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      Co-Infection with COVID-19 and Malaria in a Young Man

      Dubai Medical Journal
      S. Karger AG
      Coronavirus, Malaria, Fever, Coronavirus disease 2019

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          Malaria is an infectious disease caused by Plasmodium protozoa, which can be fatal if not diagnosed and treated promptly. COVID-19 is a newly emerging disease that can affect different body systems; however, the respiratory system is mainly reported. This case describes a 20-year-old man who presented with fever and joint pain and was found to have P. falciparum malaria in addition to a positive SARS-CoV-2 test. The patient improved after he was treated with antimalarial medications in addition to supportive therapy. A co-infection of malaria and COVID-19 can occur. Thus, more studies need to be conducted on this co-infection. Besides, other diagnoses should be highly suspected in patients presenting with symptoms suggestive of SARS-CoV-2 infection, especially in vulnerable patients.

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          COVID-19: Gastrointestinal Manifestations and Potential Fecal–Oral Transmission

          The outbreak of novel coronavirus (2019-nCoV) pneumonia initially developed in one of the largest cities, Wuhan, Hubei province of China, in early December 2019 and has been declared the sixth public health emergency of international concern by the World Health Organization, and subsequently named coronavirus disease 2019 (COVID-19). As of February 20, 2020, a total of >75,000 cumulative confirmed cases and 2130 deaths have been documented globally in 26 countries across 5 continents. Current studies reveal that respiratory symptoms of COVID-19 such as fever, dry cough, and even dyspnea represent the most common manifestations at presentation similar to severe acute respiratory syndrome (SARS) in 2003 and Middle East respiratory syndrome in 2012, which is firmly indicative of droplet transmission and contact transmission. However, the incidence of less common features like diarrhea, nausea, vomiting, and abdominal discomfort varies significantly among different study populations, along with an early and mild onset frequently followed by typical respiratory symptoms. 1 Mounting evidence from former studies of SARS indicated that the gastrointestinal tract (intestine) tropism of SARS coronavirus (SARS-CoV) was verified by the viral detection in biopsy specimens and stool even in discharged patients, which may partially provide explanations for the gastrointestinal symptoms, potential recurrence, and transmission of SARS from persistently shedding human as well. 2 Notably, the first case of 2019-nCoV infection confirmed in the United States reported a 2-day history of nausea and vomiting on admission, and then passed a loose bowel movement on hospital day 2. The viral nucleic acids of loose stool and both respiratory specimens later tested positive. 3 In addition, 2019-nCoV sequence could be also detected in the self-collected saliva of most infected patients even not in nasopharyngeal aspirate, and serial saliva specimens monitoring showed declines of salivary viral load after hospitalization. 4 Given that extrapulmonary detection of viral RNA does not mean infectious virus is present, further positive viral culture suggests the possibility of salivary gland infection and possible transmission. 4 More recently, 2 independent laboratories from China declared that they have successfully isolated live 2019-nCoV from the stool of patients (unpublished). Taken together, a growing number of clinical evidence reminds us that digestive system other than respiratory system may serve as an alternative route of infection when people are in contact with infected wild animals or sufferers, and asymptomatic carriers or individuals with mild enteric symptoms at an early stage must have been neglected or underestimated in previous investigations. Clinicians should be careful to promptly identify the patients with initial gastrointestinal symptoms and explore the duration of infectivity with delayed viral conversion. To date, molecular modelling has revealed by the next-generation sequencing technology that 2019-nCoV shares about 79% sequence identify with SARS-CoV, indicative of these 2 lineage B β-coronaviruses highly homologous, and angiotensin-converting enzyme II (ACE2), previously known as an entry receptor for SARS-CoV, was exclusively confirmed in 2019-nCoV infection despite amino acid mutations at some key receptor-binding domains. 5 , 6 It is widely accepted that coronavirus human transmissibility and pathogenesis mainly depend on the interactions, including virus attachment, receptor recognition, protease cleaving and membrane fusion, of its transmembrane spike glycoprotein (S-protein) receptor-binding domain, specific cell receptors (ACE2), and host cellular transmembrane serine protease (TMPRSS), with binding affinity of 2019-nCoV about 73% of SARS-CoV. 7 Recent bioinformatics analysis on available single-cell transcriptomes data of normal human lung and gastrointestinal system was carried out to identify the ACE2-expressing cell composition and proportion, and revealed that ACE2 was not only highly expressed in the lung AT2 cells, but also in esophagus upper and stratified epithelial cells and absorptive enterocytes from ileum and colon. 8 With the increasing gastrointestinal wall permeability to foreign pathogens once virus infected, enteric symptoms like diarrhea will occur by the invaded enterocytes malabsorption, which in theory indicated the digestive system might be vulnerable to COVID-19 infection. In contrast, because ACE2 and TMPRSS especially TMPRSS2 are co-localized in the same host cells and the latter exerts hydrolytic effects responsible for S-protein priming and viral entry into target cells, further bioinformatics investigation renders additional evidence for enteric infectivity of COVID-19 in that the high co-expression ratio was found in absorptive enterocytes and upper epithelial cells of esophagus besides lung AT2 cells. However, the exact mechanism of COVID-19–induced gastrointestinal symptom largely remains elusive. Based on these considerations, ACE2-based strategies against COVID-19 such as ACE2 fusion proteins and TMPRSS2 inhibitors should be accelerated into clinical research and development for diagnosis, prophylaxis, or treatment. Last, mild to moderate liver injury, including elevated aminotransferases, hypoproteinemia, and prothrombin time prolongation, has been reported in the existing clinical investigations of COVID-19, whereas up to 60% of patients suffering from SARS had liver impairment. The presence of viral nucleic acids of SARS in liver tissue confirmed the coronavirus direct infection in liver, and percutaneous liver biopsies of SARS showed conspicuous mitoses and apoptosis along with atypical features such as acidophilic bodies, ballooning of hepatocytes, and lobular activities without fibrin deposition or fibrosis. 9 It is believed that SARS-associated hepatotoxicity may be likely with viral hepatitis or a secondary effect associated with drug toxicity owing to high-dose consumption of antiviral medications, antibiotics, and steroids, as well as immune system overreaction. However, little is known about 2019-nCoV infection in liver. Surprisingly, recent single cell RNA sequencing data from 2 independent cohorts revealed a significant enrichment of ACE2 expression in cholangiocytes (59.7% of cells) instead of hepatocytes (2.6% of cells), suggesting that 2019-nCoV might lead to direct damage to the intrahepatic bile ducts. 10 Altogether, substantial effort should be made to be alert on the initial digestive symptoms of COVID-19 for early detection, early diagnosis, early isolation, and early intervention.
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            Chloroquine and hydroxychloroquine as available weapons to fight COVID-19

            Repositioning of drugs for use as antiviral treatments is a critical need [1]. It is commonly very badly perceived by virologists, as we experienced when reporting the effectiveness of azithromycin for Zika virus [2]. A response has come from China to the respiratory disease caused by the new coronavirus (SARS-CoV-2) that emerged in December 2019 in this country. Indeed, following the very recent publication of results showing the in vitro activity of chloroquine against SARS-CoV-2 [3], data have been reported on the efficacy of this drug in patients with SARS-CoV-2-related pneumonia (named COVID-19) at different levels of severity [4,5]. Thus, following the in vitro results, 20 clinical studies were launched in several Chinese hospitals. The first results obtained from more than 100 patients showed the superiority of chloroquine compared with treatment of the control group in terms of reduction of exacerbation of pneumonia, duration of symptoms and delay of viral clearance, all in the absence of severe side effects [4,5]. This has led in China to include chloroquine in the recommendations regarding the prevention and treatment of COVID-19 pneumonia [4,6]. There is a strong rationality for the use of chloroquine to treat infections with intracellular micro-organisms. Thus, malaria has been treated for several decades with this molecule [7]. In addition, our team has used hydroxychloroquine for the first time for intracellular bacterial infections since 30 years to treat the intracellular bacterium Coxiella burnetii, the agent of Q fever, for which we have shown in vitro and then in patients that this compound is the only one efficient for killing these intracellular pathogens [8,9]. Since then, we have also shown the activity of hydroxychloroquine on Tropheryma whipplei, the agent of Whipple's disease, which is another intracellular bacterium for which hydroxychloroquine has become a reference drug [10,11]. Altogether, one of us (DR) has treated ~4000 cases of C. burnetii or T. whipplei infections over 30 years (personal data). Regarding viruses, for reasons probably partly identical involving alkalinisation by chloroquine of the phagolysosome, several studies have shown the effectiveness of this molecule, including against coronaviruses among which is the severe acute respiratory syndrome (SARS)-associated coronavirus [1,12,13] (Table 1 ). We previously emphasised interest in chloroquine for the treatment of viral infections in this journal [1], predicting its use in viral infections lacking drugs. Following the discovery in China of the in vitro activity of chloroquine against SARS-CoV-2, discovered during culture tests on Vero E6 cells with 50% and 90% effective concentrations (EC50 and EC90 values) of 1.13 μM and 6.90 μM, respectively (antiviral activity being observed when addition of this drug was carried out before or after viral infection of the cells) [3], we awaited with great interest the clinical data [14]. The subsequent in vivo data were communicated following the first results of clinical trials by Chinese teams [4] and also aroused great enthusiasm among us. They showed that chloroquine could reduce the length of hospital stay and improve the evolution of COVID-19 pneumonia [4,6], leading to recommend the administration of 500 mg of chloroquine twice a day in patients with mild, moderate and severe forms of COVID-19 pneumonia. At such a dosage, a therapeutic concentration of chloroquine might be reached. With our experience on 2000 dosages of hydroxychloroquine during the past 5 years in patients with long-term treatment (>1 year), we know that with a dosage of 600 mg/day we reach a concentration of 1 μg/mL [15]. The optimal dosage for SARS-CoV-2 is an issue that will need to be assessed in the coming days. For us, the activity of hydroxychloroquine on viruses is probably the same as that of chloroquine since the mechanism of action of these two molecules is identical, and we are used to prescribe for long periods hydroxychloroquine, which would be therefore our first choice in the treatment of SARS-CoV-2. For optimal treatment, it may be necessary to administer a loading dose followed by a maintenance dose. Table 1 Main results of studies on the activity of chloroquine or hydroxychloroquine on coronavirusesa Table 1 Reference Compound(s) Targeted virus System used for antiviral activity screening Antiviral effect [12] Chloroquine SARS-CoV Vero (African green monkey kidney) E6 cells EC50 = 8.8 ± 1.2 μM [16] Chloroquine Vero E6 cells EC50 = 4.4 ± 1.0 μM [17] Chloroquine, chloroquine monophosphate, chloroquine diphosphate SARS-CoV (four strains) Vero 76 cells Chloroquine: EC50 = 1–4 μMChloroquine monophosphate: EC50 = 4–6 μMChloroquine diphosphate: EC50 = 3–4 μM BALB/c mice Intraperitoneal or intranasal chloroquine administration, beginning 4 h prior to virus exposure: 50 mg/kg but not 10 mg/kg or 1 mg/kg reduced for the intranasal route (but not the intraperitoneal route) viral lung titres from mean ± S.D. of 5.4 ± 0.5 to 4.4 ± 1.2 in log10 CCID50/g at Day 3 (considered as not significant) [18] Chloroquine, hydroxychloroquine SARS-CoV Vero cells Chloroquine: EC50 = 6.5 ± 3.2 μMHydroxychloroquine: EC50 = 34 ± 5 μM Feline coronavirus Crandell–Reese feline kidney (CRFK) cells Chloroquine: EC50 > 0.8 μMHydroxychloroquine: EC50 = 28 ± 27 μM [19] Chloroquine HCoV-229E Human epithelial lung cells (L132) Chloroquine at concentrations of 10 μM and 25 μM inhibited HCoV-229E release into the culture supernatant [20] Chloroquine HCoV-OC43 HRT-18 cells EC50 = 0.306 ± 0.0091 μM Newborn C57BL/6 mice; chloroquine administration transplacentally and via maternal milk 100%, 93%, 33% and 0% survival rate of pups when mother mice were treated per day with 15, 5, 1 and 0 mg/kg body weight, respectively [21] Chloroquine Feline infectious peritonitis virus (FIPV) Felis catus whole fetus-4 cells FIPV replication was inhibited in a chloroquine concentration-dependent manner [22] Chloroquine SARS-CoV Vero E6 cells EC50 = 4.1 ± 1.0 μM MERS-CoV Huh7 cells (human liver cell line) EC50 = 3.0 ± 1.1 μM HCoV-229E-GFP (GFP-expressing recombinant HCoV-229E) Huh7 cells (human liver cell line) EC50 = 3.3 ± 1.2 μM [3] Chloroquine SARS-CoV-2 Vero E6 cells EC50 = 1.13 μM CCID50, 50% cell culture infectious dose; CoV, coronavirus; EC50, 50% effective concentration (mean ± S.D.); GFP, green fluorescent protein; HCoV, human coronavirus; MERS, Middle East respiratory syndrome; SARS, severe acute respiratory syndrome; S.D., standard deviation. a See also [1] (Table 1) for additional references.
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              Emergency department management of mosquito-borne illness: malaria, dengue, and West Nile virus.

              Up to 700 million people are infected and more than a million die each year from mosquito-borne illness. While the vast majority of cases occur in endemic tropical and subtropical regions, international travel and migration patterns have increased their prevalence in North America. This review discusses the diagnosis and treatment of the 3 most common mosquito-borne illnesses seen in the United States: Plasmodium falciparum malaria, dengue, and West Nile virus. With no pathognomonic findings, it is critical that emergency clinicians in nonendemic areas maintain a high index of suspicion, conduct a thorough history/travel history, and interpret indirect findings to initiate prompt and appropriate treatment. This review gathers the best evidence from international public health resources, surveillance studies, guidelines, and academic research to give emergency clinicians tools to combat these potentially lethal infections.

                Author and article information

                Dubai Medical Journal
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )
                30 March 2021
                : 104-106
                Emergency Department, Al Ain Hospital, Al Ain, United Arab Emirates
                Author notes
                *Mustafa Mahmood Eid, Emergency Department, Al Ain Hospital, Shakboot Bin Sultan Street, Al Ain 1006 (UAE), dr.mustafa191982@ 123456gmail.com
                Copyright © 2021 by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                : 22 November 2020
                : 7 January 2021
                Page count
                Tables: 1, References: 8, Pages: 3
                Educational Corner − Case Report

                coronavirus,malaria,fever,coronavirus disease 2019
                coronavirus, malaria, fever, coronavirus disease 2019


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