Correspondence
Emergence of Zika virus: where does it come from and where is it going to? We read with great interest the Comment from Yee-Sin Leo and Angela Chow1 about the emergence of Zika virus in Singapore. The recent history of Zika virus began in 2013–14 in French Polynesia where it caused a large outbreak and the first severe complications. Zika virus then spread across the Pacific and the Americas.2 The Zika virus strains that emerged in these areas were closely related to the French Polynesian strain and belonged to the Asian lineage of Zika virus.2 It was hypothesised that mutations might have occurred in Zika virus resulting in an increased epidemicity and virulence. 2 The detection of aminoacid substitutions in the Zika virus M protein, coinciding with the emergence of Zika virus in French Polynesia, reinforced this hypothesis.3 The hypothesis of increased epidemicity and virulence associated with the new emerging strains was reinforced by reports of microcephaly cases and Zika virus circulation in Guinea-Bissau (Africa) in 2016.4 However, genetic studies showed that, while the Zika virus strain that emerged in Cape Verde (Africa) in 2015 belonged to the Asian lineage and could have been imported from Brazil, the strain isolated in GuineaBissau belonged to the African lineage.4 An imported case of Zika virus infection in Singapore in May, 2016, was suspected to have been introduced from Brazil. 5 However, the strain currently spreading in Singapore, causing the first Zika virus outbreak ever reported in southeast Asia, is closely related to a strain that previously circulated in Asia before 2007 and is not the consequence of a new introduction of the so-called www.thelancet.com/infection Vol 17 March 2017
emerging strains circulating in the Americas and Pacific.1 This is puzzling because it suggests that old Zika virus strains from the Asian and the African lineages have the potential for outbreaks and perhaps for severe disease outcomes. Nevertheless, reports of microcephaly in Guinea-Bissau and reemergence of an old Zika virus strain in Singapore might simply reflect the increased awareness and therefore testing for Zika virus after Zika virus emerged in other parts of the world and was declared an international public health emergency. The reason for the concurrent emergence or re-emergence of different Asian strains in different geographical locations and at different periods in time (Yap 2007, French Polynesia 2013–14, Singapore 2016) is unknown. The potential for theses strains to cause severe complications is also unknown and challenging in countries with other disease burden and limited resources and therefore interest. Careful monitoring, including genetic investigations, of all new emergences, would be valuable to understand the risk associated with different Zika virus strains. We declare no competing interests.
*Didier Musso, Marion C Lanteri
[email protected] Unit of Emerging Infectious Diseases, Institut Louis Malardé, 98713 Tahiti, French Polynesia (DM); Blood Systems Research Institute, San Francisco, CA, USA (MCL); Department of Laboratory Medicine, University of California San Francisco, San Francisco, CA, USA (MCL); and Cerus Corporation, Concord, CA, USA (MCL) 1.
2 3
4
Leo Y-S, Chow A. Zika virus has arrived in Singapore. Lancet Infect Dis 2016; 16: 1317–19. Musso D, Gubler DJ. Zika virus. Clin Microbiol Rev 2016; 29: 487–524. Pettersson JH, Eldholm V, Seligman SJ, et al. How did Zika virus emerge in the Pacific islands and Latin America. MBio 2016; 7: e01239–16. WHO. Zika situation report. Zika virus microcephaly Guillain-Barré syndrome 1 September 2016. http://www.who.int/ emergencies/zika-virus/situation-report/ 1-september-2016/en/ (accessed Jan 24, 2017).
5
Sadarangani SP, Hsu LY. The 2016 outbreak of Zika in Singapore. Ann Acad Med Singapore 2016; 45: 381–82.
A translucent vascularised iris granuloma in a patient with secondary syphilis We read with interest the Clinical Picture by Calogero Pagliarello and colleagues 1 describing a case of secondary syphilis. We would like to draw attention to a special ophthalmological presentation of this disease and call for vigilance also in the non-HIV-infected individual. Recently, we encountered the case of a 48-year-old heterosexual man who presented with a 2 week history of skin lesions, fever, weight loss, and cramping leg pains. Physical examination revealed bilateral conjunctival redness, pharyngitis, cervical lymphadenopathy, and a maculopapular rash on the arms and legs, palms and soles, trunk, and oral mucosa. He had unprotected oral sex 13 weeks before presentation and developed an oral lesion 3 weeks thereafter, which was considered to be a perio dontal abscess by his general practitioner. The lesion resolved in 2 weeks without intervention. Shortly after admittance to hospital he complained about blurred vision with his right eye. The corrected visual acuity was 20/20 with both eyes. The right eye showed anterior uveitis, but also, at 4–5 o’clock a translucent vascularised tumour at the iris base with locally dilated con junctival vessels and iris dimpling (figure A). With gonioscopy no tumour involvement of the trabecular system was detected; there was an open angle. With ultrasound biomicroscopy the tumour size was measured (figure B). The posterior segment was not involved. Serum Treponema pallidum IgG/IgM were positive, with 255