Naegleria (Sp.) Identified in Amebic Encephalitis

Butt, Cecil G.; Baro, Cesar; Knorr, R

doi:10.1093/ajcp/50.5.568

Cited by 67 publications

(13 citation statements)

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“…Although the aetiological agent was not identified by autopsy, later, the scientific community considered that N. fowleri was the aetiological agent (Carter, 1969;Carter et al, 1981;Marciano-Cabral, 1988). After these reports, many cases of PAM were reported in different countries, such as the USA (Butt et al, 1968;MarcianoCabral & Cabral, 2007;Yoder et al, 2010), Australia (Fowler & Carter, 1965;Norton et al, 2010) and the Czech Republic . A retrospective study of PAM showed that approximately 16 cases were identified using histological samples between 1962 and 1968 Cerva, 1969).…”

Section: Epidemiologymentioning

confidence: 99%

Naegleria fowleri after 50 years: is it a neglected pathogen?

Martínez-Castillo

Cardenas-Zuniga

Coronado-Velázquez

et al. 2016

Journal of Medical Microbiology

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It has been 50 years since the first case of primary amoebic meningoencephalitis (PAM), an acute and rapidly fatal disease of the central nervous system (CNS), was reported in Australia. It is now known that the aetiological agent of PAM is Naegleria fowleri, an amoeba that is commonly known as 'the brain-eating amoeba'. N. fowleri infects humans of different ages who are in contact with water contaminated with this micro-organism. N. fowleri is distributed worldwide and is found growing in bodies of freshwater in tropical and subtropical environments. The number of PAM cases has recently increased, and the rate of recovery from PAM has been estimated at only 5 %. Amphotericin B has been used to treat patients with PAM. However, it is important to note that there is no specific treatment for PAM. Moreover, this amoeba is considered a neglected microorganism. Researchers have exerted great effort to design effective drugs to treat PAM and to understand the pathogenesis of PAM over the past 50 years, such as its pathology, molecular and cellular biology, diagnosis and prevention, and its biological implications, including its pathogenic genotypes, its distribution and its ecology. Given the rapid progression of PAM and its high mortality rate, it is important that investigations continue and that researchers collaborate to gain better understanding of the pathogenesis of this disease and, consequently, to improve the diagnosis and treatment of this devastating infection of the CNS.

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Section: Epidemiologymentioning

confidence: 99%

Naegleria fowleri after 50 years: is it a neglected pathogen?

Martínez-Castillo

Cardenas-Zuniga

Coronado-Velázquez

et al. 2016

Journal of Medical Microbiology

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“…These observations of experimental animals dying from encephalitis led Culbertson et al (99) to predict a role for free-living amebae as agents of human disease. Human cases of amebic encephalitis were reported soon thereafter from Australia, Europe, Africa, South America, and the United States (35,57,58,64,74,142,201,280,284,344,476). However, some of these cases were identified later as primary amebic meningoencephalitis, a rapidly fatal disease of the CNS caused by another free-living ameba, Naegleria fowleri (57,268,286).…”

Section: Introductionmentioning

confidence: 99%

Acanthamoebaspp. as Agents of Disease in Humans

2003

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Acanthamoeba spp. are free-living amebae that inhabit a variety of air, soil, and water environments. However, these amebae can also act as opportunistic as well as nonopportunistic pathogens. They are the causative agents of granulomatous amebic encephalitis and amebic keratitis and have been associated with cutaneous lesions and sinusitis. Immuno compromised individuals, including AIDS patients, are particularly susceptible to infections with Acanthamoeba. The immune defense mechanisms that operate against Acanthamoeba have not been well characterized, but it has been proposed that both innate and acquired immunity play a role. The ameba's life cycle includes an active feeding trophozoite stage and a dormant cyst stage. Trophozoites feed on bacteria, yeast, and algae. However, both trophozoites and cysts can retain viable bacteria and may serve as reservoirs for bacteria with human pathogenic potential. Diagnosis of infection includes direct microscopy of wet mounts of cerebrospinal fluid or stained smears of cerebrospinal fluid sediment, light or electron microscopy of tissues, in vitro cultivation of Acanthamoeba, and histological assessment of frozen or paraffin-embedded sections of brain or cutaneous lesion biopsy material. Immunocytochemistry, chemifluorescent dye staining, PCR, and analysis of DNA sequence variation also have been employed for laboratory diagnosis. Treatment of Acanthamoeba infections has met with mixed results. However, chlorhexidine gluconate, alone or in combination with propamidene isethionate, is effective in some patients. Furthermore, effective treatment is complicated since patients may present with underlying disease and Acanthamoeba infection may not be recognized. Since an increase in the number of cases of Acanthamoeba infections has occurred worldwide, these protozoa have become increasingly important as agents of human disease

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“…Naegleria fowleri is the etiological agent of primary amoebic meningoencephalitis in humans (6,10). To date, amphotericin B is the most effective antinaeglerial drug in vitro, is able to protect mice infected with N. fowleri (9), and appears to alter favorably the outcome of primary amoebic meningoencephalitis in humans (3).…”

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confidence: 99%

Susceptibility of Naegleria fowleri to delta 9-tetrahydrocannabinol

Pringle¹,

Bradley²,

Harris³

1979

Antimicrob Agents Chemother

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Growth of the pathogenic amoeboflagellate Naegleria fowleri is inhibited by delta 9-tetrahydrocannabinol (delta 9-THC). delta 9-THC is amoebostatic at 5 to 50 micrograms/ml. delta 9-THC prevents enflagellation and encystment, but does not impair amoeboid movement. Calf serum at 10 and 20% (vol/vol) reduces the antiamoeba activity of delta 9-THC. Only 1-methoxy delta 8-tetrahydrocannabinol, of 17 cannabinoids tested, failed to inhibit growth of N. fowleri. Antinaeglerial activity was not markedly altered by opening the pyran ring, by converting the cyclohexyl ring to an aromatic ring, or by reversing the hydroxyl and pentyl groups on the benzene ring. delta 9-THC prevented the cytopathic effect of N. fowleri on African green monkey (Vero) cells and human epithelioma (HEp-2) cells in culture. delta 9-THC afforded modest protection to mice infected with N. fowleri.

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Naegleria (Sp.) Identified in Amebic Encephalitis

Cited by 67 publications

References 0 publications

Naegleria fowleri after 50 years: is it a neglected pathogen?

Naegleria fowleri after 50 years: is it a neglected pathogen?

Acanthamoebaspp. as Agents of Disease in Humans

Susceptibility of Naegleria fowleri to delta 9-tetrahydrocannabinol

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