Polio is an acute infection caused by poliovirus (enterovirus). It manifests itself in some forms:
- mild febrile state (abortive poliomyelitis);
- aseptic meningitis without paralysis (nonparalytic polio);
- lethargy and weakness of various muscle groups (paralytic poliomyelitis).
The diagnosis is clinical, although laboratory confirmation is possible. The treatment is supportive.
Polio viruses have 3 serotypes. Type 1 most often causes paralysis and epidemics. People are the only natural carrier. Infection is extremely contagious with direct contact. Asymptomatic and minor infections (abortive polio) are more common than non-paralytic or paralytic infections and are the main source of spread.
Ubiquitous vaccination almost destroyed the disease. However, cases are still reported in regions with incomplete immunization, such as sub-Saharan Africa and South Asia. In 2017, 22 cases of wild-type 1 poliovirus were recorded (Afghanistan – 14 cases; Pakistan – 8 cases) and 91 cases of circulating vaccine poliovirus (Democratic Republic of the Congo – 17 cases; Syria – 74 cases).
Most (70–75%) cases of infection are asymptomatic. Clinical disease is classified as:
- abortive polio. Most clinical manifestations of the forms of infection, especially among young children, are mild: for 1-3 days, low body temperature persists, malaise, headache, sore throat and vomiting, which develop 3-5 days after infection. There are no neurological symptoms or signs. A physical examination does not reveal anything except fever.
- paralytic polio and nonparalytic polio. Approximately 4% of patients with poliovirus infection develop a non-paralytic lesion of the central nervous system with aseptic meningitis. Patients usually complain of stiff neck muscles and/or back pain, headaches that occur after several days of prodrome, similar to abortive poliomyelitis. Manifestations last from 2 to 10 days.
- the paralytic form of poliomyelitis occurs in <1% of all cases of poliovirus infections. It can manifest itself as a two-phase disease in infants and young children with a paralytic phase that occurs several days after the symptoms of abortive polio are eliminated. The incubation period is usually 7–21 days.
Common manifestations of paralytic poliomyelitis in addition to aseptic meningitis include deep muscle pain, hyperesthesia, paresthesia. With the development of active myelitis, urinary retention, and muscle cramps may appear. Asymmetric flaccid paralysis may occur, which progresses in 2–3 days. Sometimes signs of encephalitis predominate.
Dysphagia, nasal regurgitation and nasal congestion are usually the earliest signs of a bulbar lesion, but some patients develop pharyngeal paralysis and cannot control the oral cavity secretion. As with skeletal muscle paralysis, bulbar palsy can worsen in 2-3 days and in some patients affects the respiratory and circulatory centers of the brain stem, which leads to respiratory failure. Sometimes respiratory failure develops with damage to the diaphragm or intercostal muscles.
Some patients develop post-poliomyelitis years or decades after paralytic poliomyelitis. This syndrome is characterized by muscle weakness and decreased stamina, often accompanied by fatigue, fasciculations, and atrophy.
- Lumbar puncture;
- Viral culture (feces, oropharynx, CSF);
- PCR with reverse blood transcription or CSF;
- Serological tests for serotypes of poliovirus, enteroviruses, and West Nile virus.
When there is no manifestation of the central nervous system, poliomyelitis (abortive poliomyelitis) resembles other systemic viral infections. As a rule, this disease is not taken into account, not diagnosed, except during an epidemic.
Nonparalytic polio resembles other viral lesions of the nervous system. Such patients usually undergo lumbar puncture; typical CSF results are normal glucose, slightly elevated protein, and a cell count of 10–500/μl (lymphocyte predominance). Detection of the virus in a smear from the throat, feces or CSF, or an increase in the titer of specific antibodies, confirms the poliovirus infection but is usually not required for patients with uncomplicated aseptic meningitis.
Paralytic poliomyelitis can be suspected in unimmunized children or young adults with asymmetric flaccid paralysis of the extremities or bulbar paralysis without sensitivity disturbances that occurred during acute febrile disease. However, a certain group A and B of Coxsackie viruses (especially A7), some echoviruses and enterovirus 71 can provoke such phenomena. In addition, cases of focal limb weakness or paralysis were detected after infection with enterovirus D68. West Nile virus infection can also cause acute flaccid paralysis, which is clinically indistinguishable from paralytic poliomyelitis caused by poliomyelitis viruses. Guillain-Barré syndrome causes flaccid paralysis. It can be distinguished by the following criteria:
- usually does not cause a fever;
- muscle weakness is symmetrical;
- sensory impairment is observed in 70% of patients;
- the level of protein in the CSF is usually elevated, the number of cells in the CSF is normal.
Epidemiological information (e.g. immunization history, recent travel, age, season) may help identify the disease’s cause. Since the identification of the polio-myelitis virus or other enteroviruses as the cause of acute flaccid paralysis is important for healthcare, inoculation of the virus from swabs of the nasopharynx, feces, and CSF, as well as PCR with reverse transcription of CSF and blood should be done in all cases. Specific serological tests for polioviruses, other enteroviruses, and the West Nile virus should also be performed.
In the case of non-paralytic polio, recovery is complete. In paralytic polio, approximately 2/3 of patients have a permanent residual weakness. Bulbar palsy is better treated than peripheral paralysis. Mortality is 4–6%, but increases to 10–20% in adults and in patients with severe stem disorders.
The standard polio treatment is supportive. The therapy includes rest, analgesics and antipyretics if necessary. There is no specific antiviral therapy.
During active myelitis, precautions should be taken to avoid complications of bed rest (for example, deep venous thrombosis, atelectasis, urinary tract infection), but prolonged bed rest (despite the possibility of contractures) may be necessary. Respiratory failure requires mechanical ventilation. Mechanical ventilation and bulbar palsy require intensive measures for the rehabilitation of the respiratory tract.
All infants and children should be vaccinated with the polio vaccine. The American Academy of Pediatrics recommends vaccination at the age of 2 months, 4 months and 6 to 18 months, as well as a booster dose at the age of 4-6 years (Recommended vaccination schedule at the age of 0-6 years). Vaccination in childhood gives immunity in> 95% of recipients.
An inactivated Salk poliovirus vaccine (IPV) is preferred over the live attenuated oral Sabin polio vaccine (OPV). An attenuated virus in PPV can mutate into a strain that can cause paralytic polio, which occurs in about 1 case per 2.400.000 doses of PPV. In this regard, the PVP vaccine is no longer available in the United States. In addition, type 2 poliovirus was removed from the PPV in 2016 due to outbreaks caused by a genetically dissimilar and vaccine-derived virus, despite the formal elimination of wild type 2 poliovirus. There were no severe consequences for IPV.
Adults are not usually vaccinated. Unvaccinated adults traveling to endemic or epidemic areas should be vaccinated with IPV. Vaccination includes 2 doses, administered with an interval of 4-8 weeks, the third dose after 6-12 months. At least 1 dose should be done before the trip. Vaccinated adults traveling to endemic or epidemic areas need to re-enter 1 dose of IPV. Patients with weakened immunity and their homes should not use OPV.