Primary amoebic meningoencephalitis
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
| Primary amoebic meningoencephalitis Classification and external resources | |
| ICD-10 | B60.2 |
|---|---|
| ICD-9 | 136.2 |
| eMedicine | ped/81 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [2] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview
Primary amoebic meningoencephalitis (PAM, or PAME) is a disease of the central nervous system caused by infection from the Percolozoid amoeba Naegleria fowleri and Balamuthia mandrillaris. . The organism propagates in warm, stagnant bodies of freshwater (typically during the summer months), and enters the central nervous system after insufflation of infected water by attaching itself to the olfactory nerve. It then migrates through the cribiform plate and into the olfactory bulbs of the forebrain, where it multiplies itself greatly by feeding on nerve tissue. During this stage, occurring approximately 3-7 days post-infection, the typical symptoms are parosmia, rapidly progressing to anosmia (with resultant ageusia) as the nerve cells of the olfactory bulbs are consumed and replaced with necrotic lesions.
After the organisms have multiplied and largely consumed the olfactory bulbs, the infection rapidly spreads through the mitral cell axons to the rest of the cerebrum, resulting in onset of frank encephalitic symptoms, including cephalgia (headache), nausea, and rigidity of the neck muscles, progressing to vomiting, delirium, seizures, and eventually irreversible coma. Death usually occurs within 14 days of exposure as a result of respiratory failure.
The disease is both exceptionally rare and exceptionally lethal: there have been less than 200 confirmed cases in recorded medical history, with an in-hospital case fatality rate of ~97% (3% patient survival rate).
This extreme morbidity is largely blamed on the unusually non-suggestive symptomology of the early-stage disease compounded by the necessity of microbial culture of the cerebrospinal fluid to effect a positive diagnosis. The amoeba also demonstrates a particularly rapid late-stage propagation through the nerves of the olfactory system to many parts of the brain simultaneously (including the vulnerable medulla).
Cause
Naegleria fowleri is an amoeba that is ubiquitous in soils and warm waters. Infection typically occurs during the summer months and patients typically have a history of exposure to a natural body of water. The organism specifically prefers temperatures above 32°C. The organism is extremely sensitive to chlorine (<0.5ppm). Exposure to the organism is extremely common due to its wide distribution in nature, but thus far lacks the ability to infect the body through any method other than direct contact with the olfactory nerve; the contaminated water must actually be fully insufflated into the sinus cavities for transmission to occur.
Michael Beach, a recreational waterborne illness specialist for the Centers for Disease Control and Prevention, stated in remarks to the Associated Press that the wearing of nose-clips to prevent insufflation of contaminated water would be an effective protection against contracting PAM, noting that "You'd have to have water going way up in your nose to begin with".[1]
Treatment
The current standard treatment is prompt intravenous administration of heroic doses of Amphotericin B, a systemic antifungal which is one of the few effective treatments for systemic infections of Protozoan parasitic diseases (such as leishmaniasis and toxoplasmosis). The success rate in treating PAM is usually quite poor, since by the time of definitive diagnosis most patients have already manifested signs of terminal cerebral necrosis. Even if definitive diagnosis is effected early enough to allow for a course of medication, Amphotericin B also causes significant and permanent nephrotoxicity in the heroic doses necessary to quickly halt the progress of the amoebae through the brain.
See also
External links
- http://www.dshs.state.tx.us/idcu/disease/primary_amebic_meningoencephalitis/
- http://wikidoc.org/index.php/Balamuthia_mandrillaris
Protozoal diseases (A06-A07, B50-B64) | |
|---|---|
| Apicomplexa | Coccidia (Cryptosporidiosis, Isosporiasis, Cyclosporiasis, Toxoplasmosis) - Malaria (Blackwater fever) - Babesiosis |
| Excavata | Giardiasis - Trypanosomiasis (Sleeping sickness, Chagas disease) - Leishmaniasis (Cutaneous leishmaniasis, Visceral leishmaniasis) - Trichomoniasis |
| Other | Amoebiasis - Blastocystosis - Dientamoebiasis - Microsporidiosis -Primary amoebic meningoencephalitis |
ca:Meningoencefalitis amèbica primària fr:Méningo-encéphalite amibienne primitive
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

