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Naeglaria
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- 2. Naegleria fowleri – Commonlyreferred to as the “brain-eating amoeba”, – Free-living microscopic amoeba, (single-celled living organism). – Cause a rare and devastating infection of the brain called primary amoebic meningoencephalitis (pam). – Commonly found in warm freshwater (Eg. Lakes, rivers, and hot springs) and soil. – Usually infects people when contaminated water enters the body through the nose.
- 3. – It travelsto the brain where it causes pam, which is usually fatal. – In very rare instances, naegleria infections may also occur when contaminated water from other sources (such as inadequately chlorinated swimming pool water or heated and contaminated tap water) enters the nose ■ Domain: Eukaryota ■ Genus: Naegleria ■ Species: N. fowleri
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- 5. 2. Amoeboflagellate o Temporary,nonfeeding, and non dividing stage found in culture o As a response to a change in ph or ion concentration of the amoeba’s environment o Pear shaped, flagellar apparatus at the broader end. o Flagellar apparatus consist of 2 terminal flagella, 2 basal bodies, microtubules, and a single striated rootlet or rhizoplast. o Shows rapid forward movement or slow spinning movement. o Reverts to trophozoite stage with in 24 hours.
- 6. 3. Cyst o Sphericaland about 7–15 µm in diameter o smooth, and have a double – layered cyst wall. o Single nucleus, contractile vacuoles, and food vacuoles. o In the environment of the human nasal passages it can revert to the trophozoite stage and become infective.
- 7. Culture and laboratory animals. ■ Trophozoitesare cultured in 1. Non nutrient agar inoculated with bacteria (E.coli or enterobactor sp) monoxenic culture. 2. Enriched broth such as peptone yeast extract broth without any added bacteria axenic culture. 3. Tissue culture:- Hela cells, MRC human embryonic lung cells, and monkey kidney cells. ■ Rodents, rabbits, and sheep are the laboratory animals susceptible to experimental N.fowleri infections.
- 8. Life cycle • Thelife cycle can occur in a human host, or freely in an aquatic or soil environment. • In a warm, high nutrient, aquatic environment the trophozoite stage predominates. • If pH or ionic changes occur surrounding the organism, the trophozoite can transition to the more mobile flagellated form. • If the environment becomes depleted of nutrients, cold, or dry the trophozoite can encyst to survive the unfavorable conditions. • Cysts and trophozoites can enter the human through nasal passages, usually related to water activities. • Trophozoites are infective, and their penetration of the nasal mucosa and subsequent migration to the brain results in PAM.
- 9. Pathogenesis ■ Virulence factors: –37-kDa protein: ■ Mucinolytic activity ■ Gene nfal, cytolytic function, located in pseudopodia & food cups – Cytopathic enzymes: ■ In brain tissues, N.fowleri produces food cup (amebostome) in which enzymes such as hydrolases, phospholipases, and lysosomal enzymes are secreted.
- 10. ■ N. fowleriis an amphizoic amoeba, as it can survive in a free-living state in water, soil, or in the host, which can be the human central nervous system (CNS). ■ Seen in healthy children and adults following recreational water activities, including swimming, diving, and water skiing. ■ Infect the human body by entering the host through the nose when water is splashed or forced into the nasal cavity. ■ Infectivity occurs first through attachment to the nasal mucosa, followed by locomotion along the olfactory nerve and through the cribriform plate (which is more porous in children and young adults) to reach the olfactory bulbs within the CNS.
- 11. ■ N. fowlerienters the human body in the trophozoite form. ■ Structures on the surface of trophozoites known as food cups enable the organism to ingest bacteria, fungi, and human tissue. ■ The pathogenicity of N. fowleri also dependent upon the release of cytolytic molecules, including acid hydrolases, phospholipases, neuraminidases, and phospholipolytic enzymes that play a role in host cell and nerve destruction. ■ The combination of the pathogenicity of N. fowleri and the intense immune response resulting from its presence results in significant nerve damage and subsequent CNS tissue damage, which often result in death.
- 12. Signs and symptoms ■Severe Headaches ■ Loss 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
- 13. Primary ameobic meningoencephalitis ■Naegleria fowleri is the agent of primary amebic meningoencephalitis, a fulminating, rapidly fatal disease. ■ More than 150 cases of this disease have been recorded worldwide.The disease usually affects children and young adults. ■ Incubation period:- 2 to 3 days to as long as 7 to 15 days, depending partly on the size of the inoculum and the virulence of the strain.
- 14. ■ The diseaseappears with the sudden onset of bifrontal or bitemporal headache, fever, nausea, vomiting, stiff neck, mental status change, and seizures. Symptoms progress rapidly to lethargy, confusion, and coma. ■ In all of the recorded cases, the patient died within 48 to 72 hours.
- 15. Lab diagnosis CSF ■ Microscopicexamination of fresh, unfrozen, unrefrigerated cerebrospinal fluid (CSF) – (samples cannot be frozen or refrigerated because cold temperatures kill the amebae). ■ A wet mount :- actively moving trophozoites. ■ Identified in CSF smears or cultures using hematoxylin and eosin (H&E), periodic acid-Schiff (PAS), trichrome, Giemsa, orWright-Giemsa stains. ■ Shows ameboid trophozoites with morphology typical of Naegleria ■ A nucleus with a large, centrally located and densely staining nucleolus.
- 16. Tissue ■ Microscopic examinationof hematoxylin and eosin (H&E), periodic acid- Schiff (PAS), trichrome, Giemsa, orWright-Giemsa stained smears of brain biopsy or autopsy specimens ■ Demonstrates trophozoites with morphology typical of Naegleria fowleri. ■ The ameboid trophozoites measure 10-35 µm but when rounded are usually 10-15 µm in diameter.The cytoplasm is granular and contains many vacuoles. ■ The single nucleus is large and has a large, dense karyosome. Trophozoite of Naegleria fowleri in CSF, stained with trichrome
- 17. Immunohistochemical staining ■ indirectimmunofluorescent (IIF) staining and immune alkaline phosphatase staining (IHC), use an antibody specific for Naegleria fowleri followed by microscopic examination to identify Naegleria fowleri in tissue, culture, or CSF Serology ■ indirect immunofluorescent antibody (IFA) testing is currently considered a research technique as it has not been evaluated for use as a routine diagnostic procedure.Although IFA can be performed to measure serum antibody titers in patient sera, most patients with PAM die before an immune response is mounted.
- 18. Culture ■ It involvesinoculating mammalian cell cultures and monitoring for cytopathogenicity or growth on E. coli lawns. ■ For growing on an E. coli lawn, the sample is added to a growth plate covered in bacteria that can serve as a food source for Naegleria fowleri. ■ Incubating the plate at a higher temperature (108°F/42°C) kills most free- living amebae, while selecting for thermophilic amebae, such as Naegleria fowleri . ■ This initial screen shows up as tracks made by an ameba as it moves across the plate eating the bacteria and can be identified in cultures using hematoxylin and eosin (H&E), periodic acid-Schiff (PAS), trichrome, Giemsa, orWright- Giemsa stains.
- 19. Molecular diagnosis ■ Anincreasing number of PCR-based techniques (conventional and real- time PCR) have been described for detection and identification of free- living amebic infections
- 20. Treatment ■ Amphotericin Bhas been the traditional mainstay of PAM treatment ■ Combination therapy with multiple other antimicrobials in addition to amphotericin, such as fluconazole, miconazole, rifampicin and azithromycin.
Editor's Notes
- #16 A Gram stain should be avoided as the amebae can be destroyed during heat fixation.