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Amebic meningoencephalitis , caused by Naegleria fowleri , is characterized by acute suppurative inflammation of the brain and meninges. Visit: Amoebiasis (Entamoeba histolytica)

N. fowleri is a nonparasitic, free-living soil ameba that causes rhinitis when introduced into the nasal cavity.

The amebae may subsequently invade the olfactory nerves, migrate through the cribriform plate, and proliferate in the meninges and brain. The infections are fulminating and uniformly fatal.

The disease has been recognized in many parts of the world including the United States, Europe, Australia, New Zealand, South America, and Africa.

It has been diagnosed principally on histologic evidence, with only a few cases confirmed by cultures.

Almost all patients give a history swimming in freshwater lakes or pools shortly before the onset of symptoms.

In tissue sections, trophozoites of Naegleria measure from 8 to 15 micro meter across.  Image1 ;  Image2 ; Image3 ; Image4 ; Image5.

The cytoplasm is not distinctive, but the nuclei are sharply outlined and deep stained with hematoxylin.

Some amebae have perinuclear vacuoles that tend to obscure the nuclear margin.

Cysts of the Naegleria have not been seen in tissue sections.

Clinically, acute and fulminating rhinitis and meningoencephalitis lead to death, usually within 1 to 2 weeks.

Most victims have been in their teens or younger.

The cerebrospinal fluid contains numerous neutrophils, blood, and amebae.

Grossly, the brain is swollen and soft, with vascular congestion and a thin purulent exudates on the meningeal surface, most prominent over the lateral and basal areas.

There is massive destruction of the brain by amebae, which invade the brain along the Virchow-Robin spaces.

Thrombosis and destruction of blood vessels are associated with extensive hemorrhage in the affected areas.

The olfactory tract and bulbs are enveloped and destroyed, and there is an exudate between the bulb and the inferior surface of the temporal lobe.

Histologic sections show severe damage to the olfactory tract and bulb and invasion by amebae of nerve fibres in the passages through the cribriform plate.

The exudate expands the subarachnoid space.

Extensive proliferation of Naegleria in the brain often leads to formation of solid masses of amebae (amebomas).

Meningitis can extend the full length of the cord.

The cerebellum is usually heavily involved, with amebae surrounding and damaging Purkinje cells.

There may be large areas of necrosis in the gray matter of the cerebellum and cerebrum.  

During life, diagnosis is made by finding organisms in the cerebral spinal fluid or in biopsy specimens.

The fluid may be placed directly in the counting chamber, where motile amebae are seen.

                     

 Abstract:

Primary amebic meningoencephalitis.J Assoc Physicians India. 2006 Apr;54:327-9.

Fatal case of Naegleria fowleri meningo-encephalitis in an infant: case report.Ann Trop Paediatr. 2005 Sep;25(3):223-6.

Diagnosis of the primary amoebic meningoencephalitis due to Naegleria fowleri.Parasitol Int. 2005 Dec;54(4):219-21

Review of clinical presentations in Thai patients with primary amoebic meningoencephalitis.MedGenMed. 2004 Mar 8;6(1):2.

Primary meningoencephalitis by Naegleria fowleri: first reported case from Mangalore, South India.J Clin Microbiol. 2002 Jan;40(1):309-10

Assessing the risk of primary amoebic meningoencephalitis from swimming in the presence of environmental Naegleria fowleri.Appl Environ Microbiol. 2001 Jul;67(7):2927-31

Primary amebic meningoencephalitis: a review of the clinical literature.Wilderness Environ Med. 1997 Nov;8(4):211-3

Primary amebic meningoencephalitis due to Naegleria fowleri: an autopsy case in Japan.Pathol Int. 1999 May;49(5):468-70

                       

 
May 2009

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