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Geographical Locations where the disease is found
The pathogen Naegleria fowleri thrives well in warm, bodies of stagnant freshwater (Craun et al. 243-62). This is more in particular during summer. Primary amoebic Meningoencephalitis was initially documented in Australia in the year 1965. Other cases emerged later in the United States of America in 1966. Recent cases have occurred in Stillwater, Minnesota in 2010. Another case was reported in Mims, Florida in the St. John’sRiver. Other geographical locations include the coastal city of Karachi, Pakistan.
Primary amebic Meningoencephalitis Casualties
Primary amebic Meningoencephalitis has a tendency of affecting children aged below two years. This is more in particularly during the warmer climates and months. Children who come into contact with the disease normally carry the pathogen, Naegleria Fowleri asymptomatically in their throats and noses. Primary amebic Meningoencephalitis does not demonstrate a particular racial or ethnic predilection. However, males have a higher chance of contracting the disease than their female counterparts. In fact, for every woman reported to have contracted Primary amebic Meningoencephalitis, there are two men suffering from the disease. Therefore, the ratio of women to men in a number of reported Primary amebic Meningoencephalitis cases is 1:2. However, it is not only children alone who are affected. Both children and young adults and those in particular who were previously in good health are the most targeted group by the pathogen. Again, Primary amebic Meningoencephalitis has been reported in children as young as 4 months old. Generally, most cases of Primary amebic Meningoencephalitis are mainly observed in the initial three decades of life.
Naegleria fowleri mainly propagates in bodies with warm stagnant fresh waters and more especially in the summer months. The pathogen enters into an individual’s central nervous system immediately after insufflation of the water that is infected by way of attaching itself to the olfactory nerve. The pathogen then migrates through to the cribiform plate. It later moves into the olfactory bulbs in the forebrain. At this location, it multiplies massively as it feeds on the tissue of the nerves. At this particular stage, the pathogen has taken almost 3-7 days after infection. The typical symptoms at this level begin to emerge. They include parosmia which quickly progresses into anosmia coupled with ageusia. Consequently, the olfactory nerve cells are eaten up and replaced with necrotic lesions (Craun et al. 243-62).
Signs and Symptoms
Rarely, patients suffering from Primary amebic Meningoencephalitis could experience a taste and smell that is disordered. In most cases the Primary amebic Meningoencephalitis symptoms cannot be distinguished from an acute attack by bacterial meningitis. The acute start of Primary amebic Meningoencephalitis usually occurs between several hours to about 1-2 days. Most noticeable symptoms include headache, stiff neck, high fever, vomiting and nausea. Other symptoms may include somnolence, coma, confusion and seizures. Infection could progress rapidly. This progression could result to increased cerebral herniation and ICP. Physical examination rarely assists in differentiating Primary amebic Meningoencephalitis from other disease affecting the central nervous system. Any other findings apart from the neurologic examination are absolutely exceptional. Myocarditis may rarely occur even though amoebae do not exist in the myocardium (Marciano-Cabral 5864-9).
Based on the nature of Primary amebic Meningoencephalitis suggestions have been made for physicians to give a set of antimicrobial drugs. These drugs should also include the drugs which are used to treat amoebic encephalitis. This is usually administered before the disease is indeed confirmed. The main reason for doing so is to increase the number of Primary amebic Meningoencephalitis survivors. All the same, the administration of a number of drugs simultaneously must always be carried out with a lot of caution. It is in most cases unpleasant and dangerous for the patient. The common standard treatment is the timely intravenous use of heroic doses of Amphotericin B. This is a very systematic antifungal considered as one of the very few successful treatments for all such like infections of protozoan and parasitic diseases and illnesses (Craun et al. 243-62).
The rate of success in treating Primary amebic Meningoencephalitis is normally very poor. This is mainly because; by the time of the specific diagnosis many of the patients are already showing signs and symptoms of terminal cerebral necrosis. Even though definitive diagnosis can be effective at the early stages to make medication course workable, Amphotericin B can also cause permanent and significant nephrotoxicity in the doses which are important to halt the progress of the pathogen in the brain. Rifampicin has also been administered together with amphotericin B successfully in the treatment of Primary amebic Meningoencephalitis. All the same, there is some enough evidence that it is not an effective inhibitor of the growth of Naegleria (Marciano-Cabral 5864-9).
Before the individual dies, amebic meningitis can also be diagnosed although in rare cases. The difficulties realized in the process of diagnosis and the quick progreession of Naegleria makes the situation very hard to deal with in treatment. Due to this, the diagnosis in the sick person’s CSF findings must be pursued aggressively taking the history of exposure to water and identify in whom the Gram stain of CSF is negative. Usually, the Primary amebic Meningoencephalitis infection progresses as an irresistible acute bacterial meningitis that does not respond to routine antibacterials. Therefore, the treatment of choice is purely amphotericin B. At maximally acceptable doses, amphotericin B can also be administered with doxycycline and rifampin. Effective treatment could also call for intrathecal amphotericin B. Other medications that could be of benefit include phenothiazine, qinghaosu and Sulfisoxazole. Research studies have made suggestions to employ the use of azithromycin which is an appendage to amphotericin B. Very recently, mouse models and vitro studies of the treatment of PAM have made considerations for chlorpromazine, miltefosine and rokitamycin proposing that they could have activity (Marciano-Cabral 5864-9). All the same, the effectiveness of the said treatments has not yet been fully proven. Hydrocephalus may possibly impose shunting.
After the pathogen has multiplied and eaten up the olfactory bulbs immensely, the infection spreads rapidly through the mitral cell axons. This further spreads and attacks the cerebrum leading to the onset of symptoms of frank encephalitic nature. Nausea, neck rigidity and stiffness, headache also emerges. Symptoms which may later advance to seizures, vomiting, delirium and ultimately a coma that is irreversible. Death normally occurs with a period of fourteen days (two weeks) of exposure. This is basically occasioned by the failure realized in respiration the moment the infection reaches out to the stem of the brain. In such an occasion, the autonomic nerve cells of the brain’s medulla oblongata are destroyed (Marciano-Cabral 5864-9).
Although the Primary amebic Meningoencephalitis is exceptionally a rare occurrence, it is an exceptional deadly disease. The survival rate in a number of cases is very small. Therefore, there are high chances that a person suffering from Primary amebic Meningoencephalitis will die. Studies peg the survival rate at 3% of the total number of Primary amebic Meningoencephalitis patients. The intense mortality is immensely occasioned by the unusual non-suggestive early-stage symptomology disease coupled with the need of a microbial culture associated with the cerebrospinal fluid to interfere with a positive diagnosis (Craun et al. 243-62). The moment the pathogen attacks an individual, it often has a very fast late-stage propagation right through the olfactory system nerves. This spreads over to many of the brain parts in a simultaneous manner leaving chances of survival minimal.
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