Circulating vaccine-derived poliovirus type 2 – Democratic Republic of the Congo
Emergencies preparedness, response
Disease outbreak news 13 June 2017
In the Democratic Republic of the Congo (DRC), two separate circulating vaccine-derived poliovirus type 2s (cVDPV2s) have been confirmed. The first cVDPV2 strain has been isolated from two acute flaccid paralysis (AFP) cases from two districts in Haut-Lomami province, with onset of paralysis on 20 February and 8 March 2017. The second cVDPV2 strain has been isolated from Maniema province, from two AFP cases (with onset of paralysis on 18 April and 8 May 2017) and a healthy contact in the community.
Public health response
The Ministry of Health, supported by WHO and partners of the Global Polio Eradication Initiative (GPEI), has completed a risk assessment, including evaluating population immunity and the risk of further spread.
Outbreak response plans are currently being finalized, consisting of strengthening surveillance, including active case searching for additional cases of AFP, and supplementary immunization activities (SIAs) with monovalent oral polio vaccine type 2 (mOPV2), in line with internationally-agreed outbreak response protocols.
Surveillance and immunization activities are being strengthened in neighbouring countries.
WHO risk assessment
WHO assesses the risk of further national spread of these strains to be high, and the risk of international spread to be medium.
The detection of cVDPV2s underscores the importance of maintaining high routine vaccination coverage everywhere, to minimize the risk and consequences of any poliovirus circulation. These events also underscore the risk posed by any low-level transmission of the virus. A robust outbreak response as initiated is needed to rapidly stop circulation and ensure sufficient vaccination coverage in the affected areas to prevent similar outbreaks in the future. WHO will continue to evaluate the epidemiological situation and outbreak response measures being implemented.
It is important that all countries, in particular those with frequent travel and contacts with polio-affected countries and areas, strengthen surveillance for AFP cases in order to rapidly detect any new virus importation and to facilitate a rapid response. Countries, territories and areas should also maintain uniformly high routine immunization coverage at the district level to minimize the consequences of any new virus introduction.
WHO’s International Travel and Health recommends that all travellers to polio-affected areas be fully vaccinated against polio. Residents (and visitors for more than four weeks) from infected areas should receive an additional dose of OPV or inactivated polio vaccine (IPV) within four weeks to 12 months of travel. As per the advice of the Emergency Committee convened under the International Health Regulations (2005), efforts to limit the international spread of poliovirus remains a Public Health Emergency of International Concern (PHEIC). Countries affected by poliovirus transmission are subject to Temporary Recommendations. To comply with the Temporary Recommendations issued under the PHEIC, any country infected by poliovirus should declare the outbreak as a national public health emergency and consider vaccination of all international travellers.
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A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.
On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.
The patient's legs, showing massive enlargement of the right calf and wasting on the left
What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?
An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.
A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3
Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.
Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition
The differential diagnosis of the progressive calf hypertrophy is given in the box.
Causes of calf muscle hypertrophy
Chronic partial denervation
hereditary motor and sensory neuropathy
spinal muscular atrophy
following paralytic poliomyelitis
Neuromyotonia and myokymia
continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis