Cases Of Primary Amebic Meningoencephalitis Research Articles

Naegleria and Acanthamoeba Infections: Review

Infections caused by small, free-living amebas are still unfamiliar to many clinicians, pathologists, and laboratorians. As of 31 July 1989, more than 140 cases of primary amebic meningoencephalitis caused by Naegleria fowleri and more than 40 cases of granulomatous amebic encephalitis caused by Acanthamoeba species (including two cases in patients with AIDS) and possibly by other free-living amebas had occurred worldwide. The recent increase in acanthamoeba keratitis (more than 200 cases), especially in contact lens wearers, has generated new interest in this group of amebas. Effective treatment is still lacking. Risk factors, clinical manifestations, and laboratory parameters helpful in the recognition of infections of the central nervous system (i.e., granulomatous amebic encephalitis and primary amebic meningoencephalitis) and acanthamoeba keratitis are reviewed.

Primary amebic meningoencephalitis diagnosed in the emergency department

Reported is a case of primary amebic meningoencephalitis diagnosed in the emergency department. The patient, a previously healthy teenager, developed Naegleria meningoencephalitis after swimming in a freshwater public pool. The Naegleria caused acute fulminating infection culminating in the death of the patient 36 hours after admission. Results of a spinal tap, together with the history of swimming in warm fresh water, led to the emergency department diagnosis.

A Case of Primary Amebic Meningoencephalitis in Zaria, Nigeria

A case of primary amebic meningoencephalitis due to Naegleria fowleri in a Nigerian child is described. This is probably the first authentic case from West Africa. The clinical manifestations, isolation of the ameba from the cerebrospinal fluid and nasal passages, poor response to amphotericin B, and ultimate fatal outcome all are consistent with the diagnosis of primary amebic meningoencephalitis. Subsequent identification based on morphologic features, flagellation, animal pathogenicity, and nuclear division proved conclusively that the ameba was Naegleria fowleri. The route of entry of the ameba proved to be nasal. In the absence of the history of swimming and in view of the dusty harmattan period during which the child was admitted, a possibility of infection by inhalation of dust harboring amebic cysts is suggested.

Recovery of Soil Amebas from the Nasal Passages of Children during the Dusty Harmattan Period in Zaria

Following a fatal case of primary amebic meningoencephalitis during the dusty harmattan period in an 8-month-old child in whose case Naegleria fowleri was recovered both from the cerebrospinal fluid and from material from the nose in absence of a history of swimming, it was hypothesized that dust during the harmattan might harbor amebic cysts, which may be inhaled by human beings and cause infection. A preliminary survey was thus carried out to examine the nasal passages of children for the presence of soil amebas during the harmattan. In all, 50 children were evaluated for the presence of soil amebas. Positive cultures for the soil amebas were obtained from 12 children (24%). Four species of amebas were isolated singly or in combination with other species. Pathogenic Naegleria fowleri, proved pathogenic for mice, were cultured from specimens from two children.

Fatal Disease

More than 75 cases of primary amebic meningoencephalitis (PAME) have been reported within the past twenty years. By 1970, it was obvious to most investigators that there was an association of the majority of cases of PAME with a recent history of swimming or diving in warm water of high organic content. Lakes, rivers, ponds, swimming pools, drainage ditches, hot springs, domestic waste water, septic-tank effluent, and bathtubs--all have been linked to PAME. Because of the widespread distribution and survival of the organisms and the projected growth of new power plants and new industries, it can be expected that the number of cases of PAME will increase. (CAJ)

Myocarditis associated with primary amebic (Naegleria) meningoencephalitis.

Prompted by findings of myocarditis in a patient dying from primary amebic meningoencephalitis, a retrospective search for myocarditis in autopsy material from 15 additional cases of primary amebic meningoencephalitis was undertaken. All cases were believed due to Naegleria (probably N. fowleri ). Seven of 16 cases showed either diffuse or focal myocarditis, and in two myocardial necrosis was present. Three cases showed only sparse foci of acute myocarditis. Material from ten consecutive autopsied cases of acute, fatal, purulent meningitis due to bacteria and from ten consecutive autopsied cases of acute, fatal subarachnoid hemorrhage were utilized as matched controls and reviewed for the presence of myocarditis. Only two cases (one from each control group) had myocarditis, both focal and mild in nature. The etiology as well as the pathogenesis of such myocarditis is unclear, and speculatively it could be due to a variety of factors. Nevertheless, diffuse or focal myocarditis appears to occur with a higher frequency in primary acute meningoencephalitis than in other acutely fatal central nervous system diseases, and perhaps more often than heretofore has been suspected.

Naegleria: another pathogenic ameba studies in germfree guinea pigs.

Free-living amebas of the genus Naegleria, of world-wide distribution and long considered harmless, have been linked etiologically with 57 fatal cases of primary amebic meningoencephalitis during the last decade. Naegleria from cultures derived from one of these fatal cases in Richmond, Virginia, have been inoculated intranasally, intraorally, into the conjunctival sac near the inner canthus of the eyes, and into induced skin lesions in adult germfree guinea pigs. Of 33 animals inoculated intranasally with 18 to 31 amebas, 31 developed a fatal encephalitis. There was considerable destruction of tissues of the cerebellum and the cerebrum and including the olfactory lobes. The meninges were involved to varying degrees in most of the animals. None of the animals inoculated by the three other routes developed either symptoms or lesions.

Waterborne Disease Outbreaks in 1954

For the 2-year period 1989-1990, 16 states reported 26 outbreaks due to water intended for drinking; an estimated total of 4,288 persons became ill in these outbreaks. Giardia lamblia was implicated as the etiologic agent for seven of the 12 outbreaks in which an agent was identified. The outbreaks of giardiasis were all associated with ingestion of unfiltered surface water or surface-influenced groundwater. An outbreak with four deaths was attributed to Escherichia coli O157:H7, the only bacterial pathogen implicated in any of the outbreak investigations. An outbreak of remitting, relapsing diarrhea was associated with cyanobacteria (blue-green algae)-like bodies, whose role in causing diarrheal illness is being studied. Two outbreaks due to hepatitis A and one due to a Norwalk-like agent were associated with use of well water. Eighteen states reported a total of 30 outbreaks due to the use of recreational water, which resulted in illness for an estimated total of 1,062 persons. These 30 reports comprised 13 outbreaks of whirlpool- or hot tub-associated Pseudomonas folliculitis; 13 outbreaks of swimming-associated gastroenteritis, including five outbreaks of shigellosis; one outbreak of hepatitis A associated with a swimming pool; and three cases of primary amebic meningoencephalitis caused by Naegleria. The national surveillance of outbreaks of waterborne diseases, which has proceeded for 2 decades, continues to be a useful means for characterizing the epidemiology of waterborne diseases.