Biology of Naegleria spp.

The genus Naegleria is comprised of a group of free-living ameboflagellates found in diverse habitats worldwide. Over 30 species have been isolated from soil and water but only Naegleria fowleri (N. fowleri) has been associated with human disease. Naegleria fowleri causes primary amebic meningoencephalitis (PAM), a fatal disease of the central nervous system. The pathogenesis of PAM and the role of host immunity to N. fowleri are poorly understood. Strategies for combating infection are limited because disease progression is rapid and N. fowleri has developed strategies to evade the immune system. The medical significance of these free-living ameboflagellates should not be underestimated, not only because they are agents of human disease, but also because they can serve as reservoirs of pathogenic bacteria.

The immune response to Naegleria fowleri amebae and pathogenesis of infection

Primary amoebic meningoencephalitis with Naegleria fowleri: clinical review.

Free-living amoebae causes three well-defined disease entities: (i) primary amoebic meningoencephalitis, caused by Naegleria fowleri, (ii) granulomatous amoebic encephalitis and (iii) chronic amoebic keratitis, caused by species of Acanthamoeba. Both Naegleria infections and chronic amoebic keratitis occur in healthy individuals while granulomatous amoebic encephalitis is often associated with patients with acquired immunodeficiencies. The different pathogenic behaviour of these organisms is associated with differences in life cycle, amoeboidal locomotion, enzyme composition (such as phospholipase A), and cytotoxins, as well as natural host immunity. Immunity against these amoebae (whether acquired or natural) involves a combination of complement, antibody and cell-mediated immunity. Evidence suggests that the major mechanisms of immunity against these amoebae is activation of phagocytic cells, especially neutrophils, by lymphokines and opsonization of the amoebae by antibody which promote an antibody dependent cellular destruction of the organism.

Free‐living amoebae: pathogenicity and immunity

Acute amebic meningoencephalitis caused by free-living amebae naegleria fowleri is extremely rare and uniformly fatal with only seven survivals reported till date An interesting case of naegleria meningitis diagnosed by wet mount cytology of cerebrospinal fluid (CSF) and treated with amphoterecin B, rifampicin and ornidazole with complete recovery is presented In cases of suspected pyogenic meningitis, if CSF staining, antigen detection or culture is negative for bacteria, a wet mount cytology of CSF for naegleria is suggested Early treatment with amphoterecin B and rifampicin may improve survival

Naegleria meningitis : a rare survival.

The capability of serum samples from 423 human subjects to agglutinate rounded cells of Naegleria fowleri nN68 was assessed. Sera from the umbilical cords of seven infants failed to agglutinate N. fowleri cells. The median agglutination titer was 1:4 for sera from children through age 4 years, 1:8 for sera from juveniles 5 to 15 years of age, and 1:16 for sera from subjects 15 to 30 years old. The agglutination titers of sera from older adults decreased to a median of 1:8 for the 40- to 60-year-old age group and to 1:4 for the 60- to 90-year-old subjects. Serum samples from young adults agglutinated rounded cells of both N. fowleri and N. gruberi. The agglutination activity for N. fowleri was removed by absorption with N. fowleri but not with N. gruberi. Conversely, agglutination activity for N. gruberi was removed by absorption with N. gruberi but not with N. fowleri. The agglutinating activity for N. fowleri was immunoglobulin M. Serum samples from children displayed markedly disparate capabilities to agglutinate N. fowleri and N. gruberi. Only rounded cells of N. fowleri or N. gruberi were reliably agglutinated by human serum samples. Live or paraformaldehyde-killed cells could be used in the assay, but live N. gruberi cells returned to the amoeboid form, and these agglutinated poorly.

Agglutination of Naegleria fowleri and Naegleria gruberi by antibodies in human serum.

Abstract Trichomonas gallinae is the causative protozoan parasite of avian trichomonosis, an infectious disease of wild bird species. Since an outbreak in the UK in 2005, avian trichomonosis has resulted in mass mortality events in greenfinch ( Chloris chloris ) and chaffinch ( Fringillia coelebs ) populations. Given its proximity to the UK, it is important to monitor the emergence of T. gallinae in Ireland. This study proposed to sample greenfinch, goldfinch ( Carduelis carduelis ) and feral pigeon ( Columba livia domestica ) in Ireland with the aim of culturing and isolating T. gallinae. The oral cavity of birds was sampled with an oropharyngeal swab, which was then inoculated into Biomed InPouch™ TF test kits. T. gallinae infection was diagnosed in 9 of 60 sampled birds (6 greenfinch and 3 feral pigeon), giving a total infection prevalence rate of 15% and providing evidence that avian trichomonosis is present among, but may not be limited to, greenfinch and feral pigeon populations in Ireland. It is also the first laboratory-based diagnosis of T. gallinae from live, free-living birds in Ireland to our knowledge. It is possible that avian trichomonosis is contributing to the recent decline in greenfinch populations in Ireland. Additionally, the presence of yeast cells in some positive samples did not appear to impede trichomonad growth, which may suggest a potential symbiotic relationship between T. gallinae and yeast species. 

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M F Reilly

Papers

Agglutination of Naegleria fowleri and Naegleria gruberi by antibodies in human serum.

Confirmation of avian trichomonosis among wild birds in Ireland