Our organism first found its way into medical literature in the 1960’s. Around this time there was a series of meningitis casesin the southern area of Australia. During the course of this time a series of people contracted and died from a very aggressive form of meningitis. However, within blood and CSF samples there was no causative bacteria noted, as would be expected in your typical case of meningitis. What was noted and dismissed were small motile amoeba.
In 1965, two Australian physicians M. Carter and R. Fowler take a closer look at three meningitis deaths that also occurred in the southern area of Australia. They examined the nervous tissue of the victims from gross andhistological aspects. As well as isolating what they thought was the causative agent from all of the victims bodies.
Their Findings…. IN THE GROSS ANATOMY In their post mortem examinations of the patients they note significant hemorrhaging in the cortex and frontal lobes of the brain. There are also some sulci that are flattened and misshapen. The brains themselves show swelling , as well as hemorrhaging in areas surrounding the cribiform plate and cranial nerve I. MICROSCOPICALLY Throughout much of the gross investigation a white exudate is noted in between sulci and within the ventricles of the brain. Samples of corticle tissue are taken, and smears are made of the white exudate found on the brain.Within these smears, small Eukaryotic micro-organisms are noted. Many of these specimens are prepared via Periodic-Acid – Schiff techniques or stained with haematoxylin and eosin to show morphology.
Their Conclusion…. Within the histological samples from the brain and exudate smears, numerous amoeba are noted. From their investigationt they determine that there is an illness that presents identical to bacterial meningitis. It has nearly the same symptoms, but a very different causative agent. This illness is caused byamoeba that invade the central nervous system, and then eat its functional cells, the neuron. They call this illness Primary Amoebic Meningoencephalitis.
About the caustive organism It is a single celled eukaryotic organism. It is a thermophillic organism, Don’t assume you are safe at home. and flourishes during the This organism has been isolated from, temperate summer months in air conditioners, city water supplies, select climates, when water and poorly chlorinated swimming temperatures rise above 30C. pools. Commonly it is found in stagnant This organism also comes in three fresh waters. Often it is near the different arrangements for threefloor of the body of water that it is different scenarios. in. However, the movement and stirring of the water’s bottom by Feeding - Trophozoitelimbs of larger animals, often puts Surviving - Cyst this organism into suspension Motility -Flagellated within the water.
Patho-physiology of this organism This organism infects its host bymoving into its nasal passages andusing nerves in that area to access the CNS.Water is essential to this organisms entrance to the body. The watercontaining this organism must “get up your nose” Once in your nasal passages, this organism moves up the olfactory sensory nerves, through thecribiform plate and directly to CNI and the frontal lobe of the brain.
Patho-physiology of this organism, continued Once inside the cranium, this organism causes intense inflammation and hemorrhage. The hemorrhage and inflammation causes further complications for the patient. Inflammation hinders the function of still living neurons, and blood is actually toxic to neurons; so surviving neurons can become poisoned by the bleeding in the brain and die. The brain itself may swell duringthis illness. Gyri can be flattened.Select vascular structures such as the middle meningeal artery can collapse or form lesions during this illness as well.
Tests For Diagnoses of this waterborne organism As part of routine tests aComplete Blood count is usually ordered. A lumbar puncture is the best way test for this organism.Often a direct wet mount of CSFis sufficient to see at least some of these micro-organisms Often analysis of CSF fluidobtained contains markers that indicate the presence of this organism.The fluid may be slightly cloudy Normal to low glucose levels: Up to 80 or <40(low) Increased protein values >60/100mlPresence of RBC’s (should be <0)
Under the MicroscopeWhen viewing the CSF under themicroscope this organism may be seen in its active feeding form. Known as a trophozoite Occasionally a motile form of this organism, referred to as flagellate can be noted. Chemical stains and othertechniques can be used in additionto, or instead of direct wet mount, including:Periodic-Acid-Schiff technique (P.A.S.) Haematoxylin and eosin staining Gram Stain : NegativePCR identification and direct antibody flourescence
Signs and symptoms Severe HeadachesLoss of the sense of smell (Anosmia) Cranial Nerve Palsy’s Change in personality Positive Kernigs sign Blurred vision Stiff neck Vomiting Confusion Positive Brudzinskis sign
TreatmentWhile there are many drugs that have been tried against this organism, these are the three most common utilized. Amphotericin B - An anti- fungal drug that targets ergo- sterols of the cell wall Flucanazole - Another anti- fungal drug that targets ergo- sterols of the cell wall Rifampicin - An antibacterial agent that disrupts RNA synthesis within the target cell.
While these are the standard chemotherapeutic agents used to treatinfection by this particular micro-organism, they are actually rather toxic to the host. Kidney toxicity is one of the major side effects of their use. Research continues on chemical compounds that may have a greater specificity for the cells of the infectious agent and not the host. However, at this time they are still limited to animal studies.
Prevention This organism is an equalopportunity pathogen. It infects an immunocompetant individual as effectively as it does an imunocomprimised person. With a 95% mortality rate and novaccine available, the best defense is avoiding exposure.Avoid swimming in stagnant waters during the temperate months of the year.If you do enter these types of water,wear noseplugs and avoid stirring upthe lake or creek bottom as much as possible.
Works Cited1. Fowler, M., and R. F. Carter. 1965. Acute pyogenic meningitis probably dueto Acanthamoeba sp.: a preliminary report. Br. Med. J. 2:740-742. http://search.ebscohost.com/login.aspx?direct=true&db=cmedm&AN=5825411&site=ehost-live.2. Hara, T., and T. Fukuma. 2005. Diagnosis of the primary amoebicmeningoencephalitis due to Naegleria fowleri. Parasitol. Int. 54:219-221. doi:10.1016/j.parint.2005.06.001.3. Joseph Martin, A. 2008. Survival of Naegleria fowleri primary amebicmeningocephalitis (PAM) could be improved with an intensive multi-routechemo- and biotherapeutic regimen. Med. Hypotheses. 71:969-971. doi:10.1016/j.mehy.2008.06.037.4. Kilvington, S., and J. Beeching. 1995. Development of a PCR foridentification of Naegleria fowleri from the environment. Appl. Environ.Microbiol. 61:3764-3767.5. Kilvington, S., and J. Beeching. 1995. Identification and epidemiologicaltyping of Naegleria fowleri with DNA probes. Appl. Environ. Microbiol.61:2071-2078.
Works Cited6. Qvarnstrom, Y., G. S. Visvesvara, R. Sriram, and A. J. da Silva. 2006.Multiplex Real-Time PCR Assay for Simultaneous Detection of Acanthamoebaspp., Balamuthia mandrillaris, and Naegleria fowleri. J. Clin. Microbiol.44:3589-3595. doi: 10.1128/JCM.00875-06.7. Shakoor, SadiaBeg, Mohammad AsimMahmood, Syed FaisalBandea,RebeccaSriram, RamaNoman, FatimaAli, FarheenVisvesvara,Govinda S.Zafar,Aria. 2011. Primary Amebic Meningoencephalitis Caused by Naegleriafowleri, Karachi, Pakistan. Emerging Infectious Diseases. 17:258-261. doi:10.3201/eid1702.100442.http://search.ebscohost.com.proxy.consortiumlibrary.org/login.aspx?direct=true&db=mth&AN=59634978&site=ehost-live.8. Sparagano, O., E. Drouet, R. Brebant, E. Manet, G. A. Denoyel, and P.Pernin. 1993. Use of monoclonal antibodies to distinguish pathogenicNaegleria fowleri (cysts, trophozoites, or flagellate forms) from otherNaegleria species. J. Clin. Microbiol. 31:2758-2763.9. Travis W., H. 2010. Swimming with death: Naegleria fowleri infections inrecreational waters. Travel Medicine and Infectious Disease. 8:201-206. doi:10.1016/j.tmaid.2010.06.001.
Works Cited10. Vargas-Zepeda, J., A. V. Gómez-Alcalá, J. A. Vázquez-Morales, L. Licea-Amaya, J. F. De Jonckheere, and F. Lares-Villa. 2005. Successful Treatment ofNaegleria fowleri Meningoencephalitis by Using Intravenous Amphotericin B,Fluconazole and Rifampicin. Arch. Med. Res. 36:83-86. doi:10.1016/j.arcmed.2004.11.003.11. Bauman, R.W. 2011. Antimicrobials against Eukaryotes: Antifungal Drugs.In Microbiology with Diseases by Taxonomy. Benjamin Cummings PublishingCo.. Glenview Il.
Image CreditsSlide 1Artist unknown. Neuron on Black background. Retrieved 11/1/2011, fromhttp://encefalus.com/wp-content/uploads/2008/07/neuron.jpgSlide 2Jacobs, Bob. Professor, Colorado College. Golgi Stained Neuron. Retrieved11/1/2011, from http://www.snl.salk.edu/~nikoosh/outreach2006.htmlSlide 3Dunn, Greg. Artist. Hippocampal Pyrimidal Neurons. Retrieved 11/1/2011from, http://gregadunn.com/images/MrTwit-MasterFolderForNewWebsite/comission/zoomifySFNLARGE/hippocampal-pyramidal.htmlSlide 4Artist Unspecified. Work type unspecified. Retrieved 11/1/2011 fromhttp://3.bp.blogspot.com/_gDNe1xZsxX4/TQd1JlvCgqI/AAAAAAAAAEE/vsPpsINhlmc/s1600/Pyramidal_hippocampal_neuron_40x.jpg
Image CreditsSlide 5Schultz, Thomas. Diffusion MRI image (saggital view). Retrieved11/22/2011 from, http://en.wikipedia.org/wiki/File:DTI-sagittal-fibers.jpgSlide 6Pearson education, Educational. Work type unknown. Retreived 11/1/2011fromhttp://science.kennesaw.edu/~jdirnber/Bio2108/Lecture/LecBiodiversity/28_Labeled_Images/28_03lAmoeba-L.jpgSlide 7Neumeyer, Ron. Proprietor, Micro-Imaging services. Work type unknown.Retreived 11/1/2001 fromhttp://www.microimaging.ca/protozoa/21ameoba.jpg.Gray’s Anatomy. Lithograph of Cribiform Plate and Olfactory filaments.Retreived 11/1/2011 fromhttp://www.ganfyd.org/images/1/16/Olfactory_Nerve.png