Information

15.6C: Amoebic Meningoencephalitis - Biology


Amoebic meningoencephalitis is an often-fatal central nervous system infection caused by Naegleria fowleri.

Learning Objectives

  • Summarize the route of transmission and effects of infection by Naegleria fowleri

Key Points

  • Amoebic meningoencephalitis is not actually caused by an ameoba but rather Naegleria fowleri a protist found in warm fresh water.
  • Once Naegleria fowleri enters deep into the nasal passage, digesting through the olfactory bulbs it then migrates into the forebrain, where the protists eat neuronal tissue in the brain, leading to death within 14 days from initial exposure.
  • The disease is largely asymptomatic until its final stages; often by the time it is diagnosed, it is too late to treat, causing a very high mortality rate.
  • Antimicrobial drugs can combat Naegleria fowleri infection if it is treated soon enough. Avoiding the infection by wearing nose plugs when swimming in warm water is a good preventative measure.

Key Terms

  • anosmia: Inability to smell; to perceive odors.
  • protist: Any of the eukaryotic unicellular organisms including protozoans, slime molds and some algae; historically grouped into the kingdom Protoctista.
  • parosmia: A distorted sense of smell, often resulting in phantom, non-existent, and mostly unpleasant, smells.
  • ageusia: Partial or complete loss of the sense of taste.

Primary amoebic meningoencephalitis (PAM, or PAME) is a disease of the central nervous system caused by infection from Naegleria fowleri.

Naegleria fowleri is commonly referred to as an amoeba but is actually a unicellular parasitic protist that is ubiquitous in soils and warm, stagnant bodies of freshwater, especially during the summer months. 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 or in water heated by geothermal activity. The organism is extremely sensitive to chlorine (<0.5 ppm). Exposure to the organism is extremely common due to its wide distribution in nature.

However, thus far the only route for Naegleria fowleri to enter the central nervous system is via deep insufflation of infected water as it attaches itself to the olfactory nerve, which is exposed only at the extreme vertical terminus of the paranasal sinuses.

When this occurs, 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 when the infection spreads to the brain stem, destroying the autonomic nerve cells of the medulla oblongata.

The disease is both exceptionally rare and highly lethal: there have been fewer than 200 confirmed cases in recorded medical history as of 2004, and 300 cases as of 2008, with an in-hospital case fatality rate of ~97% (3% patient survival rate). Its high mortality rate is largely blamed on the unusually non-suggestive symptomology in its early stages, 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).

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 nasal uptake 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”.

PAM can be effectively treated with antimicrobiotics, if the patient is treated early enough.


15.6C: Amoebic Meningoencephalitis - Biology

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Claims

1. A live, chimeric non-human Mononegavirales vector which allows a cell to express at least one protein from at least one human pathogen.

2. The non-human Mononegavirales vector of claim 1, wherein the natural host of the non-human Mononegavirales vector is a non-human animal.

3. The non-human Mononegavirales vector of claim 1, wherein the natural host of the non-human Mononegavirales vector is from the order Rodentia.

4. The non-human Mononegavirales vector of claim 1, wherein the non-human Mononegavirales vector is a murine pneumonia virus (MPV).

5. The non-human Mononegavirales vector of claim 1, wherein the at least one human pathogen is bacteria or a virus.

6. The non-human Mononegavirales vector of claim 1, wherein the at least one human pathogen is a virus.

7. The non-human Mononegavirales vector of claim 1, wherein the at least one human pathogen is a human Pneumoviridae virus.

8. The non-human Mononegavirales vector of claim 1, wherein the at least one human pathogen is an Orthopneumovirus.

9. The non-human Mononegavirales vector of claim 1, wherein the at least one pathogen is a human respiratory syncytial virus (RSV).

10. The non-human Mononegavirales vector of claim 1, wherein the at least one protein is RSV F protein.

11. The non-human Mononegavirales vector of claim 1, wherein the non-human Mononegavirales vector comprises a sequence with at least 90% sequence identity to SEQ ID NO: 56 or SEQ ID NO: 58.

13. The non-human Mononegavirales vector of claim 1, wherein the at least one protein is RSV G protein.

14. The non-human Mononegavirales vector of claim 1, comprising a sequence with at least 90% sequence identity to SEQ ID NO: 60.

15. The non-human Mononegavirales vector of claim 1, comprising a sequence with at least 90% sequence identity to SEQ ID NO: 61.

16. The non-human Mononegavirales vector of claim 1, comprising a sequence with at least 90% sequence identity to SEQ ID NO: 62.

17. A composition comprising the non-human Mononegavirales vector of claim 1, and a pharmaceutically acceptable carrier.

18. The composition of claim 17, wherein the composition is formulated for intranasal administration.

23. A method of making a live, chimeric non-human Mononegavirales vector which allows a cell to express at least one protein from at least one human pathogen, comprising inserting a non-native gene that encodes at least one protein from at least one human pathogen in a non-human Mononegavirales vector.

24. A kit for eliciting an immune response, the kit comprising:

(a) the composition of claim 17 and (b) at least one container for holding the composition.

49. A method of eliciting an immune response to at least one human pathogen comprising administering the non-human Mononegavirales vector of claim 1 to a human.


Balamuthia mandrillaris and Acanthamoeba Amebic Encephalitis with Neurotoxoplasmosis Coinfection in a Patient with Advanced HIV Infection

Fig 1 MRI T1 and T2 fluid attenuated inversion recovery (FLAIR) images on admission show a ring-enhancing lesion (2.3 by 2.3 by 2.4 cm) in the left parietal/occipital lobe with surrounding vasogenic edema. Fig 2 (A) Deep sections revealed these structures suggestive of amebae (arrows). H&E stain magnification, ×200. (B to E) Higher magnification of amebalike trophozoites. (B and C) H&E stain magnification, ×1,000. (D and E) Giemsa stain magnification, ×1,000. Fig 3 (A) Vascular dissemination, showing degenerating amebas (at arrows) within capillaries. (B) Degenerating amebas in reaction with the anti- Balamuthia antibodies. (C) Degenerating amebas in reaction with the anti- Acanthamoeba antibodies.