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CRISBERT I. CUALTEROS, M.D. (+63919)8586556


The polioviruses are non-enveloped, positive-stranded RNA viruses belonging to the Picornaviridae family, in the genus Enterovirus, and include three antigenically distinct serotypes (types 1, 2, and 3). Polioviruses spread from the intestinal tract to the central nervous system (CNS), where they cause aseptic meningitis and poliomyelitis, or polio. The polioviruses are extremely hardy and can retain activity for several days at room temperature, and can be stored indefinitely frozen at -20°C. They are rapidly inactivated by heat (>56°C), formaldehyde, chlorination, and ultraviolet light. Polioviruses grow well in many cell cultures and rapidly cause cytopathic effects.

In 1952 there were 57,879 reported cases of polio in the United States, including 21,269 cases of paralytic polio that resulted in more than 3,000 deaths, with similar epidemics being reported in Europe. These epidemics appeared to affect mostly adolescents and young adults and were growing at a steady pace, which spurred development of the Salk inactivated poliovirus vaccine, and Sabin, Cox, and Koprowski live attenuated vaccines. The universal use of the Salk and Sabin vaccines has resulted in the almost complete global eradication of polio.
The most devastating result of poliovirus infection is paralysis, but more than 90% of infections are asymptomatic or inapparent but do induce protective immunity. Clinically apparent but nonparalytic illness occurs in about 5% of all infections, with paralytic polio occurring in about 1 out of 1,000 infections among infants to about 1 out of 100 infections among adolescents. Prior to the introduction of vaccines in the United States and Europe, improvements in sanitation had limited the fecal-oral spread of polioviruses, resulting in epidemics of infection occurring later in life, when 1 in every 100 infections resulted in paralysis. Thus, in developed countries prior to universal vaccination, epidemics of paralytic poliomyelitis were observed among adolescents. Conversely, in developing countries where sanitation was and continues to be poor, infection early in life results in infantile paralysis. Undoubtedly, good sanitation explains the virtual eradication of polio as a disease from the United States in the early 1960s, when only about two thirds of the population was immunized with the Salk vaccine, and the subsequent absence of circulating wild-type poliovirus in the United States and Europe. In contrast, poor sanitation and crowding have permitted the continued transmission of poliovirus in certain poor countries in Africa and Asia, despite massive global efforts to eradicate polio, in some areas with an average of 12–13 doses of polio vaccine administered to children younger than 5 yr of age.
Humans are the only known reservoir for the polioviruses. Poliovirus has been isolated from feces more than 2 wk before paralysis to several weeks after the onset of symptoms.
Polioviruses infect cells by adsorbing to specific genetically determined receptors, including poliovirus receptor (PVR). The virus penetrates the cell and is then uncoated and releases RNA. The RNA is translated to produce proteins responsible for replication of the RNA, shut-off of host-cell protein synthesis, and synthesis of structural elements that compose the capsid. Mature virus particles are produced in 6–8?hr and are released into the environment by disruption of the cell.
In the contact host, polioviruses gain entry through the gastrointestinal tract. The pathology of vaccine-associated poliomyelitis (VAPP) mimics natural disease. The primary site of replication may be in M cells lining the mucosa of the small intestine. Regional lymph nodes are infected, and primary viremia occurs after 2–3 days. The virus seeds multiple sites, including the reticuloendothelial system, the brown fat deposits, and skeletal muscle. Poliovirus probably accesses the CNS along peripheral nerves. Because poliovirus replicates in endothelial cells, the theory of viremic spread to the CNS was favored; however, poliovirus has almost never been cultured from the cerebrospinal fluid (CSF) of patients with paralytic disease, and patients with aseptic meningitis caused by poliovirus never have paralytic disease. With the first appearance of non-CNS symptoms, a secondary viremia probably occurs as a result of enormous viral replication in the reticuloendothelial system.
The exact mechanism of entry into the CNS is not known. Once entry is gained, however, the virus may traverse neural pathways, and multiple sites within the CNS are often affected. The effect on motor and vegetative neurons is most striking and correlates with the clinical manifestations. Perineuronal inflammation, a mixed inflammatory reaction with both polymorphonuclear leukocytes and lymphocytes, is associated with extensive neuronal destruction. Petechial hemorrhages and considerable inflammatory edema also occurs in areas of poliovirus infection. The poliovirus primarily infects motor neuron cells in the spinal cord (the anterior horn cells) and the medulla oblongata (the cranial nerve nuclei). Because of the overlap in muscle innervation by adjacent 2–3 segments of the spinal cord, clinical signs of weakness in the limbs develop when more than 50% of motor neurons are destroyed. In the medulla, less extensive lesions cause paralysis and involvement of the reticular formation that contains the vital centers controlling respiration and circulation, which may have a catastrophic outcome. Involvement of the intermediate and dorsal horn and dorsal root ganglia in the spinal cord cause the typical hyperesthesia and myalgias that are seen in acute poliomyelitis. Other neurons affected are the nuclei in the roof and vermis of the cerebellum, the substantia nigra, and occasionally the red nucleus in the pons; there may be variable involvement of thalamic, hypothalamic, and pallidal nuclei and the motor cortex.
Apart from the histopathology of the CNS, inflammatory changes occur generally in the reticuloendothelial system. Inflammatory edema and sparse lymphocytic infiltration are prominently associated with hyperplastic lymphocytic follicles.
Infants acquire immunity transplacentally from their mothers; the immunity disappears at a variable rate during the first 4–6 mo of life. Active immunity after natural infection is probably lifelong but protects against the infecting serotype only; infections with other serotypes are possible. Poliovirus neutralizing antibodies develop within several days after exposure as a result of replication of the virus in the M cells in the intestinal tract and deep lymphatic tissues. This early production of circulating immunoglobulin (Ig) G antibodies protects against CNS invasion. Local (mucosal) immunity, conferred mainly by secretory IgA, is an important defense against subsequent re-infection of the gastrointestinal tract.
Clinical Manifestations.
The incubation period of poliovirus from contact to initial clinical symptoms is usually considered to be 8–12 days, with a range of 5–35 days. Poliovirus infections may follow one of several courses: inapparent infection, which occurs in 90–95% of cases and causes no disease and no sequelae; abortive poliomyelitis; nonparalytic poliomyelitis; or paralytic poliomyelitis. Paralysis, if it occurs, appears 3–8 days after the initial symptoms.
In about 5% of patients, a nonspecific influenza-like syndrome occurs 1–2 wk after infection; this is termed abortive poliomyelitis. Fever, malaise, anorexia, and headache are prominent features, and there may be sore throat and abdominal or muscular pain. Vomiting occurs irregularly. The illness is short-lived (up to 2–3 days). The physical examination may be normal or may reveal nonspecific pharyngitis, abdominal or muscular tenderness, and weakness. Recovery is complete, and no neurologic signs or sequelae develop.
In about 1% of all infected patients, the signs of abortive poliomyelitis are present but headache, nausea, and vomiting are more intense, and there is soreness and stiffness of the posterior muscles of the neck, trunk, and limbs. Fleeting paralysis of the bladder and constipation are frequent. Approximately two thirds of these children have a short symptom-free interlude between the first phase (minor illness) and the second phase (CNS disease or major illness). This two-phase course is less common in adults, in whom the evolution of symptoms is more insidious. Nuchal and spinal rigidity are the basis for the diagnosis of nonparalytic poliomyelitis during the second phase.
Physical examination reveals nuchal-spinal signs and changes in superficial and deep reflexes. In cooperative patients the nuchal-spinal signs are first sought by active tests. The patient is asked to sit up unassisted. If this causes undue effort and if the

knees flex upward and the patient writhes a bit from side to side in sitting up and uses the hands on the bed to assume the tripod supporting position, spinal rigidity is unmistakable. While sitting, the patient is asked to flex the chin to the chest and is observed for nuchal rigidity. Alternatively, in the supine position, with the knees held down gently, the patient is asked to sit up and kiss his or her knees. If the knees draw up sharply or if the maneuver cannot be adequately completed, there is stiffness of the spine, which is a result of muscle spasm. If the diagnosis is still uncertain or in infants, attempts should be made to elicit the Kernig and Brudzinski signs. Gentle forward flexion of the occiput and neck will elicit nuchal rigidity. Head drop is demonstrated by placing the hands under the patient's shoulders and raising the trunk. Although normally the head follows the plane of the trunk, in poliomyelitis it often falls backward limply but is not due to true paresis of the neck flexors. In struggling infants it may be difficult to distinguish voluntary resistance from clinically important true nuchal rigidity. One may place the infant's shoulders flush with the edge of the table, support the weight of the occiput in the hand, and then flex the head anteriorly. True nuchal rigidity will persist during this maneuver. When open, the anterior fontanel may be tense or bulging.
In the early stages the reflexes are normally active and remain so unless paralysis supervenes. Changes in reflexes, either increased or decreased, may precede weakness by 12–24?hr; hence, it is important to test reflexes, especially in nonparalytic patients managed at home. The superficial reflexes, the cremasteric and abdominal reflexes, and the reflexes of the spinal and gluteal muscles are usually the first to diminish. The spinal and gluteal reflexes may disappear before the abdominal and cremasteric reflexes. Changes in the deep tendon reflexes generally occur 8–24?hr after the superficial reflexes are depressed and indicate impending paresis of the extremities. Tendon reflexes are absent with paralysis. Sensory defects do not occur in poliomyelitis.
Paralytic poliomyelitis develops in about 0.1% of persons infected with poliovirus, causing three clinically recognizable syndromes that represent a continuum of infection differentiated only by the portions of the CNS most severely affected. These are (1) spinal paralytic poliomyelitis, (2) bulbar poliomyelitis, and (3) polioencephalitis.
Spinal Paralytic Poliomyelitis. Spinal paralytic poliomyelitis may occur as the second phase of a biphasic illness, the first phase of which corresponds to abortive poliomyelitis. The patient then appears to recover and feels better for 2–5 days, after which severe headache and fever occur with exacerbation of the previous systemic symptoms. Severe muscle pain is present and sensory and motor phenomena (e.g., paresthesia, hyperesthesia, fasciculations, and spasms) may develop. On physical examination the distribution of paralysis is characteristically spotty. Single muscles, multiple muscles, or groups of muscles may be involved in any pattern. Within 1–2 days, asymmetric flaccid paralysis or paresis occurs. Involvement of one leg is most common, followed by involvement of one arm. The proximal areas of the extremities tend to be involved to a greater extent than the distal areas. To detect mild muscular weakness, it is often necessary to apply gentle resistance in opposition to the muscle group being tested. Examination at this point may reveal nuchal stiffness or rigidity, muscle tenderness, initially hyperactive deep tendon reflexes (for a short period) followed by absent or diminished reflexes, and paresis or flaccid paralysis. In the spinal form there is weakness of some of the muscles of the neck, abdomen, trunk, diaphragm, thorax, or extremities. Sensation is intact; sensory disturbances, if present, suggest a disease other than poliomyelitis.
The paralytic phase of poliomyelitis is extremely variable; some patients progress during observation from paresis to paralysis, whereas others recover, which may be slow or rapid. The extent of paresis or paralysis is directly related to the extent of neuronal involvement; paralysis occurs if more than 50% of the neurons supplying the muscles are destroyed. The extent of involvement is usually obvious within 2–3 days; only rarely does progression occur beyond this interval. Paralysis of the lower limbs is often accompanied by bowel and bladder dysfunction ranging from transient incontinence to paralysis with constipation and urinary retention.
The onset and course of paralysis are variable and age-related. Infants and young children most frequently manifest the biphasic course, with prominent prodromal symptoms. Older persons may have a single phase in which prodromal symptoms and paralysis occur in a continuous fashion. In developing countries, where a history of intramuscular injections precedes paralytic poliomyelitis in about 50–60% of patients, patients may present initially with fever and paralysis without the characteristic biphasic course (provocation paralysis). The degree and duration of muscle pain are also variable; some patients have none, and others complain for days or weeks. Spasm and increased muscle tone with a transient increase in deep tendon reflexes occur in some patients, whereas in others flaccid paralysis may occur abruptly. Once the temperature returns to normal, no further paralytic manifestations are noted in most patients. Little recovery from paralysis is noted in the first days or weeks but, if it is to occur, is usually evident within 6 mo. The return of strength and reflexes is slow and may continue to improve as long as 18 mo after the acute disease. Lack of improvement from paralysis within the first several weeks or months after onset is usually evidence of permanent paralysis. Atrophy of the limb, failure of growth, and deformity is common and is especially evident in the growing child.
Bulbar Poliomyelitis. Bulbar poliomyelitis may occur as a clinical entity without apparent involvement of the spinal cord. Yet the infection is a continuum, and designation of the disease as bulbar implies only dominance of the clinical manifestations by dysfunctions of the cranial nerves and medullary centers. The clinical findings seen with bulbar poliomyelitis with respiratory difficulty (other than paralysis of extraocular, facial, and masticatory muscles) include (1) nasal twang to the voice or cry caused by palatal and pharyngeal weakness (hard-consonant words such as “cookie” or “candy” bring this out best); (2) inability to swallow smoothly, resulting in accumulation of saliva in the pharynx, indicates partial immobility (holding the larynx lightly and asking the patient to swallow will confirm such immobility); (3) accumulated pharyngeal secretions, which may cause irregular respirations because each inspiration must be “planned” to avoid aspirating; the respirations may thus appear interrupted and abnormal even to the point of falsely simulating intercostal or diaphragmatic weakness; (4) absence of effective coughing, shown by constant fatiguing efforts to clear the throat; (5) nasal regurgitation of saliva and fluids as a result of palatal paralysis, with inability to separate the oropharynx from the nasopharynx during swallowing; (6) deviation of the palate, uvula, or tongue; (7) involvement of vital centers in the medulla, which are manifested by irregularities in rate, depth, and rhythm of respiration; by cardiovascular alterations including blood pressure changes (especially increased blood pressure), alternate flushing and mottling of the skin, and cardiac arrhythmias; and by rapid changes in body temperature; (8) paralysis of one or both vocal cords, causing hoarseness, aphonia, and ultimately asphyxia unless this is recognized by laryngoscopy and managed by immediate tracheostomy; and (9) the rope sign, an acute angulation between the chin and larynx caused by weakness of the hyoid muscles (the hyoid bone is pulled posteriorly, narrowing the hypopharyngeal inlet).
Uncommonly, bulbar disease may culminate in an ascending paralysis (Landry type), in which there is progression cephalad from initial involvement of the lower extremities. Hypertension and other autonomic disturbances are common in bulbar involvement and may persist for a week or more or may be transient.

Occasionally, hypertension is followed by hypotension and shock and is associated with irregular or failed respiratory effort, delirium, or coma. This kind of bulbar disease may be rapidly fatal.
The course of bulbar disease is variable; some patients die as a result of extensive, severe involvement of the various centers in the medulla; others recover partially but require ongoing respiratory support, and others recover completely. Cranial nerve involvement is seldom permanent. Atrophy of muscles may be evident, patients immobilized for long periods may develop pneumonia, and renal stones may form as a result of hypercalcemia and hypercalciuria secondary to bone resorption.
Polioencephalitis. Polioencephalitis is a rare form of the disease in which higher centers of the brain are severely involved. Seizures, coma, and spastic paralysis with increased reflexes may be observed. Irritability, disorientation, drowsiness, and coarse tremors not explained by inadequate ventilation are noted; peripheral or cranial nerve paralysis coexists or ensues. Hypoxia and hypercapnia caused by inadequate ventilation due to respiratory insufficiency may produce disorientation without true encephalitis. The manifestations are common to encephalitis of any cause and can only be attributed to polioviruses by specific viral diagnosis or if accompanied by flaccid paralysis.
Paralytic Poliomyelitis with Ventilatory Insufficiency. A number of components acting together may produce ventilatory insufficiency resulting in hypoxia and hypercapnia, which may produce profound effects on many other systems. Because respiratory insufficiency may develop rapidly, close continued clinical evaluation is essential. Despite weakness of the respiratory muscles, the patient may respond with so much respiratory effort (associated with anxiety and fear) that overventilation may occur at the outset, resulting in respiratory alkalosis. Such effort is fatiguing and contributes to respiratory failure.
There are certain characteristic patterns of disease. Pure spinal poliomyelitis with respiratory insufficiency involves tightness, weakness, or paralysis of the respiratory muscles (chiefly the diaphragm and intercostals) without discernible clinical involvement of the cranial nerves or vital centers that control respiration, circulation, and body temperature. The cervical and thoracic spinal cord segments are chiefly affected. Pure bulbar poliomyelitis involves paralysis of the motor cranial nerve nuclei with or without involvement of the vital centers. Involvement of the 9th, 10th, and 12th cranial nerves results in paralysis of the pharynx, tongue, and larynx with consequent airway obstruction. Bulbospinal poliomyelitis with respiratory insufficiency affects the respiratory muscles and results in coexisting bulbar paralysis.
The clinical findings associated with involvement of the respiratory muscles include (1) anxious expression; (2) inability to speak without frequent pauses, resulting in short, jerky, “breathless” sentences; (3) increased respiratory rate; (4) movement of the ala nasi and of the accessory muscles of respiration; (5) inability to cough or sniff with full depth; (6) paradoxical abdominal movements caused by diaphragmatic immobility due to spasm or weakness of one or both leaves; and (7) relative immobility of the intercostal spaces, which may be segmental, unilateral, or bilateral. When the arms are weak, and especially when deltoid paralysis occurs, there may be impending respiratory paralysis because the phrenic nerve nuclei are in adjacent areas of the spinal cord. Observation of the patient's capacity for thoracic breathing while the abdominal muscles are splinted manually indicates minor degrees of paresis. Light manual splinting of the thoracic cage will help to assess the effectiveness of diaphragmatic movement.
Poliomyelitis should be considered in any unimmunized or incompletely immunized child with nonspecific febrile illness, aseptic meningitis, or paralytic disease. VAPP should be considered in any child with paralytic disease occurring 7–14 days after receiving oral poliovirus vaccine. VAPP can occur at later times after administration, and should be considered in any child with paralytic disease in countries or regions where wild type poliovirus has been eradicated and OPV has been administered to the child or a contact. The combination of fever, headache, neck and back pain, asymmetric flaccid paralysis without sensory loss, and pleocytosis does not regularly occur in any other illness.
The World Health Organization (WHO) currently recommends that the laboratory diagnosis of poliomyelitis be confirmed by isolation and identification of poliovirus in the stool, with specific identification of wild-type and vaccine type strains. In suspected cases of acute flaccid paralysis, 2 stool specimens should be collected 24–48?hr apart, as soon as possible after the diagnosis of poliomyelitis is suspected. Poliovirus concentrations are high in the stool in the first week after the onset of paralysis, which is the optimal time for collection of stool specimens. Polioviruses may be isolated from 80 to 90% of acutely ill patients, whereas less than 20% may yield virus within 3–4 wk after onset of paralysis. Because most children with spinal or bulbospinal poliomyelitis have constipation, rectal straws may be used to obtain specimens; ideally a minimum of 8–10 grams should be collected. In laboratories that can isolate poliovirus, isolates should be sent to either the Centers for Disease Control and Prevention or to one of the WHO-certified poliomyelitis laboratories where DNA sequence analysis can be performed to distinguish between wild poliovirus and neurovirulent, revertant oral poliovirus vaccine strains. With the current WHO global plan for eradication of poliomyelitis worldwide, most regions of the world (the Americas, Europe, and Australia) have been certified wild-poliovirus free; in these areas, poliomyelitis is most often caused by vaccine strains. Hence it is critical to differentiate between wild type and revertant vaccine type strains.
The CSF, while often normal during the minor illness, demonstrates a pleocytosis between 20 and 300 cells/mm3 with CNS involvement; the cells in the CSF may be polymorphonuclear early in the disease but shift to mononuclear cells soon afterward. By the second week of the major illness, the CSF cell count falls to near-normal values. In contrast, the CSF protein is normal or only slightly elevated at the outset of CNS disease but usually rises to between 50–100?mg/dL by the second week of illness. In polioencephalitis the CSF may remain normal or show minor changes. Serologic testing demonstrates seroconversion or a fourfold or greater increase in antibody titers, when measured during the acute phase of illness and 3–6 wk later.
Poliomyelitis should be considered in the differential diagnosis of any case of paralysis, and is only one of many causes of acute flaccid paralysis in children and adults. The possibility of polio should be considered in any case of acute flaccid paralysis even in countries where polio has been eradicated. The diagnoses most often confused with polio are the Guillain-Barré syndrome, transverse myelitis, and traumatic paralysis due to sciatic nerve injury. In Guillain-Barré syndrome, which is the most difficult to distinguish from poliomyelitis, the paralysis is characteristically symmetric and sensory changes and pyramidal tract signs are common; these are absent in poliomyelitis. Fever, headache, and meningeal signs are less notable, and there are few cells but an elevated protein level in the CSF. Transverse myelitis progresses rapidly over hours to days, causing an acute symmetric paralysis of the lower limbs with concomitant anesthesia and diminished sensory perception. Autonomic signs of hypothermia in the affected limbs are common, and there is bladder dysfunction. The CSF is usually normal. Traumatic neuritis occurs from a few hours to a few days after the traumatic event, is asymmetric, acute, and affects only one limb. There is reduced or absent muscle tone and deep tendon reflects in the affected limb with pain in the gluteus. The CSF is normal.
There are numerous other causes of acute flaccid paralysis ( Table 228–1 ). In most conditions, the clinical features are sufficient to differentiate between these various causes, but in


TABLE 228-1 -- Differential Diagnosis of Acute Flaccid Paralysis
Site, Condition, Factor, or Agent
Clinical Findings
Onset of Paralysis
Progression of Paralysis
Sensory Signs and Symptoms
Reduced or Absent Deep Tendon Reflexes
Residual Paralysis
Anterior Horn Cells of Spinal Cord
Poliomyelitis (Wild and VAPP)
Incubation period
7–14 days
(4–35 days)
24–48?hr to onset of full paralysis; proximal > distal, asymmetric
Aseptic meningitis (moderate polymorphonuclear leukocytes at 2–3 days)
Nonpolio enterovirus
Hand-foot-and-mouth disease, aseptic meningitis, AHC
As in poliomyelitis
As in poliomyelitis
As in poliomyelitis
Other Neurotropic Viruses
Rabies virus

Months to years
Acute, symmetric, ascending
Varicella-zoster virus
Exanthematous vesicular eruptions
Incubation period
10–21 days
Acute, symmetric, ascending
Japanese encephalitis virus

Incubation period
5–15 days
Acute, proximal, asymmetric
Guillain-Barré Syndrome
Acute inflammatory polyradiculoneuropathy
Preceding infection, bilateral facial weakness
Hours to 10 days
Acute, symmetric, ascending (days to 4 wk)
Acute motor axonal neuropathy
Fulminant, widespread paralysis, bilateral facial weakness, tongue involvement
Hours to 10 days
1–6 days
Acute Traumatic Sciatic Neuritis
Intramuscular gluteal injection
Acute, asymmetrical
Hours to 4 days
Complete, affected limb
Acute transverse myelitis
Preceding Mycoplasma pneumoniae, Schistosoma, other parasitic or viral infection
Acute, symmetric hypotonia of lower limbs
Hours to days
Yes, early
Epidural abscess
Headache, back pain, local spinal tenderness, meningismus

Spinal cord compression; trauma

Hours to days
Exotoxin of Corynebacterium diphtheriae
In severe cases, palatal paralysis, blurred vision
Incubation period 1–8 wk (paralysis 8–12 wk after onset of illness)


Toxin of Clostridium botulinum
Abdominal pain, diplopia, loss of accommodation, mydriasis
Incubation period 18–36?hr
Rapid, descending, symmetric

Tick bite paralysis
Ocular symptoms
Latency period 5–10 days
Acute, symmetric, ascending

Diseases of the Neuromuscular Junction
Myasthenia gravis
Weakness, fatigability, diplopia, ptosis, dysarthria

Disorders of Muscle
Neoplasm, autoimmune disease
Subacute, proximal > distal
Weeks to months

Viral myositis

Hours to days

Metabolic Disorders
Hypokalemic periodic paralysis

Proximal limb, respiratory muscles
Sudden postprandial
ICU Weakness
Critical illness polyneuropathy
Flaccid limbs and respiratory weakness
Acute, following SIRS/sepsis
Hours to days
AHC = acute hemorrhagic conjunctivitis; ICU = intensive care unit; SIRS = systemic inflammatory response syndrome.
Modified from Marx A, Glass JD, Sutter RW: ifferential diagnosis of acute flaccid paralysis and its role in poliomyelitis surveillance. Epidemiol Rev 2000;22:298–316.


some cases nerve conduction studies and electromyograms in addition to muscle biopsies may be required.
Conditions causing pseudoparalysis do not present with nuchal-spinal rigidity or pleocytosis. These causes include unrecognized trauma, transient (toxic) synovitis, acute osteomyelitis, acute rheumatic fever, scurvy, and congenital syphilis (pseudoparalysis of Parrot).
Inasmuch as there are no specific antiviral agents for treating poliomyelitis, the management is supportive and aimed at limiting progression of disease, prevention of ensuing skeletal deformities, and preparation of the child and family for prolonged treatment required and for permanent disability if this seems likely. Patients with the nonparalytic and mildly paralytic forms of poliomyelitis may be treated at home. All intramuscular injections and surgical procedures are contraindicated during the acute phase of the illness, especially in the first week of illness, because these may result in progression of disease.


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