Polio vaccination coverage in Somalia On May 5, 2014, WHO declared polio a public health emergency of international concern.1 Somalia has not eradicated polio yet and has done five national immunisation campaigns in 2013, at considerable expense. Much attention has been given to low immunisation coverage in the conflictaffected south of Somalia. A cooperation between the Ministry of Health, Save the Children, UNICEF, and the UK Department for International Development looking at barriers to accessing health care in Puntland, an area not affected by conflict, found an unexpected low polio vaccination coverage rate in March, 2014, in the Karkaar region— an arid desert where pastoralism is the main activity. Although the study was not designed as a polio coverage survey, it met Lot Quality Assurance Sampling criteria. The study looked at whether children younger than 5 years old had received at least one polio vaccination, using a combination of card and caretaker recall. We noted a proportion of children younger than 5 years who had been vaccinated against polio at least once in their lifetime of 81·5% (SD 4·9, range 77–92) in small towns, of 58·8% (SD 23·9, range 20–90) in small villages, and of 34·4% (SD 24·5, range 0–79) in pastoralist populations. This survey was not designed to measure polio coverage and the sample size (385) is rather small. No reliable population estimates are available for the region, but the Ministry of Planning estimates that pastoralists represent 60–70% of the Karkaar population, while Puntland health authorities’ estimates are at 40–50%. Pastoralists can freely cross unmarked borders. Moreover, Karkaar region is an important crossroad (connecting Gulf states, South Central Somalia [the epicentre of the 2013 polio outbreak], Ethiopia, and Kenya, but also between Yemen and Ethiopia). www.thelancet.com Vol 383 June 28, 2014
The WHO–UNICEF Joint Strategic Action Plan for the Polio Outbreak Response in the Horn of Africa in November, 2013, focused on the South Central region of Somalia where polio immunisation is hampered by ongoing insecurity. However, our data are from a region that has not been affected by conflict for at least a decade, and polio immunisation coverage still seems very low, especially in the population most likely to act as a vector for polio transmission. The recent WHO statement1 will lead to a new round of planning to contain polio, and our data suggest that attention should also be given to transmission vectors outside the conflict area. Our observations highlight that pastoralist populations are underserved. Because polio is a global concern, undoubtedly funding will be found for this specific intervention. It should however also be a wake-up call that pastoralist populations need health-care services, and thus funding. We declare no competing interests.
*Harry Jeene, Abdirizak Hersi Hassan
[email protected] RALSA Foundation, PO Box 637, 00502 Nairobi, Kenya (HJ); and Ministry of Health, Puntland, Somalia (AHH) 1
WHO. WHO statement on the meeting of the International Health Regulations Emergency Committee concerning the international spread of wild poliovirus. http://who.int/ mediacentre/news/statements/2014/ polio-20140505/en/ (accessed June 10, 2014).
Polio will go, acute flaccid paralysis will stay The Global Polio Eradication Initiative has made tremendous progress since its launch by WHO in 1988, reducing polio cases from an estimated 350 000 in 1988 to about 407 in 2013. The number of countries that have never interrupted wild poliovirus transmission decreased from more than 125 to only three countries (Nigeria, Afghanistan, and Pakistan).1 In 1999, the eradication of wild poliovirus
type 2 was achieved.2 The last case of poliovirus type 3 occurred on Nov 10, 2012, in Nigeria. The remaining goal of the Global Polio Eradication Initiative is to stop the transmission of all wild poliovirus and vaccine-derived poliovirus through supplementary immunisation activities, and environmental and acute flaccid paralysis surveillance. It is therefore realistic to be optimistic that the global eradication of polio might be feasible in the not too distant future. But as the Global Polio Eradication Initiative and the scientific community plan to celebrate polio eradication sooner or later, there is need for recognition that the risk of acute flaccid paralysis due to other enteroviruses is still high. Acute flaccid paralysis is a weakness in one or more limbs or the respiratory or bulbar muscles, resulting from damaged lower motor neurons. The most common viral causes are polio and nonpolio enteroviruses. As polio gradually disappears globally, there is major concern about the probable emergence of other neurotropic enteroviruses to occupy the niche and cause infections mimicking acute paralytic poliomyelitis. Enterovirus 71 for example has been regarded as the second most important neurotropic enterovirus, causing frequent outbreaks of paralytic disease.3 A crude mortality rate of 16% in children younger than 14 years was observed during an enterovirus 71 outbreak between 1998 and 2005 in Taiwan.4 Also, and equally important, is recombination between vaccine-derived poliovirus and other enteroviruses, which might result in the emergence of novel recombinant viruses causing similar paralytic diseases.5 Over the past decades, several non-polio enteroviruses have been discovered and some implicated in acute flaccid paralysis of unprecedented severity. Therefore, as polio eradication is near attainment, future efforts by WHO should probably focus on improved funding for vaccine designs and enhanced epidemiological surveillance for other neurotropic enteroviruses.
Karen Kasmauski
Correspondence
For more on the Global Polio Eradication Initiative see http:// www.polioeradication.org/
2209
Correspondence
We declare no competing interests.
*James A Ayukekbong, Tomas Bergström
[email protected] Department of Infectious Diseases, Section of Clinical Virology, Institute of Biomedicine, University of Gothenburg, Gothenburg 41346, Sweden 1
2
3
4
5
CDC. Progress toward eradication of polioworldwide—Nigeria, January 2011–September 2012. MMWR Morb Mortal Wkly Rep 2012; 61: 899–904. CDC. Progress toward the global interruption of wild poliovirus type 2 transmission, 1999. MMWR Morb Mortal Wkly Rep 1999; 48: 736–38. da Silva EE, Winkler MT, Pallansch MA. Role of enterovirus 71 in acute flaccid paralysis after the eradication of poliovirus in Brazil. Emerg Infect Dis 1996; 2: 231–33. Chen SC, Chang HL, Yan TR, Cheng YT, Chen KT. An eight-year study of epidemiologic features of enterovirus 71 infection in Taiwan. Am J Trop Med Hyg 2007; 77: 188–91. Combelas N, Holmblat B, Joffret ML, Colbere-Garapin F, Delpeyroux F. Recombination between poliovirus and coxsackie A viruses of species C: a model of viral genetic plasticity and emergence. Viruses 2011; 3: 1460–84.
Diagnostic and treatment challenges in giant cell arteritis Colm McAlinden and colleagues’ Case Report (March 29, p 1182)1 of a patient with biopsy-proven giant cell arteritis in the absence of elevated inflammatory markers highlights a rare presentation of a sight-threatening and potentially fatal condition. We wish to raise additional points to further aid the reader in what is often a difficult diagnostic. The ocular and systemic symptoms and signs in this case were highly suggestive of giant cell arteritis. An ischaemic optic neuropathy with profound visual loss, a relative afferent pupillary defect, and an ipsilateral temporal headache (even without jaw claudication) arguably suggest that the diagnosis is unequivocal. However, it is important for clinicians to remain mindful of patients who might present with silent or occult giant cell arteritis in which systemic symptoms or signs are absent; the incidence ranges between 5% and 38%.2 2210
Aside from the commonly increased erythrocyte sedimentation rate and C-reactive protein, a thrombocytosis might support a diagnosis of giant cell arteritis,3 particularly when the aforementioned inflammatory markers are only equivocally raised and the diagnosis is suspected. A rising platelet count can commence as early as 1 year before the diagnosis of giant cell arteritis.4 Temporal artery biopsy is still considered the gold standard for diagnosis and a positive result is indeed confirmatory. However, a negative biopsy does not exclude the diagnosis. A false negative rate of 5–13% has been reported, depending on the length of the specimen, the presence of skip lesions, and the duration of preceding corticosteroid treatment. 5 Where there is a high clinical suspicion, the commencement of therapy should not be delayed, because the biopsy sensitivity might not be substantially affected if performed within 2 weeks.6 Corticosteroid therapy should not be discontinued after a negative biopsy result if there is enough evidence to make the diagnosis. Finally, vascular imaging might also add diagnostic value in giant cell arteritis. Colour duplex ultrasonography and MRI might detect changes in the orbital and superficial temporal vasculature consistent with giant cell arteritis. These alone lack diagnostic sensitivity, but might serve to target biopsy site. Recently, ¹⁸F-fluorodeoxyglucose PET scanning of the aorta and its large branches has shown substantial sensitivity (80%) and specificity (79%) in confirmed cases of giant cell arteritis,7 although its role in biopsy-negative cases has yet to be established. Giant cell arteritis should be considered in the differential diagnosis of all patients with an ischaemic optic neuropathy, irrespective of the absence of elevated inflammatory markers or a negative temporal artery biopsy. We declare no competing interests.
*Philip J Banerjee, Petros Petrou, Gordon T Plant philip.banerjee@moorfields.nhs.uk Moorfields Eye Hospital, London EC1V 2PD, UK (PJB, PP, GTP); and National Hospital For Neurology and Neurosurgery, London, UK (GTP) 1
2
3
4
5
6
7
McAlinden C, Ioannidis P, Roberts S, Skiadaresi E. Giant cell arteritis. Lancet 2014; 383: 1182. Rahman W, Rahman FZ. Giant cell (temporal) arteritis: an overview and update. Surv Ophthalmol 2005; 50: 415–28. Foroozan R, Danesh-Meyer H, Savino PJ, Gamble G, Mekari-Sabbagh ON, Sergott RC. Thrombocytosis in patients with biopsy-proven giant cell arteritis. Ophthalmology 2002; 109: 1267–71. Lincoff NS, Erlich PD, Brass LS. Thrombocytosis in temporal arteritis rising platelet counts: a red flag for giant cell arteritis. J Neuro-Ophthalmol 2000; 20: 67–72. Poller DN, van Wyk Q, Jeffrey MJ. The importance of skip lesions in temporal arteritis. J Clin Pathol 2000; 53: 137–39. Achkar AA, Lie JT, Hunder GG, O’Fallon WM, Gabriel SE. How does previous corticosteroid treatment affect the biopsy findings in giant cell (temporal) arteritis? Ann Intern Med 1994; 120: 987–92. Prieto-Gonzalez S, Depetris M, Garcia-Martinez A, et al. Positron emission tomography assessment of large vessel inflammation in patients with newly diagnosed, biopsy-proven giant cell arteritis: a prospective, case-control study. Ann Rheum Dis 2014; 73: 1388–92.
Authors’ reply We thank Philip Banerjee and colleagues for furthering this discussion on giant cell arteritis. We agree that giant cell arteritis can be a diagnostic challenge at times. The biomarkers are imperfect as was evident in our Case Report. 1 We concur that elevated platelets might also support a diagnosis of giant cell arteritis, but might also be normal, as was also evident in our case. An additional clinical sign highly suggestive of giant cell arteritis is an initial pulsatile superficial temporal artery, which later becomes absent. This is best palpated just anterior and superior to the tragus (above the zygomatic arch of the temporal bone). Although other investigations including ultrasonography and MRI are attractive methods because of their non-invasiveness, they still fall short on sensitivity and specificity compared with temporal artery biopsy. www.thelancet.com Vol 383 June 28, 2014
