ovarian tumour DNA. We now report that in all four transfectants the newly acquired sequences consist of human centromeric alpha satellite repeat DNA. In at least three transfectants the alphoid DNA originates from the centromere of chromosome three. Analysis of the sequences of the recombination site in one transfectant revealed that a homologous sequence of five base pairs (CAGCA) is present in both parental strands, and might thus have contributed to the recombinational event. To establish a conclusive role for alphoid DNA in the activation of mas, we performed a co-transfection experiment in NIH3T3 cells with cloned alphoid DNA and the mas coding sequence. We show that the transfectants expressing a transformed phenotype contain amplified mas linked to alphoid DNA. NIH3T3 cells transfected with plasmids that contained alphoid sequences cloned directly upstream of the mas coding sequence, and injected into nude mice, gave rise to tumours with amplified mas sequences (7/7). In six of these tumours the alphoid sequences were amplified as well. Our data suggest a novel mechanism of oncogene activation: recombination with normal alphoid repeat DNA resulting in amplification of the oncogene.

The natural course of multiple endocrine neoplasia type IIb. A study of 18 cases.

BACKGROUND: Multiple endocrine neoplasia (MEN) type IIb is an autosomal dominantly inherited disorder associated with medullary thyroid cancer, pheochromocytoma, and a characteristic phenotype. The present study was performed to investigate the natural course of the syndrome and to describe its expression. METHODS: The medical records of 18 patients with MEN IIb, seven male and 11 female, were reviewed. RESULTS: The mean age at diagnosis of MEN IIb was 18 years (range, 8 to 41 years). All 18 patients had medullary thyroid cancer. In three patients, medullary thyroid cancer was diagnosed via screening. In two of these patients, the calcitonin value normalized after thyroidectomy. One patient died of metastases from medullary thyroid cancer at the age of 20 years (median duration of follow-up, 10 years). Eight of the 18 patients had pheochromocytomas. All of our patients had neuromas and bumpy lips, and all but one had a marfanoid habitus. A large proportion of the patients had intestinal abnormalities (75%), thickened corneal nerves (69%), skeletal abnormalities (87%), and delayed puberty (43%). CONCLUSIONS: The course of medullary thyroid cancer in MEN IIb is not always as aggressive as is generally thought. Periodic examination of relatives who are at risk may lead to early diagnosis and curative treatment. Intestinal abnormalities, skeletal abnormalities, and delayed puberty are commonly found in association with MEN IIb.

Spi-1 oncogene activation in Rauscher and Friend murine virus-induced acute erythroleukemias.

The Friend viruses, like the Rauscher virus, cause murine acute erythroleukemias which evolve in a similar multistep process. In previous studies it has been described that the late malignant proerythroblastic transformation induced by the polycythemia-inducing strain of Friend spleen focus-forming virus (SFFVP) is correlated with Spi-1 oncogene activation by insertional mutagenesis. In this paper we report that Spi-1 genomic rearrangements were also observed in 90% of tumors induced by the anemia-inducing strain of Friend spleen focus-forming virus (SFFVA) and in all Rauscher-induced tumors analyzed. SFFVA and Rauscher proviral insertions occurred in the viral integration cluster previously characterized in SFFVP-induced tumors. The Spi-1 1.4-Kb messenger RNA was found highly expressed in all SFFVA and Rauscher-induced malignant cells as compared to normal tissues. The nucleotide sequence of Spi-1 cDNA isolated from a library constructed from SFFVA-induced tumor cells revealed no difference between the Spi-1 gene transcripts expressed in both SFFVP and SFFVA-induced leukemic cells. These results indicate that Spi-1 gene activation is a general feature in the malignant proerythroblastic transformation which occurs in mice infected with Friend and Rauscher viruses.

Molecular cloning of the Rauscher murine leukemia virus. Disease spectrum and integration pattern.

After transfection of NIH 3T3 cells with DNA from molecularly cloned Rauscher MuLV, virus was isolated which showed a disease spectrum comparable to that of R-MuLV cloned biologically by endpoint dilution. In both cases sites of proviral integration vary from 2-5 per leukemic tissue and occur apparently at random.

Nucleotide sequence of both reciprocal translocation junction regions in a patient with Ph positive acute lymphoblastic leukaemia, with a breakpoint within the first intron of the BCR gene.

Breakpoints on chromosome 22 in the translocation t(9;22) found in Philadelphia positive acute lymphoblastic leukaemia patients fall within two categories. In the first the breakpoint is localized within the breakpoint cluster region of the BCR gene, analogous to the chromosome 22 breakpoint in chronic myeloid leukaemia. The second category has a breakpoint 5' of this area, but still within the BCR gene. We have previously shown that these breakpoints occur within the first intron of the BCR gene and cloned the 9q+ junction from such a patient. We have now determined the sequences around the breakpoints on both translocation partners from this patient as well as the germline regions. The chromosome 9 ABL sequence around the breakpoint shows homology to the consensus Alu sequence whereas the chromosome 22 BCR sequence does not. At the junction there is a 6 bp duplication of the chromosome 22 sequence which is present both in the 9q+ and in the 22q- translocation products. Possible mechanisms for the generation of the translocation are discussed.

Oncogene expression in Rauscher murine leukemia virus induced erythroid, myeloid and lymphoid cell lines.

A comparative study on the expression of nuclear and cytoplasmic oncogenes was carried out using the Northern blotting technique, in Rauscher virus induced primary leukemias and the more malignant transformed cell lines derived from them. The latter grow permanently in vitro. Hyperplastic spleens obtained from mice recovering from anemia were analysed as controls. In addition to the detection of mRNAs, Southern blotting was carried out to observe whether rearrangement or amplification of oncogenes had occurred. The results show that the nuclear oncogenes c-myc, c-myb and p53 are strongly expressed in leukemic tissue, whereas c-fos transcripts show a much weaker hybridization. The expression of two of these oncogenes, c-myc and c-myb was followed during differentiation in myeloid leukemic cells and showed a gradual decrease when compared with the actin gene, which is constitutively transcribed. A large number of cytoplasmic oncogenes is expressed in the leukemic cells lines, i.e. c-abl, c-fms, c-fes, c-src, c-ros, c-H-ras, c-K-ras and N-ras. Of these, transcripts coding for c-abl and c-src were absent in blast cells of acute erythroid leukemias. Transcripts coding for c-erb, c-mos and c-sis could also not be detected. A number of putative oncogenes which are reported to play a role in Moloney and Friend virus induced leukemias for instance pim-1, fis-1, fim-1 and fim-2 were also used for screening. Only expression of pim-1 in Rauscher virus induced myeloid leukemic cells and in primary acute erythroid leukemias could be observed. At the DNA level no rearrangement or amplification of any of the oncogenes investigated could be detected. The results show that a number of oncogenes are expressed simultaneously in the same leukemic tissue or cell lines. It therefore seems likely that the presence of transcripts of different oncogenes is associated with the progression of leukemia, but is not the primary cause of leukemogenesis or of the transformation of these cells into established cell lines.