Amebic
Meningoencephalitis
Caused by
Balamuthia
mandrillaris
D a v i d A. G r i e s e m e r , M D * ,
Leslie L. B a r t o n , M D * ,
Charles M. Reese, MD*,
P e t e r C. J o h n s o n , M D ~,
Jill A . B . G a b r i e l s e n , MD//,
D i n e s h T a l w a r , M D ~, a n d
G o v i n d a S. V i s v e s v a r a , P h D * *

Griesemer DA, Barton LL, Reese CM, Johnson PC, Gabrielsen JAB, Talwar D, Visvesvara GS. Amebic meningoencephalitis caused by Balamuthia mandrillaris. Pediatr Neurol 1994;10:249-254.

Introduction
Free-living amebae, although ubiquitous in soil and water, have only been etiologically associated with central
nervous system (CNS) disease in humans in the last two
decades. Known pathogens include Naegleria fowleri,
Acanthamoeba spp, and recently, leptomyxid ameba
[1-3]. We report 2 children with granulomatous meningoencephalitis caused by a newly identified leptomyxid
ameba, Balamuthia mandrillaris. In addition, we reviewed all previously reported children with amebic meningoencephalitis who have now been retrospectively
identified through immunofluorescent studies to have had
B. mandrillaris infection.
Case Reports

Free-living amebae etiologically associated with central
nervous system (CNS) infection in children have included Acanthamoeba, Naegleria, and recently, leptomyxid ameba. Two previously healthy children are reported with CNS infection caused by leptomyxid
ameba, recently classified as Balamuthia mandriUaris.
One child, a 27-month-old boy, had right hemiparesis
and aphasia, and the other, a 13-year-old girl, had
headache, right hemiparesis, diplopia, and left facial
weakness. Cerebrospinal fluid studies of both children revealed a mononuclear pleocytosis and mildly
elevated protein. The younger child developed seizures
and progressive cerebrovascular occlusions; both developed hydrocephalus and coma progressing to death
16 days after onset of symptoms. The younger child at
autopsy had necrotizing meningoencephalitis, left internal carotid arteritis, and amebic trophozoites and
cysts in brain. Perivascular trophozoites were difficult
to distinguish morphologically from macrophages in
the older child, who had no cyst forms. Indirect immunofluorescence test revealed CNS infection with
B. mandrUlaris in both. This leptomyxid ameba, formerly considered an innocuous soil organism, should
be considered in the differential diagnosis of progressive or atypical childhood stroke.

Patient I. A 27-month-old previously healthy boy developed an acute
fight hemiparesis. One week earlier he was diagnosed with a left otitis
media and was treated with amoxicillin. He had low-grade fever that
resolved before the day of hospitalization. The day of admission he
awoke with vomiting and the inability to sit without support. He did not
speak, eat, or drink on the day of admission. Medical history was remarkable only for multiple episodes of otitis media. The family lived in
a trailer with a dog, two cats, guinea pig, rabbit, and fish.
Rectal temperature on hospital admission was 37°C; pulse 108 beats/
min, respiratory rate 28 breaths/min, and blood pressure 117/62 mm Hg.
He was sleepy, but arousable and cried intermittently. He spoke no
intelligible words. The left tympanic membrane was pink and retracted.
His neck was supple. He had right facial weakness, uncoordinated
tongue movements, and a hoarse cry. He withdrew his left arm and leg
from painful stimuli, but had weakness of the right leg and did not move
his fight arm. Deep tendon reflexes were symmetric and plantar responses were flexor bilaterally.
Magnetic resonance imaging (MRI) revealed increased T2-signal in the
left middle cerebral artery distribution, left caudate, and lentiform nucleus (Fig 1A). Absence of flow void signal suggested occlusion of the
left internal carotid artery (Fig 1B). Paranasal sinuses were normal.
Initial laboratory studies included hematocrit 37%; 8,900 leukocytes/
mm 3 with 68% neutrophils, 24% lymphocytes, 6% monocytes, 1%
eosinophils, 1% basophils, 510,000 platelets/mm 3, prothrombin time
(PT) 13.0 s, partial thromboplastin time (PTT) 28.5 s, protein C 134
p.g/ml and protein S 141 p~g/ml (normal), anti-thrombin III 140% (normal), sedimentation rate 25 mrn/hr, antinuclear antibody (ANA) <1:20,
and normal urinalysis, chest radiography, and echocardiography. Lumbar puncture revealed cerebrospinal fluid (CSF) with 90 leukocytes/mm 3
(100% mononuclear cells), 2 erythrocytes/mm 3, protein 64 mg/dl, and

From the *Division of Pediatric Neurology, Department of Neurology;
Medical U~versity of South Carolina.; Charleston, South Carolina;
Sections of TInfectious Diseases and 1'Pediatric Neurology;
Departments of//Pediatrics and *Pathology~ University of Arizona
Health Sciences Center; Tucson, Arizona; ~Department of
Neuropathology; Barrow Neurological Institute; St. Joseph's Hospital
and Medical Center; Phoenix, Arizona; and **Parasitic Diseases
Branch, Division of Parasitic Diseases; National Center for Infectious
Diseases; Centers for Disease Control and Prevention; Atlanta,
Georgia.

Communications should be addressed to:
Dr. Griesemer; Division of Pediatric Neurology, Department of
Neurology; Medical University of South Carolina; 171 Ashley
Avenue; Charleston, SC 29425.
Received December 2, 1993; accepted January 25, 1994.

© 1994 by Elsevier Science Inc. • 0887-8994/94/$7.00

Griesemer et al: Balamuthia mandriUaris

249

A

B

Figure 1. (A ) T2-weighted axial MRI. Increased signal in the distribution of the left middle cerebral artery, left caudate, and lentiJbrm nuclei
(B) Tl-weighted axial MRI. Absence of flow void signal of the left internal carotid artery, suggesting occlusion of the left vessel.
glucose 34 mg/dl. Intravenous ampicillin and cefotaxime were administered.
On the second hospital day, he had increased movement of his right
arm and leg. Magnetic resonance angiography disclosed diminished caliber of the left internal carotid artery, particularly in the cavernous segment (Fig 2). Severe stenosis also extended to the proximal segments of
the middle cerebral artery and the anterior cerebral artery.
On the third hospital day, the child's right-sided weakness increased.
Repeated CSF studies demonstrated 280 leukocytes/mm3 (99% mononuclear cells, among which were numerous plasma cells, and 1% segmented nuclear cells), 13 erythrocytes/mm3, protein 71 mg/dl, and glucose 95 mg/dl. The next day, angiography disclosed complete occlusion
of the left internal carotid artery near its apex, distal to the anterior
choroidal artery (Fig 3). Stenosis was seen at the origin of the left
ophthalmic artery. Collateral flow to the left hemisphere occurred via
leptomeningeal supply from the posterior cerebral artery and through the
anterior communicating artery. Intravenous dexamethasone was administered. The patient subsequently developed a left sixth nerve palsy and
increasing lethargy. On the eighth hospital day repeated CSF studies
demonstrated 555 leukocytes/mm3 (77% mononuclear cells, 18% plasma
cells, and 5% segmented nuclear ceils), 2,920 erythrocytes/mm3, protein
69 mg/dl, and glucose 48 mg/dl. Two days later, he had a seizure and
phenytoin and phenobarbital were administered.
Subsequently, the patient's condition deteriorated despite administration of praziquantel, fluconazole, ampicillin, cefotaxime, tdmethoprirnsulfamethoxazole, vancomycin, isoniazid, rifampin, and pyrazinamide.
By day 12 of hospitalization, he had nonreactive pupils, no gag or cough
reflex, no withdrawal from painful stimuli, and was apneic. Cranial
computed tomography (CT) revealed changes suggesting infarction in
the fight basal ganglia, hemorrhagic transformation of the left middle
cerebral artery distribution infarct, and dilated ventricles. He was intubated and a ventriculostomy tube was placed; however, he died on day
16 of hospitalization.
All cultures, serologies, and skin tests were negative for bacteria,

250

PEDIATRIC NEUROLOGY

Vol. 10 No. 3

fungi, mycobacteria, viruses including human immunodeficiency virus
and Epstein-Barr, mycoplasma, Rochalimaea spp.. Treponema pallidum, and Taenia solium.
Autopsy revealed diffuse brain edema with prominent cerebellar tonsils. Leptomeninges overlying the left cerebral cortex appeared hemorrhagic without visible signs of meningitis; those around the pyramids of
the medulla were thickened and discolored. Gross sections revealed proteinaceous debris in the lateral ventricles with diffuse necrosis of gray
and white matter. Hemorrhage (0.5 cm) was evident in the anterior left
medulla. The distal left internal carotid artery was completely occluded
by thrombus extending to the middle cerebral artery. The distal right
internal carotid artery had a thickened, firm wall with a patent lumen.
Histologic examination revealed marked thickening of the leptomeninges with prominent chronic inflammatory infiltrate, giant cells,
and necrotizing vasculitis. Around vessels in the Virchow-Robin spaces
and scattered throughout the meninges were numerous cells with vesicular nuclei, prominent nucleoli, and eosinophilic cytoplasm, ranging in
size from 15 to 40 I~m, consistent with trophozoite forms of ameba (Fig
4). Rare, spherical, double-walled cysts were also identified. Sections of
the left and right internal carotid artery revealed chronic necrotizing
vasculitis with numerous trophozoite and cyst forms of ameba present
within the wall of the vessel.
Autopsy also revealed multiple, well-demarcated hemorrhagic foci in
the lungs. Histologically, multinodular lymphohistiocytic lesions manifested interstitially and in alveoli of the lungs. No amebic trophozoites or
cysts were observed in the lungs. No skin lesions were identified.
On the basis of histopathologic features of the amebic trophozoites and
the presence of cysts in tissue sections, the infectious agent was considered to be either Acanthamoeba or Balamuthia. To differentiate between
the two, indirect immunofluorescence test was performed using rabbit
antisera against a number of Acanthamoeba spp. belonging to three
groups as well as B. mandriUaris. The sections were deparaffinized and
covered with a 1:100 dilution of the various antisera and incubated for 30
min at 37°(2. The slides then were washed three times, 10 rain/wash, with

Figure 2. Magnetic resonance angiography, coronal view, demonstrating diminished caliber of the left internal carotid artery with stenosis
of the left anterior cerebral artery and left middle cerebral artery (Patient 1).
phosphate-buffered saline at pH 7.6. After the third wash, the sections
were covered with fluorescein isothiocyanate-conjugated goat anti-rabbit
immunoglobulins at a dilution of 1:50. Evan's blue was used as the
counterstain. The slides were incubated and washed as described above,

Figure 3. Cerebral angiogram, left lateral view, disclosing complete
occlusion of the left internal carotid artery near its apex, distal to the
anterior choroidal artery with stenosis of the left ophthalmic artery (Patient 1).

Figure 4. Photomicrograph of cerebral cortex demonstrating numerous trophozoite-forms of ameba (arrow) in a perivascular distribution.
Trophozoites appear as large cells (15-40 lain) with vesicular nucleus,
prominent nucleolus, and granular eosinophilic cytoplasm (Patient 1).

examined, and photographed with an Olympus BH-2 microscope
equipped with epi-illumination.
The amebas in the sections did not react with any of the antiAcanthamoeba sera (i.e., A. astronyxis: group 1; A. castellanii, A. polyphaga, and A. rhysodes: group 2; and A. culbertsoni: group 3) at a 1:100
dilution, whereas amebas in tissue sections reacted strongly with the
anti-Balamuthia serum at that dilution (Fig 5), indicating that Balamuthia is antigenically distinct from Acanthamoeba. Based on these
findings, it was concluded that the infectious agent belongs to the Balamuthia genus.
Patient 2. A 13-year-old, previously healthy girl developed severe
frontal and temporal headache with double vision and progressive vomiting 4 days before hospitalization. Medical history was remarkable for
travel 4 weeks previously to Mexico where she had eaten " b a d " pork.
Oral temperature on hospital admission was 38.2°C. She was alert and
oriented to her surroundings, but she had meningismus. Grade III to IV
papilledema was observed bilaterally. Abducens nerve palsies occurred
bilaterally and her tongue deviated to the right. She had a right hemiparesis with greater involvement of the arm and an extensor plantar response on the right.
Cranial CT revealed a large mass in the right frontal region with
multiple cystic lesions. Initial laboratory studies included hemoglobin
12.0 mg/dl, 8,300 leukocytes/mm3 with 79% neutrophils, 19% lymphocytes, and 2% monocytes, sedimentation rate 53 mm/hr, and normal
creatine phosphokinase. Intravenous dexamethasone was administered.
Lumbar puncture on the fourth hospital day disclosed CSF with 470
leukocytes/mm3 (98% mononuclear cells, 1% neutrophils, and 1%
eosinophils), 2 erythrocytes/mm3, protein 50 mg/dl, and glucose 70 mg/
dl. The next day praziquantel was administered for presumed cysticer-

Griesemer et al: Balamuthia mandrillaris

251

foci described on gross examination contained large numbers of cells
characterized by a prominent nucleus with nucleolus-like, centrally
placed chromatin and by a sharply circumscribed cytoplasmic border.
The foamy cytoplasm of these cells occasionally contained phagocytized
erythrocytes and were consistent with trophozoite forms of ameba. No
cysts were identified.
Indirect immunofluorescent test was performed using rabbit antisera as
described above. The amebas in the sections did not react with any of the
anti-Acanthamoeba sera, but fluoresced brightly with the antiBalamuthia serum.

Discussion

Figure 5. lmmunofluorescence patterns of Balamuthia amebas in brain
of Patient 1. Note the distribution of amebas within the vascular walls:
original magnification, ×200.

cosis; headache, vomiting, and low-grade fever persisted. MRI on hospital day 7 demonstrated progression of cystic lesions. Her level of
consciousness began to decline and mannitol was administered. A ventriculostomy was placed and a biopsy of the frontal lobe lesion revealed
necrotic brain tissue. She died on hospital day 12.
Serology was negative for T. solium.
Autopsy revealed brain weight of 1,330 gin; diffuse softening of the
brainstem and cerebellum occurred but herniation was not evident. Multiple hemorrhagic necrotic loci, approximately 1.0 cm in diameter, were
observed in the right parietal and occipital lobes (Figs 6A, 6B). A 2.0-cm
area of softening with yellow discoloration was evident in the left frontal
lobe.
Histologic examination revealed an inflammatory infiltrate of the leptomeninges and extensive vascular wall necrosis. Sections of abnormal

Figure 6.

Differential diagnosis of stroke in children includes infection, although this association often j o i n t l y occurs with
bacterial meningitis or viral encephalitis. Clinical findings
of a progressive encephalopathy with m o n o n u c l e a r pleocytosis in these children, however, suggested a granulomatous process. Coccidioidomycosis, tuberculosis, and
cysticercosis were c o n s i d e r e d p o s s i b l e etiologies and
treatment was instituted without benefit. Serial n e u r o i m aging studies demonstrated multiple infarctions in the distribution of both large and small blood vessels. Light microscopy and i m m u n o f l u o r e s c e n t testing f o l l o w i n g autopsy identified the infectious agent.
A m o n g hundreds of free-living a m e b a e , only those of
the A c a n t h a m o e b a and Naegleria genera previously have
been k n o w n to cause disease in h u m a n s . N a e g l e r i a f o w l e r i
causes acute and f u l m i n a t i n g primary amebic m e n i n g i t i s
(PAM) in children who have b e e n s w i m m i n g or playing in
freshwater lakes and ponds. A c a n t h a m o e b a species cause
g r a n u l o m a t o u s a m e b i c e n c e p h a l i t i s ( G A E ) of several

(A,B) Horizontal sections of brain of Patient 2, revealing multiple foci of hemorrhagic necrosis.

252 PEDIATRIC NEUROLOGY Vol. 10 No. 3

SUBKINGDOM PROTOZOA

I
t
Subphylum Sarcodina
I
Suparclass Rhizopodea

Phylum Sarcomastigophora

Class Lobosea

Class Acarpomyxea

I

Subclass Gymnamoebia

'
Order Amoebida

Order Schizopyrenida

Sub Order Acanthopodina
'I
Family Acanthamoebidae

FamilyVahlkampfidae

I

Genus Acanthamoeba

I

L

Genus Naegleria

Order Leptomyxida

I

-f ":-amily Leptomyxidae
Genus Leptomyxa
L- Genus Balamuthia

Figure 7. Classification of Balamuthia.

weeks duration in immunocompromised or debilitated patients. Several cases of GAE believed to be caused by
Acanthamoeba, however, have been reidentified as caused
by leptomyxid ameba. Leptomyxid ameba, previously believed to be innocuous, was first isolated from brain of a
pregnant mandrill baboon that developed fight hemiparesis and died of meningoencephalitis [1]. Subsequently,
leptomyxid ameba was not only identified in brain sections of several human GAE patients, but also was isolated
into culture from a human patient [1,2]. The trophic and
cyst stage of leptomyxid ameba, especially in formalinfixed tissue sections, appears to be similar to Acanthamoeba spp. at the light microscopic level. Characteristic differences, however, exist between the two at the
ultrastructural level, as well as in physiologic and antigenic properties [1,3]. Leptomyxid ameba recently was
classified as B. mandrillaris of the order Leptomyxida
(Fig 7).
Our patients were not immunocompromised and had no
exposure to standing freshwater. Consequently, there was
little consideration of ameba as the infectious agent.
Pathogenic amebae, however, may at times be found in
the mouth or nasopharynx of healthy children [4-6]. We
speculate that environmental perturbations with increased
moisture in a desert climate may increase the likelihood of
soil amebae occurring as "normal flora."

Table 1.

Retrospective testing has identified infection by B.
mandrillaris as the cause of fatal GAE in 7 previously
reported children (Table 1). On the basis of clinical findings and morphology of the organism, previous reports
have presumptively attributed infection to Acanthamoeba
spp., despite absence of confirmatory immunofluorescence studies. The fourth child in the series, an 8Y2month-old girl, was previously reported only in a tabular
list [1]; however, additional clinical information was
available from one of the authors (GSV). This child developed high fever and fight Vlth nerve palsy 4 days before hospitalization. Lumbar puncture on admission disclosed CSF with 206 leukocytes/mm3 (83% mononuclear
cells, 17% segmented nuclear cells), 160 erythrocytes/
mm 3, protein 93 mg/dl, and glucose 33 mg/dl (serum
level: 113 mg/dl). Therapy with intravenous penicillin,
chloramphenicol, phenobarbital, dexamethasone, and
mannitol was initiated. She rapidly developed fight facial
weakness, left-sided extremity weakness, and then fightsided extremity weakness. Isoniazid, ethambutol, and rifampin were added to her treatment regimen. Cranial CT
on hospital day 7 revealed multifocal lucencies in the supra- and subtentofial regions. Brain biopsy disclosed perivascular cuffing and lymphocytic infiltrate with intranuclear cytoplasmic inclusion bodies. Increased intracranial
pressure and coma ensued, progressing to brain death on
hospital day 14. All cultures and serologies were negative
for bacteria, fungi, mycobactefia, and viruses, including
herpes simplex and cytomegalovirus. At autopsy, leptomeninges were translucent but focally hemorrhagic over
the entire cerebrum and cerebellum, with slight thickening
at the base of the brain. Significant edema occurred with
uncal and tonsillar notching. Multiple soft, reddish brown
areas, 2-3 mm in diameter, were evident diffusely in gray
and white matter, particularly in frontal and parietal lobes.
Histologic examination of the leptomeninges disclosed extensive inflammatory infiltrates with numerous monocytes
and occasional plasma cells. In areas of underlying cortex
demonstrating extensive necrosis, there were pefivascular
collections of large trophozoite forms of ameba appearing
as mononuclear cells with central nucleolus, occasional
pefinuclear halos and cytoplasmic vesicles, and rare in-

Children with amebic meningoencephalitis who by immunofluorescent studies have proved B. mandr///ar/s infection

Reference
Number

Date

Age (yrs)

Location

[7]
[8]
[9]
[1]
[ 10]

1974
1978
1979
1983
1986

2.5
0.3
2.5
0.8
11

Australia
So. Carolina
Pennsylvania
California
Texas

[ 1]
[ 11 ]
Patient 1
Patient 2

1988
1989
1993
1993

7
12
2.3
13

Venezuela
Argentina
Arizona
Arizona

Clinical Course
Fluctuating ataxia, cranial nerve palsies, headache; died in 30 days
Fever, vomiting, diarrhea, dehydration, lethargy, seizures; died in 37 days
Progressive hemiparesis over 6 mos, headache, vomiting; died in 240 days
Diarrhea, cough, fever, Vlth nerve palsy, hemiparesis; died in 15 days
Fever, focal seizure, focal MRI lesions, Vlth nerve palsy, papilledema, headache,
vomiting, hemiparesis; died in 180 days
Exophthalmos, Pyle disease, pneumonitis; died in 210 days
Malar rash for 2 years; cranial nerve palsies, dysarthria, hemiparesis; died in 21 days
Hemiparesis, seizures; died in 16 days
Headache, diplopia, hemiparesis; died in 16 days

Griesemer et al: Balamuthia mandrillaris 253

gested erythrocytes. A section from the right caudate nucleus revealed numerous smaller cysts with a prominent
outer wall. A retrospective review of the brain biopsy
revealed small clusters of trophozoite forms similar to
those observed at autopsy.
Like Acanthamoeba spp., B. mandrillaris produces a
subacute or chronic granulomatous encephalitis with death
occurring from 1 week to several months after onset of
symptoms. Both cause infection in patients who are immunocompromised, but B. mandrillaris also affects immunocompetent children. The presence of a marked granulomatous, histiocytic response in our patients supports
the presumed immunocompetence of these children [2],
despite treatment with steroids. Meningoencephalitis
caused by Acanthamoeba spp. is reported to spread hematogenously from a primary respiratory or cutaneous infection. It is possible that GAE secondary to B. mandrillaris may arise in a similar manner; however, our patients
had no apparent skin lesions. Pathologic examination of
the lungs in Patient 1 revealed multinodular lymphohistiocytic infiltrates, but there was no evidence of amebae.
Microscopic examination of brain sections from our patients demonstrated trophozoite forms clustered around
blood vessels and direct invasion of brain parenchyma.
Cyst forms, which are not evident with fulminant PAM,
also were observed in Patient 1. Cyst forms develop in
vitro in older tissue cultures [3] and presumably occur in
vivo with chronic infection, where the tissue substrate is
less nutritionally supportive. The thick-walled cyst stage
suggests that B. mandrillaris is well adapted for surviving
extreme environmental conditions. These amebae appear
not only capable of surviving in the Sonoran desert climate
of southern Arizona, but they also can be successfully
cryopreserved [3]; however, B. mandrillaris is more fastidious than other soil amebae because it grows only when
provided with nutrient living tissue culture cells [2]. When
amebic meningoencephalitis is a diagnostic consideration,
tissue samples for amebic culture should be obtained along
with samples for bacterial, mycobacterial, fungal, and viral cultures [1,2,12]. Because trophozoites and cysts of
Acanthamoeba spp. and B. mandrillaris are morphologically indistinguishable in formalin-fixed tissue sections,
sufficient tissue or number of trophozoites are needed for
premortem serologic diagnosis [2]. Despite reluctance to
possibly compromise a child's deteriorating clinical condition, brain biopsy should be performed in the absence of
an identifiable etiologic agent [13]. In addition to facilitating definitive diagnosis, culture of this pathogen by
biopsy may have value in determining in vitro sensitivities.

254 PEDIATRIC NEUROLOGY

Vol. 10 No. 3

Further studies are necessary to define the frequency,
clinical spectrum, and antimicrobial therapy for CNS infection with B. mandrillaris. It should be suspected in
children who present with stroke associated with cranial
nerve palsies, dysarthria, and CSF mononuclear pleocytosis.
We gratefully acknowledge the efforts of Stanley D. Johnsen, MD.
Andreas A. Theodoreau, MD, and Ziad M. Shehab, MD in caring for the
patients: Joachim F. Seeger, MD and N. Troy McDaniel, Jr, MD in
interpreting neuroradiologic studies; Naomi E. Rance, MD, PhD in reviewing pathologic specimens; and Sara V. Wallace for expert technical
assistance.
References

[1] Visvesvara GS, Martinez AJ. Schuster FL. et al. Leptomyxid
ameba, a new agent of amebic meningoencephalitis in humans and animals. J Clin Microbiol 1990;28:2750-6.
[2] Gordon SM, Steinberg JP, DuPuis MH, Kozarsky PE, Nickerson JF, Visvesvara GS. Culture isolation of Acanthamoeba species and
leptomyxid amebas from patients with amebic meningoencephalitis, including two patients with AIDS. Clin Infect Dis 1992;15:1024-30.
[3] Visvesv~rn GS, Schuster FL, Martinez AJ Balamuthia mandriUaris, N.G., N. Sp., agent of amebic meningoencephalitis in humans
and other animals. J Euk Microbiol 1993:40:504-14
[4] RIvera F, Rosas I, Castillo M, et al. Pathogenic and free-living
protozoa cultured from the nasopharyngeal and oral regions of dental
patients. II. Environ Res 1986;39:364-71.
[5] Lawamle RV, Abraham SN, John I. Egler LJ. Recovery of soil
amebae from the nasal passages of children during the dusty harmattan
period in Zaria. Am J Clin Pathol 1979;71:201-3.
[6] Wang SS, Feldman HA. Isolation of Hartmannella species from
human throats. N Engl J Med 1967:277:1174-9.
[7] Carter RF, Cullity GJ. Ojeda VJ. Silberstein P, Willaert E. A
fatal case of meningoencephalitis due to a free-living ameba of uncertain
identity--probably Acanthamoeba sp. Pathology 1981; 13:51-68.
[8] Cox EC. Amoebic menmgoencephalitis caused by Acanthamoeba species in a four month old child. J SC Med Assoc 1980-76:
459-62.
[9] Wessel HB, Hubbard J, Martinez AJ, Willaert E. Granulomatous amebic encephalitis (GAE) with prolonged clinical course, C,T.
scan findings, diagnosis by brain biopsy, and effect of treatment. Neurology 1980;30:442.
[10] Matson DO, Rouah E, Lee D, Armstrong RT, Parke JT, Baker
CJ. Acanthamoeba meningoencephalitis masquerading as neurocysticercosis. Pediatr Infect Dis J 1988;7:121-4.
[11] Taratuto AL, Monges J, Acefe JC, Meli F, Paredes A, Martinez AJ. Leptomyxid amoeba encephalitis: Report of the first case in
Argentina. Trans R Soc Trop Med Hyg 1991;85:77.
[12] Ma P, Visvesvara GS, Martinez AJ, Theodore FH, Daggett
PM, Sawyer TK. Naegleria and Acanthamoeba infections: Review. Rev
Infect Dis 1990;12:490-513.
[13] Soong S-J, Watson NE, Caddell GR, Alford CA, Whitley RJ,
NIAID Collaborative Antiviral Study Group. Use of brain biopsy for
diagnostic evaluation of patients with suspected herpes simplex encephalitis: A statistical model and its clinical implications. J Infect Dis 1991;
163:17-22.