Naegleria fowleri Hemorrhagic Meningoencephalitis: Report of Two Fatalities in Children

2004 ◽  
Vol 19 (3) ◽  
pp. 231-233 ◽  
Author(s):  
Darin T. Okuda ◽  
Hank J. Hanna ◽  
Stephen W. Coons ◽  
John B. Bodenstelner

Two cases of hemorrhagic meningoencephalitis secondary to Naegleria fowleri infection confirmed by postmortem analysis are described. The first patient is a 5-year-old boy who presented with a severe headache, neck stiffness, and lethargy. His neurologic examination was significant for somnolence and nuchal rigidity. Cerebrospinal fluid studies and structural neuroimaging were consistent with hemorrhagic meningoencephalitis. Another 5-year-old boy presented to a different institution 2 miles away in the same week with similar complaints. Both patients declined rapidly and expired within 48 hours of admission secondary to transtentorial herniation caused by the mass effect of inflammation, edema, and hemorrhage with displacement of the brain stem. Histopathologic and immunochemistry analysis of brain tissue revealed the presence of Naegleria trophozoites in both cases.

2015 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This chapter contains 4 highly rendered figures, 7 tables, 16 references, and 5 MCQs.


2018 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This review contains 4 highly rendered figures, 8 tables, and 17 references.


2020 ◽  
Vol 12 (1) ◽  
pp. 195-202
Author(s):  
Ikrame Zeouk ◽  
Ines Sifaoui ◽  
Aitor Rizo-Liendo ◽  
Iñigo Arberas-Jiménez ◽  
María Reyes-Batlle ◽  
...  

2020 ◽  
Vol 8 (5) ◽  
pp. 789
Author(s):  
Aitor Rizo-Liendo ◽  
Ines Sifaoui ◽  
Luis Cartuche ◽  
Iñigo Arberas-Jiménez ◽  
María Reyes-Batlle ◽  
...  

Naegleria fowleri is an opportunistic pathogenic free-living amoeba which is able to rapidly colonize the central nervous system (CNS) and causes a lethal infection known as primary amoebic meningoencephalitis (PAM). Furthermore, more than 98% of the known cases of PAM are fatal and affect mainly children under 12 and young adults. Until now, no fully effective therapeutic agents against N. fowleri are available and hence the urgent need to find novel agents to treat PAM. At present, PAM therapy is based on the combination of amphotericin B, miltefosine, among others, with unwanted toxic effects. Recently, our team isolated various indolocarbazoles (ICZs) from the culture of a mangrove strain of Streptomyces sanyensis which showed activity against kinetoplastids and the Acanthamoeba genus. Hence, in this study, the activity of the previously isolated ICZs, staurosporine (STS), 7-oxostaurosporine (7OSTS), 4′-demethylamino-4′-oxostaurosporine, and streptocarbazole B, was evaluated against two type strains of N. fowleri. Furthermore, the performed activity assays revealed that STS was the most active ICZ presenting an inhibitory concentration 50 (IC50) of 0.08 ± 0.02 µM (SI 109.3). Moreover, STS induced programmed cell death (PCD) in the treated amoebae by triggering DNA condensation, mitochondrial disfunction, cell membrane disruption, and reactive oxygen species (ROS) generation. Therefore, STS could be a promising therapeutic agent against PAM.


Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1320 ◽  
Author(s):  
Andrea Güémez ◽  
Elisa García

Naegleria fowleri is a free-living amoeba (FLA) that is commonly known as the “brain-eating amoeba.” This parasite can invade the central nervous system (CNS), causing an acute and fulminating infection known as primary amoebic meningoencephalitis (PAM). Even though PAM is characterized by low morbidity, it has shown a mortality rate of 98%, usually causing death in less than two weeks after the initial exposure. This review summarizes the most recent information about N. fowleri, its pathogenic molecular mechanisms, and the neuropathological processes implicated. Additionally, this review includes the main therapeutic strategies described in case reports and preclinical studies, including the possible use of immunomodulatory agents to decrease neurological damage.


Author(s):  
Rubén Martín-Escolano ◽  
Lyto Yiangou ◽  
Eleanna Kazana ◽  
Gary K. Robinson ◽  
Martin Michaelis ◽  
...  

2001 ◽  
Vol 38 (2) ◽  
pp. 216-218 ◽  
Author(s):  
Y. Noda ◽  
H. Yokoyama ◽  
T. Katsuki ◽  
S. Kurashige ◽  
Y. Uchinuno ◽  
...  

Eight newborn calves showing ataxia were necropsied and examined histologically. Six of seven cerebrospinal fluid samples collected from these animals had neutralizing antibody for Akabane virus (AKV). All examined calves had nonsuppurative encephalomyelitis, localized mainly in the midbrain and spinal cord. Corresponding to the encephalitic lesion, AKV antigen was demonstrated in neuroglial cells in the brain stem and neuronal cells in the ventral horn of the spinal cord. This is the first study to demonstrate AKV antigen by immunohistochemistry in naturally infected newborn calves.


Author(s):  
M. Estée Török ◽  
Fiona J. Cooke ◽  
Ed Moran

This chapter covers both acute bacterial and viral, and chronic, meningitis, as well as tuberculous, cryptococcal, coccidioidal, and Histoplasma meningitis, describing meningeal symptoms (headache, neck stiffness, vomiting, photophobia) and cerebral dysfunction (confusion, coma). The chapter also covers neurocysticercosis (including parenchymal and extra-parenchymal cysts), encephalitis (an inflammatory process in the brain characterized by cerebral dysfunction), as well as brain abscess, cerebritis, subdural empyema, epidural abscess, and cerebrospinal fluid shunt infections.


1957 ◽  
Vol 55 (4) ◽  
pp. 464-474 ◽  
Author(s):  
D. M. McLean ◽  
D. Cameron

Eleven cases of aseptic meningitis occurred in a Cambridgeshire village between 17 October and 11 November 1955. The syndrome consisted of severe headache, backache, vomiting, fever and neck stiffness together with lymphocytes and frequently some granulocytes in the cerebrospinal fluid. Principally, it affected persons aged between 10 and 30 years. Out of a total population twenty-three at risk, seventeen were infected and eight became ill. A further three contacts who were living in Cambridge became ill.Identical strains of virus were isolated from the faeces of two patients by inoculation of trypsin-dispersed human amnion cells and from the faeces of another two patients by inoculation of monkey kidney cultures. Bourn virus, which belonged to the ECHO group, Type 9, multiplied readily and produced cytopathogenic effects in human amnion and monkey kidney cultures, but it was not cytopathogenic in HeLa cell cultures. These investigations strongly suggest that Bourn virus caused the epidemic.We wish to thank Dr M. G. P. Stoker for his advice and criticism and Mrs B. M. Cook for technical assistance.We are indebted to Dr J. O'H. Tobin and Dr F. K. Sanders for advice on certain technical procedures.It is a pleasure to acknowledge the assistance given by many colleagues and friends, including Dr D. I. Annear, Miss D. K. Bell, Mrs D. Ditchburn, Dr R. M. Fry, Dr D. Gairdner, Dr J. E. Power, Dr D. Simpson, Dr P. Tyzer and Dr P. J. Wormald.


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