Anish Chaudhary Department of Microbiology Poliomyelitis Anish Chaudhary Department of Microbiology

Introduction: Poliomyelitis (polios = grey; myelitis: inflammation of spinal cord) is an acute infectious disease that in its serious form affects the central nervous system (CNS). Transmitted by faeco-oral route; less oftenly by droplet infection and conjunctival transfer. The destruction of motor neurons in the spinal cord results in flaccid paralysis. However, most poliovirus infections are subclinical. Belongs to the Picornaviridae in the genera: Enterovirus. Enterovirus of medical importance include: poliovirus 1-3, Coxsackievirus A types 1-24, Coxsackievirus B types 1-6, Echovirus types 1-34 and Enterovirus types 68-71.

The worldwide prevalence of poliomyelitis has decreased by more than 99% due to improved socioeconomic conditions and availability of vaccines. Morphology: Spherical particles about 27 nm in diameter Composed of 60 subunits, each consisting of four viral proteins (VP1-VP4) arranged in icosahedral symmetry. VP1 which faces outside; contains the major antigenic site for combination with type-specific neutralizing antibodies. Genome consists of single stranded positive sense RNA which can be directly translated by host ribosomes to form a polyprotein. The genome is polyadenylated at the 3′ end and has a small viral-coded protein (VPg) covalently bound to the 5′ end.

Antigenic properties: Classified into 3 serotypes (type: 1, 2 and 3) on the basis of neutralization test. Type 1 is the most common and cause most of the epidemics. Type 2 usually causes endemic infections. Type 3 strains have caused epidemics. Immunity is type specific. Two antigens, C (coreless or capsid) and D (dense) are recognized by enzyme-linked immunosorbent assay or precipitation test.

Pathogenesis: Reservoir of infection: Infected humans excreting poliovirus in their stool. Source of infection: Infected stool containing poliovirus throat secretions containing polio virus during early stage of the illness may also be another source of infection. Mode of infection: primarily by the fecal–oral route by ingestion of food and water contaminated with human faeces. Inhalation or entry through conjunctiva of droplets of respiratory secretions. Poor sanitation, low socioeconomic status, and crowded living conditions facilitate transmission of infection.

Steps in pathogenesis: Through faeco-oral route or any other route enters the body. Infects and multiplies in the tonsils and Peyer’s patch of the ileum. Spreads to regional lymph nodes and enters the blood, causing a primary viremia. On continued infection and multiplication of virus in the reticuloendothelial cells, it invades the blood stream again and causes secondary viremia. During this period of viremia, the poliovirus crosses the blood–brain barrier or gains access to the brain by transfer through nerves from infected muscles.

Direct neural transmission to the central nervous system may also occur under special circumstances (poliomyelitis following tonsillectomy). In CNS, multiplies selectively in the neurons, anterior horn cells of the spinal cord, dorsal root ganglia, and motor neurons and destroys them. Destruction of motor neurons leads to paralysis of the muscles innervated by those neurons. Infected neurons undergo degeneration. Earliest change in neuron: degeneration of nissil body. Also infects the brain stem, causing bulbar poliomyelitis associated with respiratory paralysis. Pathological changes in the CNS is solely responsible for symptoms of the disease.

Causes wide spectrum of illness in unvaccinated people like: Clinical features: Causes wide spectrum of illness in unvaccinated people like: asymptomatic illness Abortive poliomyelitis nonparalytic poliomyelitis Paralytic polio Postpoliomyelitis syndrome Incubation period: usually 10 days but may range from 4 days to 4 weeks. Asymptomatic illness: 90–95% of exposed individuals develop inapparent and asymptomatic infection. This is due to viral infection confined to oropharynx or intestine. This types of infection leads to seroconversion alone.

Abortive poliomyelitis: Minor illness occuring in 5% of infected individuals. Febrile illness characterised by fever, headache, sore throat, loss of appetite, vomiting, and abdominal pain. Neurological symptoms: typically absent The duration of illness: usually less than 5 days. Nonparalytic poliomyelitis: also known as aseptic meningitis caused by invasion of virus into the CNS Symptoms similar to those of abortive poliomyelitis but are more intense. Stiffness of the posterior muscles of the neck, trunk, and limbs is present in addition to the symptoms of the minor illness. occurs in 1–2% of infected patients.

Most severe manifestation of poliomyelitis Paralytic polio: Major illness, which occurs in 0.1–2% of individuals infected with poliovirus. Most severe manifestation of poliomyelitis Appears 3–4 days after the abortive poliomyelitis has subsided. This condition results due to invasion of virus from blood to the anterior horn cells of the spinal cord and the motor cortex of the brain. Depending on the various tissues or organs affected and the intensity of neuronal infection, poliomyelitis may be of two types, as follows: Paralytic poliomyelitis: Bulbar poliomyelitis:

Paralytic poliomyelitis: Also called spinal paralysis. characterized by spinal paralysis involving one or more limbs. typical manifestation: asymmetrical flaccid paralysis with no sensory loss Caused mostly by poliovirus type 1 Also seen in vaccinated individuals following vaccination. The condition may progress to death or may recover completely with residual paralysis. Bulbar poliomyelitis: caused due to involvement of the cranial nerves, most commonly 9th, 10th, and 12th.

Post-poliomyelitis syndrome: condition tends to be more severe with involvement of the muscles of the pharynx, vocal cords, and respiration. may cause death in 75% of the patients. Post-poliomyelitis syndrome: Sequelae of poliomyelitis, which may develop 20–40 years after infection with poliovirus. Seen in 20–80% of patients who have recovered from poliomyelitis. Recurrence of weakness or fatigue is observed in this condition. Usually involves the muscles that were initially affected by the poliovirus.

Laboratory Diagnosis: Specimen: Stool, throat swab, and cerebrospinal fluid (CSF) Viruses can be isolated from feces for more than 30 days during the illness and from the throat swab during the first few days of the illness. Rarely from CSF. Microscopy: Microscopic examination of CSF shows predominantly lymphocytic pleocytosis with the presence of 25–500 cells/mm3. Virus rarely demonstrated in CSF. Electron microscopy of faeces is helpful.

Isolation of the virus: Isolation of viruses from clinical specimen by tissue culture is the most specific method in the diagnosis of poliomyelitis. Cell culture: Specimens (faeces and throat swab) are inoculated into monkey kidney, human amnion, HeLa, Hep-2, Buffalo green monkey (BGM), MRC-5, and other cell cultures. Cytopathic effect produced by the virus is observed after 48 hours. Cytopathic effects: cell retraction, increased refractivity, cytoplasmic granularity, and nuclear pyknosis. Identification of serotype: by neutralization test

Serodiagnosis: less frequently used for diagnosis of poliomyelitis. Based on detection of 4th fold rise in antibody titre collected during acute and convalescent phase of illness. Neutralization or complement fixation test is done. Molecular technique: PCR Treatment: no specific treatment Prevention: maintaining proper sanitation and vaccination.

Polio vaccine: 2 types: oral polio vaccine and injectable or inactivated polio vaccine Live attenuated oral polio vaccine: Also called Sabin vaccine. Developed by Albert Sabin in the year 1962. Contains live attenuated strains of the three serotypes of poliovirus cultured in monkey kidney cells or human diploid cells. Given orally, which causes natural infection.

Elicits production of both local secretory IgA antibodies in the pharynx and alimentary tract, and humoral IgG antibodies in the serum The virus lacks the capability to multiply in the CNS, hence is non-neurovirulent. The vaccine virus is excreted for several weeks in the feces during which the vaccine virus spread may occur to close contacts, inducing or boosting immunity in them. The first dose of vaccine is given to infants at age of 1½ months along with DPT. Second, third, and fourth doses of vaccine are given when children are raised to 2½, 3½, and 16–24 months, respectively.

Injectable or inactivated polio vaccine: Also called as Salk vaccine Developed by Jonas Salk in 1956 The vaccine contains formalin inactivated strains of the three serotypes of the poliovirus grown in monkey kidney cell culture. The vaccine is given by deep subcutaneous or intramuscular injections in three doses. The vaccine is given at 2 months, 4 months, and at school entry, which is usually at 4 years.

It does not cause development of vaccine-associated poliomyelitis (VAP). The vaccine elicits the production of higher IgG antibody titers in the serum, but it does not stimulate the production of detectable level of secretory IgA in the gut. Can be safely used for immunization in immunocompromised hosts.