
There is a deadly amoeba attacking throughout the south. It lives in freshwater lakes and thrives in the summer months. A quick dip in the lake could lead to an invasion of brain-eating micro-organisms. There have been three deaths this year caused by this zombie bug. The worst part about it is the fact that it kills before doctor's can correctly diagnose it. This brain eater it called primary amoebic meningoencephalitis or PAM. Realistically the chances of you contracting this bug is millions to one.
Here is the Wikipedia article on PAM:
Click HERE for link to article
Primary amoebic meningoencephalitis
From Wikipedia, the free encyclopedia
| Primary amoebic meningoencephalitis |
| Classification and external resources |

Histopathology of amebic meningoencephalitis due to Naegleria fowleri. Direct fluorescent antibody stain. (CDC) |
| ICD-10 | A06.6, B60.2 |
| ICD-9 | 136.2 |
| eMedicine | ped/81 |
Primary amoebic meningoencephalitis (
PAM, or
PAME) is a disease of the
central nervous system caused by infection from
Naegleria fowleri.
[1][2]
[edit] Presentation
Naegleria fowleri 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.
[3] It then migrates through the
cribiform plate and into the
olfactory bulbs of the
forebrain,
[4] 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 when the infection spreads to the
brain stem, destroying the autonomic nerve cells of the
medulla oblongata.
The disease is both exceptionally rare and exceptionally lethal: there had been fewer than 200 confirmed cases in recorded medical history as of 2004,
[5] 300 cases as of 2008,
[6] with an in-hospital
case fatality rate of ~97% (3% patient
survival rate).
[7]
This extreme
mortality 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 parasite 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).
For those reasons, it has been suggested that physicians should give an array of antimicrobial drugs, including the drugs used to treat amoebic encephalitis, before the disease is actually confirmed in order to increase the number of survivors. However, administering several of those drugs at once (or even some of them known to treat the condition) is often very dangerous and unpleasant for the patient.
Naegleria fowleri is commonly referred to as an amoeba but is actually a unicellular parasite 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, as might be found in a tropical climate
[citation needed] or in water heated by geothermal activity.
[8] The organism is extremely sensitive to chlorine (<0.5 ppm). 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, which is only exposed at the extreme vertical terminus of the
paranasal sinuses; the contaminated water must actually be deeply 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".
[9]
[edit] Outbreaks
This form of nervous system infection by amoeba was first documented in Australia in 1965.
[10][11] In 1966, four cases were reported in the USA. By 1968 the causative organism, previously thought to be a species of
Acanthamoeba or
Hartmanella, was identified as
Naegleria. This same year, occurrence of 16 cases over period of two years (1963-1965) was reported in
Ústí nad Labem.
[12] In 1970, the species of amoeba was named
N. fowleri.
[13]
[edit] 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 doses necessary to quickly halt the progress of the amoebae through the brain.
Rifampicin has also been used with amphotericin B in successful treatment.
[14][15][16] However, there is some evidence that it does not effectively inhibit Naegleria growth.
[17]
Two cases of similar amoebic infections (caused by
Balamuthia mandrillaris) were successfully treated for amoebic encephalitis and recovered, including a 5-year-old girl and a 64-year-old man.
[18]
[edit] See also
[edit] References
- ^ Cabanes PA, Wallet F, Pringuez E, Pernin P (July 2001). "Assessing the risk of primary amoebic meningoencephalitis from swimming in the presence of environmental Naegleria fowleri". Appl. Environ. Microbiol. 67 (7): 2927–31. doi:10.1128/AEM.67.7.2927-2931.2001. PMC 92963. PMID 11425704. http://aem.asm.org/cgi/pmidlookup?view=long&pmid=11425704.
- ^ Sarica, FB; Tufan; Cekinmez; Erdoğan; Altinörs (2009). "A rare but fatal case of granulomatous amebic encephalitis with brain abscess: the first case reported from Turkey". Turkish neurosurgery 19 (3): 256–9. PMID 19621290. edit
- ^ Centers for Disease Control and Prevention (CDC) (May 2008). "Primary amebic meningoencephalitis--Arizona, Florida, and Texas, 2007". MMWR Morb. Mortal. Wkly. Rep. 57 (21): 573–7. PMID 18509301. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5721a1.htm.
- ^ Cervantes-Sandoval I, Serrano-Luna Jde J, García-Latorre E, Tsutsumi V, Shibayama M (September 2008). "Characterization of brain inflammation during primary amoebic meningoencephalitis". Parasitol. Int. 57 (3): 307–13. doi:10.1016/j.parint.2008.01.006. PMID 18374627. http://linkinghub.elsevier.com/retrieve/pii/S1383-5769(08)00007-X.
- ^ Wiwanitkit V (2004). "Review of clinical presentations in Thai patients with primary amoebic meningoencephalitis". MedGenMed 6 (1): 2. PMC 1140726. PMID 15208515. http://www.medscape.com/viewarticle/468088.
- ^ Caruzo G, Cardozo J (October 2008). "Primary amoebic meningoencephalitis: a new case from Venezuela". Trop Doct 38 (4): 256–7. doi:10.1258/td.2008.070426. PMID 18820207. http://td.rsmjournals.com/cgi/pmidlookup?view=long&pmid=18820207.
- ^ "Amebic Meningoencephalitis". http://emedicine.medscape.com/article/996227-overview. Retrieved 2010-07-16.
- ^ "Geothermal activity". http://www.ew.govt.nz/Environmental-information/Natural-hazards/Geothermal-activity/. Retrieved 2008-01-09. [dead link]
- ^ "6 die from brain-eating amoeba in lakes", Chris Kahn/Associated Press, 9/28/07"
- ^ Fowler M, Carter RF (September 1965). "Acute pyogenic meningitis probably due to Acanthamoeba sp.: a preliminary report". Br Med J 2 (5464): 740–2. PMC 1846173. PMID 5825411.
- ^ Symmers WC (November 1969). "Primary amoebic meningoencephalitis in Britain". Br Med J 4 (5681): 449–54. doi:10.1136/bmj.4.5681.449. PMC 1630535. PMID 5354833.
- ^ Červa L.; K. Novák (April 5, 1968). "Ameobic meningoencephalitis: sixteen fatalities". Science 160 (3823): 92. doi:10.1126/science.160.3823.92. PMID 5642317.
- ^ Gutierrez, Yezid (15). "Chapter 6: Free Living Amebae". Diagnostic Pathology of Parasitic Infections with Clinical Correlations (2 ed.). USA: Oxford University Press. pp. 114–115. ISBN 0195121430.
- ^ Poungvarin N, Jariya P (February 1991). "The fifth nonlethal case of primary amoebic meningoencephalitis". J Med Assoc Thai 74 (2): 112–5. PMID 2056258.
- ^ Jain R, Prabhakar S, Modi M, Bhatia R, Sehgal R (December 2002). "Naegleria meningitis: a rare survival". Neurol India 50 (4): 470–2. PMID 12577098. http://www.neurologyindia.com/article.asp?issn=0028-3886;year=2002;volume=50;issue=4;spage=470;epage=2;aulast=Jain.
- ^ Vargas-Zepeda J, Gómez-Alcalá AV, Vásquez-Morales JA, Licea-Amaya L, De Jonckheere JF, Lares-Villa F (2005). "Successful treatment of Naegleria fowleri meningoencephalitis by using intravenous amphotericin B, fluconazole and rifampicin". Arch. Med. Res. 36 (1): 83–6. doi:10.1016/j.arcmed.2004.11.003. PMID 15900627.
- ^ "Proceedings of the Oklahoma Academy of Science". http://digital.library.okstate.edu/OAS/oas_htm_files/v77/p133_136nf.html. Retrieved 2009-01-02.
- ^ Deetz TR, Sawyer MH, Billman G, Schuster FL, Visvesvara GS (200). "Successful treatment of Balamuthia amoebic encephalitis: presentation of 2 cases". Clin Infect Dis 37 (10): 1304–12. doi:10.1086/379020. PMID 14583863.
[edit] External links