due to Polio Type III surrounding the anterior spinal artery Poliovirus enters the body through the mouth, infecting the first cells with which it comes in contact – the
pharynx and
intestinal mucosa. It gains entry by binding to an
immunoglobulin-like receptor, known as the poliovirus receptor or
CD155, on the cell membrane. The virus then hijacks the
host cell's own machinery, and begins to
replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the
tonsils (specifically the
follicular dendritic cells residing within the tonsilar
germinal centers), the intestinal
lymphoid tissue including the
M cells of
Peyer's patches, and the deep
cervical and
mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream. Known as
viremia, the presence of a virus in the bloodstream enables it to be widely distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks. In a small percentage of cases, it can spread and replicate in other sites, such as
brown fat, the
reticuloendothelial tissues, and muscle. This sustained replication causes a major viremia, and leads to the development of minor influenza-like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local
inflammatory response. In most cases, this causes a self-limiting inflammation of the
meninges, the layers of tissue surrounding the
brain, which is known as nonparalytic aseptic meningitis. The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance event – largely independent of the age, gender, or
socioeconomic position of the individual. The destruction of neuronal cells produces
lesions within the
spinal ganglia; these may also occur in the
reticular formation,
vestibular nuclei,
cerebellar vermis, and deep
cerebellar nuclei. The likelihood of developing paralytic polio increases with age, as does the extent of paralysis. In children, nonparalytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only one in 1000 cases. In adults, paralysis occurs in one in 75 cases. In children under five years of age, paralysis of one leg is most common; in adults, extensive paralysis of the
chest and
abdomen also affecting all four limbs –
quadriplegia – is more likely. Paralysis rates also vary depending on the serotype of the infecting poliovirus; the highest rates of paralysis (one in 200) are associated with poliovirus type 1, the lowest rates (one in 2,000) are associated with type 2.
Spinal polio s in the
anterior horn cells of the
spinal column Spinal polio, the most common form of paralytic poliomyelitis, results from viral invasion of the motor neurons of the
anterior horn cells, or the
ventral (front)
grey matter section in the
spinal column, which are responsible for movement of the muscles, including those of the
trunk,
limbs, and the
intercostal muscles. Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron
ganglia. When spinal neurons die,
Wallerian degeneration takes place, leading to weakness of those muscles formerly
innervated by the now-dead neurons. With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles
atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed. The extent of spinal paralysis depends on the region of the cord affected, which may be
cervical,
thoracic, or
lumbar. The virus may affect muscles on both sides of the body, but more often the paralysis is
asymmetrical. Any
limb or combination of limbs may be affected – one leg, one arm, or both legs and both arms. Paralysis is often more severe
proximally (where the limb joins the body) than
distally (the
fingertips and
toes).
Bulbar polio Making up about two percent of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the
bulbar region of the
brain stem. The bulbar region is a
white matter pathway that connects the
cerebral cortex to the brain stem. The destruction of these nerves weakens the muscles supplied by the
cranial nerves, producing symptoms of
encephalitis, and causes
difficulty breathing, speaking and swallowing. Critical nerves affected are the
glossopharyngeal nerve (which partially controls swallowing and functions in the throat, tongue movement, and taste), the
vagus nerve (which sends signals to the heart, intestines, and lungs), and the
accessory nerve (which controls upper neck movement). Due to the effect on swallowing, secretions of
mucus may build up in the airway, causing suffocation. Other signs and symptoms include
facial weakness (caused by destruction of the
trigeminal nerve and
facial nerve, which innervate the cheeks,
tear ducts, gums, and muscles of the face, among other structures),
double vision, difficulty in chewing, and abnormal
respiratory rate, depth, and rhythm (which may lead to
respiratory arrest).
Pulmonary edema and
shock are also possible and may be fatal.
Bulbospinal polio Approximately 19 percent of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory or bulbospinal polio. Here, the virus affects the upper part of the cervical spinal cord (
cervical vertebrae C3 through C5), and paralysis of the
diaphragm occurs. The critical nerves affected are the
phrenic nerve (which drives the diaphragm to inflate the
lungs) and those that drive the muscles needed for swallowing. By destroying these nerves, this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a
ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions. == Diagnosis ==