Paralytic Polio Or Poliomyelitis

Paralytic polio or poliomyelitis has been known since the late 18th century, perhaps even since ancient Egypt. The disease is caused by poliovirus, a member of the genus Enterovirus, family Picornaviridae. Until now have been isolated three strains of polio virus type 1 (Brunhilde), type 2 (Lansing), and type 3 (Leon). Infection can occur by one or more types. Widespread epidemics are usually caused by type 1. The virus is relatively resistant to almost all disinfectants (ethanol, isopropanol, lisol, quaternary ammonium, etc.). This virus does not have a fat envelope of fat that are resistant to solvents including ether and chloroform. The virus can diinaktifasi by formaldehyde, glutaraldehyde, a strong acid, sodium hypochlorite, and chlorine. Polio virus becomes inactive by heating above 42 degrees Celsius. In addition, drying and ultraviolet light can also eliminate the polio virus activity.

Poliovirus transmission mainly through the faecal-oral route and requires close contact. Prevalence of infection was highest in those who live with sufferers. Usually if one family member is infected, then the others also infected. Fecal contamination to the fingers, stationery, toys, food and beverages, is the main source of infection.
Travel Polio Disease

Now we discuss the course of the disease after being infected with polio virus. Polio virus attacks the only primates, including humans. Poliovirus entry through the gastrointestinal tract. Once inside, the virus will replicate (reproduce itself). It is not yet known for certain, specific cell types and places used these viruses to replicate the first time. Only, this virus can be isolated from lymphoid tissues in the gastrointestinal tract, so the first thought to place the virus replication in lymphoid tissue is the gastrointestinal tract, especially “Peyer patches” and tonsils. Even so, it is unclear whether the polio virus is replicating in that place or “just absorbed” by the lymphoid tissue after epithelial cells replicate in the gastrointestinal tract. This phase lasts 3-10 days, can be up to 3 weeks. Polio virus in this phase can be found in saliva and feces, and was instrumental in the process of transmission.

After multiply in the gut lymphoid tissue, the polio virus will spread through the blood (viremia) to go the other reticuloendothelial system, including lymph nodes, sunsum bone, liver, and spleen, and possibly to other places such as brown fat tissue and muscle.

Most of those infected with polio virus did not show any symptoms, or showed symptoms of the so-called abortive poliomyelitis (some call it a minor clinical phase of poliovirus infection). The symptoms resemble viral infections in general, namely fever, sore throat, gastrointestinal disturbances (nausea, vomiting, discomfort in the abdomen, constipation or diarrhea may be), and or influenza-like symptoms, characterized by headache, myalgia (muscle pain) , and the body felt weak. Most of those infected can cope with infections that occur before the second viremia arises.

About 5% of those infected, the virus after propagation in the reticuloendothelial system and elsewhere, will be the spread of the virus in the blood (viremia) the second. Although the central nervous system (probably) can be infected when the first viremia, but the majority occur after the second viremia (Here are the main points of the importance of polio vaccination. The explanation is more detail in a future article). Poliovirus infection in the central nervous system can cause meningitis (inflammation of the lining of the brain) aseptic (not accompanied by bacterial infection) of non-paralytic or paralytic poliomyelitis may include (paralytic = lose the ability to move / paralysis, partial or total). Infections of the central nervous system is what feared the polio virus infection.
Polio Virus Distribution Method

Polio virus is mainly transmitted from human to human, especially in the acute phase, along with a high titer of poliovirus in the pharynx and the feces. Suspected polio virus can spread through the respiratory system due to respiratory secretions is a material that proved infectious for other entero viruses. Even so, the respiratory tract has not been proven to be a pathway for transmission of polio virus. Oral transmission usually have a dominant role in the spread of polio virus in developed countries, whereas the fecal-oral transmission is most prevalent in poor areas. Food and drinks can be contaminated by flies or due to low hygienic. Another possible source of infection is the role of soil and water contaminated with fecal material, rice fields fertilized human feces, and irrigation water contaminated with poliovirus.

Poliovirus transmission mainly through the faecal-oral route and requires close contact. Prevalence of infection was highest in those who live with sufferers. Usually if one family member is infected, then the others also infected. Fecal contamination to the fingers, stationery, toys, food and beverages, is the main source of infection.

Factors affecting the spread of the virus is the population density, level of hygiene, water quality, and waste treatment facilities. In areas with good sanitation and drinking water are not contaminated, other transmission routes may be important. Materials are considered to be infectious for the polio virus is the feces and respiratory secretions of infected patients who received the polio virus or OPV (oral poliovirus vaccine) and laboratory products used for the experiment by using the polio virus. Materials that are considered potentially infectious pharyngeal secretions and feces collected for any purpose of the areas that still have wild poliovirus. Blood, serum and cerebrospinal fluid is not classified as infectious for poliovirus.

Globalization has made controlling the spread of the virus becomes more difficult. Population mobility endemic countries to various countries makes the virus quickly spread. When an outbreak of polio in 2005 in Sukabumi and polionya virus is a virus that originated from west Africa. Is uncertain how the virus is far from Africa’s get to Sukabumi. One estimate is viral entry through the journey overland from Jakarta. Other estimates of the population is through the pilgrims, may also from Indonesia manpower in the Middle East.
Invasion of Polio Virus in the Central Nerve System

At 5% of those infected with polio virus, will experience major viremia. Viremia is associated with so-called abortive poliomyelitis. Of those who experienced major viremia, there was a later show symptoms and signs of invasion of the polio virus in the central nervous system. Invasion of the polio virus can cause central nervous non-paralytic aseptic meningitis and paralytic poliomyelitis.

Non-paralytic aseptic meningitis occurs in 1-2% of poliovirus infections, and is associated with high heat (maybe with pharyngitis), myalgia, anorexia, nausea, vomiting, headache, stiff neck, back and lower limbs. On examination of cerebrospinal fluid can be found an increase in leukocytes (10-200 cells/mm3) and a slight increase in protein (40-50 mg / dL).

Paralytic poliomyelitis is not accompanied by changes in sensation or cognition. Based on its specific manifestations, paralytic poliomyelitis can be divided into spinal poliomyelitis, bulbar poliomyelitis, and bulbospinal poliomyelitis.

Factors affecting the occurrence of spinal poliomyelitis is not known with certainty. It’s just that, alleged physical activity and intramuscular injection when clinically minor phase plays an important role (that’s why, once when the incidence of polio infection remains high, some have argued that children should not be injected hot, because who knows the heat is caused by infection with the polio virus). Spinal poliomyelitis preceded by myalgia (muscle pain), muscle spasm (contraction of muscles that are not conscious and abnormal), then followed by a decrease in muscle strength asymmetry, especially the lower limbs and became maximal after 48 hours. This is due to destruction of motor nerve cells (nervous system of the front horn of the spine), which was followed by skeletal muscle denervation disarafinya.

Bulbar poliomyelitis (part of the brain stem) usually only minimal interference with muscle motion in the bottom. Usually occurs in children, and often found in those with tonsils and adenoidnya (= tonsils) are already taken (that’s why if an epidemic of polio surgical removal of the tonsils should be postponed). Bulbar poliomyelitis possessed a high mortality rate, due to vasomotor disturbances such as hypertension, hypotension, circulatory collapse (shock), autonomic dysfunction, dysphagia (difficulty swallowing), dysphonia (voice problems) and respiratory failure.
Bulbospinal poliomyelitis occurred since the invasion of the polio virus in the brain stem and spinal nerve systems. Besides the polio virus can also cause encephalitis (brain inflammation) Acute.

The mechanism of polio virus infects the central nervous system is still not known with certainty. There are three hypotheses, the first, polio virus infects the central nervous system via the transport of axons (the long nerve cells that conduct nerve signals) in the opposite direction (the nerve signals move from the central nervous system to muscles, the virus moves from muscle to central nervous system). Immune Response Against Polio Virus Infection

Immune response / natural immunity plays an important role in determining the network trofisme and pathogenicity of poliovirus. CD155 transgenic mice, non-neural tissues that are not being targeted for polio virus replication showed increased activity of interferon-stimulated genes and response interferonnya faster than neural networks. This raises an alleged key role of interferon in protecting non-neural tissue such. When CD155 transgenic mice mentioned interferon-alpha knock-out its beta, poliovirus titer in non-neural tissue increases and an increase in the frequency of paralysis compared with wild CD155 transgenic mice (but the mechanism is unclear, interested in researching?).

Humoral immune response plays an important role in the protection and long-term immunity.
Antibodies produced after infection with wild polio virus, or after vaccination with oral polio vaccine (OPV / oral poliovirus vaccine. Some call it the polio vaccine “live”) or IPV (inactivated polio vaccine, or polio vaccine has been called “dead”) can prevent the occurrence of poliomyelitis due to preventing the occurrence of viremia, thereby preventing infection of the central nervous system. Compared with IPV, wild poliovirus infections or the oral polio vaccine would produce more circulating IgG and IgA secretion in the small intestine. As a result, the dose required by the polio virus to re-infection will increase. In addition, if re-infection occurs, the amount and duration of poliomyelitis virus in the feces expenditure will decline. The number and duration of spending poliovirus in stool was instrumental in the deployment process of poliovirus. More and more and the longer the polio virus via feces expelled by the patient, the risk of spread will be even greater.

In addition to humoral immune response, cellular immune system may also play a major role in dealing with poliovirus infections. Theoretically, CD4 + T cells help B cells in humoral immune responses. Sitolitik T cells may have a role in the virus cleaning process in a way directly lyse virus-infected cells. Or gamma delta T cells and NK cells (which are part of the natural immune response) may play a role in adaptive immune response of T cells Even so, the actual mechanism of how the cellular immune system in the face of polio virus infection is still unclear (interested in researching?). The second hypothesis is the virus penetrates the blood brain barrier, independent of the presence of cellular receptors for poliovirus (CD155). And the third hypothesis, poliovirus imported into the central nervous system through macrophage cells (Trojan horse mechanism). Until now, the majority of scientific evidence supports the first hypothesis.

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