Polio – The old foe and new challenges: An update for clinicians

Abstract

The Global Polio Eradication Initiative since 1988 has seen the impact of poliovirus decline from frequent global epidemics in the early 1900s to being now only endemic in two countries today. Global vaccination programmes and surveillance for the disease have resulted in the landmark eradication of two of the three poliovirus strains in the last 5 years. Australia continues to contribute to global surveillance efforts for the disease via the Australian Paediatric Surveillance Unit and the Paediatric Active Enhanced Disease Surveillance Network, which aim to detect cases of acute flaccid paralysis in children, the key clinical feature of poliomyelitis. Today, in the era of the polio 'endgame', there is growing recognition of non-polio enteroviruses causing paralytic diseases that are polio-like, particularly in children, with an increased need for awareness and vigilance by paediatric clinicians.

Bridging the gap between emerging models and humans by learning from polio animal studies: A systematic review

“…Like many other enteroviruses, the first replication site of poliovirus in humans is the gastrointestinal tract 14,15,39,42,43,45,51,53–55,59–62 . From there, the poliovirus reaches the CNS, either by retrograde axonal transport or by entering the bloodstream, where it replicates in the brain stem and the motor neurons localized in the anterior horns of the spinal cord 14,15,39,41,42,45–47,50,51,55,59–64 . The intracerebral route of infection caused the virus to replicate almost exclusively in the CNS 17,18,32,33,65,66 .…”

“…14,15,39,42,43,45,51,[53][54][55][59][60][61][62] From there, the poliovirus reaches the CNS, either by retrograde axonal transport or by entering the bloodstream, where it replicates in the brain stem and the motor neurons localized in the anterior horns of the spinal cord. 14,15,39,41,42,[45][46][47]50,51,55,[59][60][61][62][63][64] The intracerebral route of infection caused the virus to replicate almost exclusively in the CNS. 17,18,32,33,65,66 Other organs such as kidney, muscle, pancreas, liver, spleen, heart and, lung were also involved in PVRTg-IFNAR mice after intravenous infection, 36 in NMRI mice after intracerebral infection, 28 in PVRTg (ICR) mice after intranasal infection, 57 and in cPVR mice after intraperitoneal infection.…”

“…In humans, the damage of the motor neurons in the anterior horns of the spinal cord leads to movement impairment, muscle weakness, and flaccid paralysis 14,15,39-52,54,59-62 64,67 predominantly in children below five years of age, eventually leading to death in less than 1% of cases. 41,43,45,47,51,52,60,62 All tested Tg mouse models manifested paralysis upon different infec-tion routes but never after oral infection 17,18,24,[30][31][32][68][69][70][71][72][73][74][75] (Table S2D). Neurovirulence was evaluated in OF1 mice (exhibiting neither signs of paralysis or death), 29 in CAG-PVRTg, IPS knockout mice, and TICAM knockout mice (only mortality was documented).…”

First evidence of enterovirus A71 and echovirus 30 in Uruguay and genetic relationship with strains circulating in the South American region

“…The epidemiology of EVs is a dynamic phenomenon that deserves continuous surveillance since novel EV types are frequently discovered, and types originally associated with a specific disease, could emerge associated with novel conditions [ 4 – 9 ]. During the last decades, poliovirus has been a priority for public health surveillance systems worldwide due to its high incidence in AFP cases [ 10 ]. In the poliovirus eradication era, other non-polio EVs are being studied for their role as emerging pathogens associated with AFP, or as causing agents of central nervous system (CNS) disease outbreaks [ 10 – 13 ].…”

“…During the last decades, poliovirus has been a priority for public health surveillance systems worldwide due to its high incidence in AFP cases [ 10 ]. In the poliovirus eradication era, other non-polio EVs are being studied for their role as emerging pathogens associated with AFP, or as causing agents of central nervous system (CNS) disease outbreaks [ 10 – 13 ]. Human enterovirus A71 (EV-A71) has been historically associated with HFMD, including severe forms of the disease, and also is strongly associated with severe and sometimes fatal CNS infections.…”