These procedures are especially strict in island nations where rabies is not yet present, such as Australia. The incubation period for rabies can be lengthy, ranging from several weeks or months to over a year. As the virus replicates, it moves from the site of the bite into motor and sensory axons of peripheral nerves and spreads to multiple nerves, eventually making its way to the CNS through the spinal ganglia.
Once rabies virus reaches the brain, the infection leads to encephalitis caused by the disruption of normal neurotransmitter function, resulting in the symptoms associated with rabies. After the rabies virus infects the brain, it can continue to spread through other neuronal pathways, traveling out of the CNS to tissues such as the salivary glands, where the virus can be released.
As a result, as the disease progresses the virus can be found in many other tissues, including the salivary glands, taste buds, nasal cavity, and tears. The early symptoms of rabies include discomfort at the site of the bite, fever, and headache. Once the virus reaches the brain and later symptoms appear, the disease is always fatal. Terminal rabies cases can end in one of two ways: either furious or paralytic rabies. Individuals with furious rabies become very agitated and hyperactive.
Hydrophobia a fear of water is common in patients with furious rabies, which is caused by muscular spasms in the throat when swallowing or thinking about water.
Excess salivation and a desire to bite can lead to foaming of the mouth. These behaviors serve to enhance the likelihood of viral transmission, although contact with infected secretions like saliva or tears alone is sufficient for infection.
The disease culminates after just a few days with terror and confusion, followed by cardiovascular and respiratory arrest. In contrast, individuals with paralytic rabies generally follow a longer course of disease.
The muscles at the site of infection become paralyzed. Over a period of time, the paralysis slowly spreads throughout the body. This paralytic form of disease culminates in coma and death. Before present-day diagnostic methods were available, rabies diagnosis was made using a clinical case history and histopathological examination of biopsy or autopsy tissues, looking for the cytophatic effectt of rabies virus, Negri bodies. There are no tests that can detect rabies virus in humans at the time of the bite or shortly thereafter.
Once the virus has begun to replicate but before clinical symptoms occur , the virus can be detected using an immunofluorescence test on cutaneous nerves found at the base of hair follicles. Saliva can also be tested for viral genetic material. Even when these tests are performed, most suspected infections are treated as positive and rabies immunoglobulin injections are administered.
Poliomyelitis polio , caused by poliovirus, is a primarily intestinal disease that, in a small percentage of cases, proceeds to the nervous system, causing paralysis and, potentially, death. Poliovirus is highly contagious, with transmission primarily occurring by the fecal-oral route; aerosol or droplet transmission is possible. In about one case in every , the poliovirus affects cells in the CNS. After it enters through the mouth, viral replication begins in the pharynx and gastrointestinal tract.
As the infection progresses, poliovirus is usually present in the throat and in the stool before the onset of symptoms. One week after the onset of symptoms, there is less poliovirus in the throat, but for several weeks, poliovirus continues to be excreted in the stool.
Poliovirus invades local lymphoid tissue, enters the bloodstream, and then may infect cells of the CNS. Replication of poliovirus in motor neurons of the anterior horn cells in the spinal cord, brain stem, or motor cortex results in cell destruction and leads to flaccid paralysis. In severe cases, this can involve the respiratory system, leading to death. Patients with impaired respiratory function are treated using positive-pressure ventilation systems.
In the past, patients were sometimes confined to Emerson respirators , also known as iron lungs Figure 4. Treatment is limited to various supportive measures. These include pain relievers, rest, heat therapy to ease muscle spasms, physical therapy and corrective braces if necessary to help with walking, and mechanical ventilation to assist with breathing if necessary.
Figure 4. Two different vaccines were introduced in the s that have led to the dramatic decrease in polio worldwide Figure 5. The Salk vaccine is an inactivated polio virus that was first introduced in This vaccine is delivered by intramuscular injection. The Sabin vaccine is an oral polio vaccine that contains an attenuated virus; it was licensed for use in Figure 5. Attenuated viruses from the Sabin vaccine are shed in the feces of immunized individuals and thus have the potential to infect nonimmunized individuals.
By the late s, the few polio cases originating in the United States could be traced back to the Sabin vaccine. In these cases, mutations of the attenuated virus following vaccination likely allowed the microbe to revert to a virulent form. For this reason, the United States switched exclusively to the Salk vaccine in Because the Salk vaccine contains an inactivated virus, there is no risk of transmission to others see Vaccines.
Currently four doses of the vaccine are recommended for children: at 2, 4, and 6—18 months of age, and at 4—6 years of age. That goal is now close to being realized. Polio is now endemic in only a few countries, including Afghanistan, Pakistan, and Nigeria, where vaccination efforts have been disrupted by military conflict or political instability. Although there was no armed conflict, the two super powers were diplomatically and economically isolated from each other, as represented by the so-called Iron Curtain between the Soviet Union and the rest of the world.
After , migration or travel outside of the Soviet Union was exceedingly difficult, and it was equally difficult for foreigners to enter the Soviet Union. The United States also placed strict limits on Soviets entering the country. During the Eisenhower administration, only 20 graduate students from the Soviet Union were allowed to come to study in the United States per year. Yet even the Iron Curtain was no match for polio. The Salk vaccine became widely available in the West in , and by the time the Sabin vaccine was ready for clinical trials, most of the susceptible population in the United States and Canada had already been vaccinated against polio.
Neisseria meningitidis, Streptococcus pneumonia and Haemophilus influenza type b are common causes of bacterial meningitis. The bacteria infect the meninges by spreading from the ears or sinuses, or by moving from the nose or mouth into the blood stream.
Meningitis can also be spread by person-to-person contact but it is usual for people to have the bacteria that can cause the infection on their skin and in their nose as a harmless commensal organism. A second form of meningitis, called aseptic meningitis, or viral meningitis, is caused by enteroviruses that can travel from the digestive tract or are spread by insect bites.
Other viruses that can cause aseptic meningitis are the herpes simplex virus, Epstein—Barr virus, HIV, varicella zoster virus and mumps virus. Central nervous system infections, like most infections, stimulate an immune response.
This involves white blood cells moving to the area of infection to attack the pathogens, which inevitably leads to excess fluid and plasma in the area. This causes inflammation and swelling, which is in itself highly dangerous when this raises fluid pressure inside the skull. Some types of infection in the central nervous system can be distinguished by specific symptoms and the severity of symptoms:.
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Central nervous system infections caused by bacteria or fungi can cause illnesses such as: Brain abscesses. This is a collection of pus and infected tissue within the brain. Bacterial meningitis. This happens when bacterial infections enter the bloodstream and travel to the brain and spinal cord.
Symptoms of bacterial or fungal central nervous system infections may include: Severe headache Back pain Stiff neck Confusion Weakness Fever Seizures Paralysis Central nervous system infections caused by viruses can cause illnesses such as: Viral meningitis.
This is inflammation of the layers of tissue that cover the brain and spinal cord. Morbidity and mortality is very high. Viruses that cause this condition include herpes simplex , rabies and some of the arboviruses. The arboviruses are a miscellaneous group of enveloped, ssRNA viruses that infect animals.
They are transmitted from one vertebrate host to another via blood sucking arthropods. The main reservoirs are wild birds and small mammals. Man may be infected if bitten by the insect vector. In South Africa, there are no enzootic arboviruses that specifically cause encephalitis. Rarely, however, encephalitis may occur as part of the clinical course of infection with viruses such as, West Nile virus, Rift Valley fever virus and Sinbis virus. These viruses are enzootic in livestock herds in certain parts of the country and farm workers or vets may occasionally be infected.
Rabies: Rabies virus is an enveloped bullet shaped ssRNA virus. It primarily infects warm blooded vertebrates. It is enzootic in most parts of the world.
Virus is shed in the saliva of infected animals and humans are occasionally infected if bitten by an infected animal. The behaviour of the infected animal is altered and it is more likely to bite humans or other animals that it comes into contact with thus ensuring the viruses survival.
The most common sources of human infection are dogs and bats. Pathogenesis: Virus is introduced into the tissues through a bite. It enters peripheral nerves and travels up the axon to the brain where it replicates. It causes a fatal encephalitis. Incubation period: It varies from days, depending on the severity and site of the bite. Incubation period is determined by how long the virus takes to reach the brain.
Bites on the foot take longer than bites on the face. The disease can be prevented in an exposed person by administration of post exposure prophylaxis in the form of rabies vaccine and rabies immunoglobulin. This syndrome is due to direct infection of motor neurones grey matter in the spinal cord by a virus. Patients present with fever and flaccid paralysis of a group of muscles. Signs of meningitis such as headache and neck stiffness are frequent accompanying features.
The most common aetiological agents include the Polioviruses 1, 2 and 3 , but with the reduction in prevalence of wild type polio due to successful global vaccination, other non polio enteroviruses are responsible for most cases.
This uncommon complication may develop in the convalescent phase, following a number of common viral infections, including: measles, mumps, rubella and primary varicella-zoster virus infection. In addition it may develop following exposure to certain vaccines, such as: vaccinia virus and the older neurotissue rabies vaccines. Widespread demyelinating lesions develop involving the white matter in the brain and spinal cord.
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