The public health threat from Balamuthia Mandrillaris in the southern United States.
The objectives of this review and meta-analysis are to describe and to analyze laboratory-confirmed cases of Balamuthia mandrillaris amebic encephalitis (BAE) in the US for any consistent behavioral, environmental, genetic, iatrogenic, recreational, or regional risk factors for pathogen exposures and typically fatal infections.
MATERIALS AND METHODS
Initially, Medline, Pub Med, Google[R], and Google Scholar[R] search engines were queried for references using all key words listed as query terms. The only cases of Balamuthia amebic encephalitis (BAE) included in this meta-analysis were published cases with laboratory-confirmed detection of Balamuthia mandrillaris infective life forms (trophozoites) by direct microscopic observation, by immunohistopathological techniques, by isolation in culture, or by species-specific deoxyribonucleic acid (DNA) as detected by polymerase chain reaction (PCR) in cerebrospinal fluid (CSF), brain or skin biopsies, or brain necropsy tissue. (11-13) Significant behavioral, demographic, environmental, ethnic, iatrogenic, occupational, recreational, and regional exposure factors for BAE were identified over the study period, 1980-2010, in order to make recommendations for the early diagnosis, management, and prevention of BAE and to determine any potential regional threats to public health posed by Balamuthia mandrillaris.
The ages of case-patients were stratified by gender and by age 18 and older (adults) versus age less than 18 years (children) and were compared for statistically significant differences by two-tailed, unpaired t-tests. Statistical significance was indicated by p-values less than or equal to 0.05. Selected behavioral, demographic, environmental, ethnic, occupational, recreational, and regional exposure factors previously presumed to be associated with BAE were also stratified by age and gender, described, and compared by proportions (percentages) and rates. Since this investigation was a comparative descriptive and statistical analysis of previously reported cases, institutional review board approval was not required.
Balamuthia mandrillaris caused typically fatal granulomatous encephalitis without many consistent epidemiological patterns in both children and adults, in immunocompetent and immunosuppresssed patients, and in few case-patients with documented environmental exposures to soil or freshwater. Most cases occurred in immunocompetent patients (n = 29, 83%), unlike Acanthamoeba-associated granulomatous encephalitis, which has remained more common in immunosuppressed patients (Table 1). (7, 8) Table 1 contrasts clinical, diagnostic laboratory, and neuroimaging features of primary amebic meningoencephalitis with the only two known causes of granulomatous amebic encephalitis, Acanthamoeba and Balamuthia mandrillaris. (1, 2 6-39)
There were 35 laboratory-confirmed cases of Balamuthia mandrillaris amebic encephalitis (BAE) in the US during the reporting study period, 1980-2010 (Tables 2-3). (13-29) The mean age of the study population of males was 23.49 ([+ or -] 25.01) years, with males (n = 25, 71%) outnumbering females 2.5:1.0 (n = 10, 29%). Tables 2 and 3 display the demographic, epidemiologic, clinical, and diagnostic presenting features of BAE in laboratory-confirmed male (Table 2) and female (Table 3) case-patients. There were no statically significant differences in the mean ages of male and female cases, and there were few survivors of Balamuthia mandrillaris GAE (n = 6, 3 males and 3 females) for an overall case fatality rate of 83%.
The stratified comparative analysis of BAE cases by gender (Table 4) and by age (Table 5) demonstrated the following consistent epidemiological patterns. (1) Most case-patients, especially children (n = 19, 95%), were immunocompetent and not immunosuppressed by medications or congenital immunodeficiencies. (2) Most cases occurred in the southern-most tier of the continental US from Florida to California (FL, MS, TX, AZ, CA; n = 31, 89%). (3) Cases occurred in patients of Hispanic ethnicity more often than anticipated by population demographics, even in the southern-most tier, Mexican border-states (n = 15, 43%), and especially in children (n = 11, 55%) and in California (n = 8, 53%). (4) BAE was almost uniformly fatal in children (case fatality rate = 90%) and adults (case fatality rate = 73%). (5) With the exceptions of male gender, southern tier state of residence, and Hispanic ethnicity, there were few remaining potential, predisposing risk factors for BAE. (6) Soil exposures did indeed occur prior to some cases in all segments of the stratified study population (n = 6), but were inconsistent and ranged from two cases in children (10%) to four cases in adult males (16%). (6) Lastly, recent cases demonstrated that, like Acanthamoeba granulomatous amebic encephalitis (GAE), Balamuthia mandrillaris infections were also transmitted from organ donors with laboratory confirmed BAE to organ transplant recipients with high case fatality rates, even following accurate diagnosis and aggressive treatment of transplant recipients with recommended conventional and experimental drugs (n = 3, 38%).
[FIGURE 1 OMITTED]
Balamuthia mandrillaris was first isolated from the brain of a pregnant mandrill baboon that died of acute meningoencephalitis at the San Diego Zoo in 1990. (30) Since then, Balamuthia mandrillaris has been identified, usually by indirect immunofluorescent methods using rabbit Balamuthia antiserum, in about 200 cases of typically fatal human encephalitis throughout the world. (13, 19, 29, 31) Balamuthia amebic encephalitis (BAE) or balamuthiasis is a chronic infection of the brain that may disseminate to other organs hematogenously and occurs in immunocompetent patients, immunosuppressed patients with the acquired immunodeficiency syndrome (AIDS) or organ transplants, and in patients receiving chemotherapy for cancer or tuberculosis. (12-14) The portal of entry for Balamuthia mandrillaris is through the respiratory tract or via ulcerating skin wounds with hematogenous spread to the CNS and, less commonly, with systemic dissemination to other organs in the severely immunocompromised. (5, 11-14) The life cycle of Balamuthia mandrillaris is depicted in Figure 1, and an infective trophozoite of B. mandrillaris in brain biopsy tissue is depicted in Figure 2.
[FIGURE 2 OMITTED]
Besides immunocompromise, other potential risk factors for balamuthiasis may include contact with stagnant freshwater or with contaminated dust or soil, often through agricultural work, desert motorcycling, dirt-biking, or even gardening and yard work. (5, 12) In some cases, BAE has occurred following indolent skin lesions originating in soil-contaminated puncture wounds or presumed insect bites (Table 2, male case numbers 11, 13, 16, 26). In other cases, BAE has occurred following potential inhalational exposures to aerosols of dirt, dust, and potting soils (Table 2, male case numbers 19, 22, 23, 24; Table 3, female case number 9). A genetic predisposition to Balamuthia mandrillaris GAE has now been identified in American Hispanics, who appear less able to produce effective antibodies against some free living amebae, and may be predisposed by more frequent contact with Balamuthia-contaminated soils and aerosols in agricultural and landscaping occupations. (31, 32)
The incubation period for BAE can extend for weeks or months after primary inoculation in the skin, sinuses, or lungs, with subsequent draining ulcers, chronic sinusitis, or pneumonia. (5, 13-29) However, the incubation period typically exhibits a mean of 8.5 days with a range of 1-30 days following primary inoculation. (12) The clinical presentation of BAE may include early behavioral and personality changes, fever, depressed mental status, seizures, photophobia, visual loss, and nonspecific cranial nerve dysfunction, followed by signs of increased intracranial pressure, including headache, nausea, vomiting, and loss of consciousness. (13-29, 33)
The laboratory diagnosis of BAE is usually based on microscopic identification of characteristic trophozoites in CSF, skin, or brain biopsies. Trophozoites are more often identified in fixed and stained skin ulcer biopsies, brain biopsies, and post-mortem brain tissue than in wet or fixed and stained mounts of CSF (Figure 2). (11, 12) Recently, immunodiagnostic tests using indirect immunofluorescent methods, such as indirect immunofluorescent ultraviolet microscopy and indirect immunofluorescent antibody ultraviolet microscopy with specific anti-pathogen antibodies, and new PCR assays for identification of pathogen DNA have been developed for diagnostic specimens. (34)
Neuroimaging studies by axial computerized tomography (CT) and/or magnetic resonance imaging (MRI) in BAE are nonspecific and often include single to multiple space-occupying lesions in the brain from the frontal cortex to the cerebellum with ring--enhancing and other focal effects slightly more common in balamuthiasis than in other free-living amebic infections of the brain, such as acanthamoebiasis and primary amebic meningoencephalitis (PAM). (35, 36) Evidence of cerebral edema will often be present and may include midline shifts, cisternal and ventricular compression, and hydrocephalus, with hydrocephalus more common in children than adults. (35, 36)
Treatment strategies for BAE will include combinations of critical care techniques to reduce increased intracranial pressure, craniotomy for biopsy or excision of mass lesions, and combination pharmacotherapy with antifungals, anti-protozoal agents, synergistic antibiotics, and several experimental therapies that have shown promise in vitro, such as oral and intravenous treatment with phenothiazines. (37-39) Although case fatality rates in BAE are high ([greater than or equal to] 90%), some successful drug treatment combinations in balamuthiasis have included azoles (albendazole, fluconazole, or itraconazole), flucytosine, pentamidine, sulfadiazine; and synergistic anti-protozoal therapy with macrolide antibiotics (azithromycin or clarithromycin), phenothiazines (thioridazine or trifluoperazine), and the experimental anti-Leishmania agent used to treat visceral leishmaniasis, miltefosine. (37-39) The optimum duration of drug therapy for BAE is unknown, but most survivors have been treated for weeks to months. (12, 37-39) Like Acanthamoeba-caused amebic infections of the brain, Balamuthia mandrillaris infections may also be disseminated hematogenously and were recently associated with two case clusters of organ transplant-transmitted infections in southern tier US states (AZ, MS) with three deaths in transplant recipients (Table 2, male case numbers 21, 22; Table 3, female case number 10). (24, 25)
Prevention and control strategies for BAE should include (1) consideration of BAE in organ transplant and immunocompromised patients with encephalitis and skin ulcers not improving with standard therapies, especially in southern tier US states; (2) recognition of genetic risk factors for acanthamoebiasis and balamuthiasis in Hispanics; and (3) recognition of other soil or stagnant freshwater risk factors in both immunocompetent and immunosuppressed patients with skin ulcers, chronic sinusitis, and unexplained meningoencephalitis. (31, 32)
The results of this study have demonstrated the following public health threats from Balamuthia mandrillaris in the US. (1) BAE occurs sporadically in patients of all ages and affects both immunosuppressed patients and immunocompetent patients with few predisposing factors. (2) The few predisposing factors include male gender, exposure in a southern tier US state, and Hispanic ethnicity. (3) Most cases of BAE will not be diagnosed in time for aggressive medical intervention and will be fatal. (4) BAE can be transmitted from infected organ donors with undiagnosed causes of infectious meningoencephalitis to immunosuppressed transplant recipients.
Clinicians should suspect free-living amebic infections of the CNS in all refractory cases of meningoencephalitis initially managed as aseptic or bacterial infections, especially in patients predisposed to such infections by behavioral practices, environmental or occupational exposures, ethnicity, or immunosuppression by chemotherapy or organ transplant anti-rejection therapy.
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James H. Diaz, MD, MPH&TM, DrPH, FACPM, FCCM
Dr. Diaz is a professor of public health and preventive medicine, program head of the Environmental and Occupational Health Sciences School of Public Health at Louisiana State University Health Sciences Center in New Orleans (LSUHSC-NO), In addition, he is professor of anesthesiology/critical care medicine in the School of Medicine at LSUHSC-NO.
Table 1. Comparison of the clinical features of primary amebic meningoencephalitis and granulomatous amebic encephalitis. (1,2,6-39) Infections Primary amebic Granulomatous amebic meningoencephalitis encephalitis (GAE) (PAM) caused by either Acanthamoeba species or Balamuthia mandrillaris) Pathogens Naegleria fowleri Acanthamoeba spp. Distribution Worldwide in warm Worldwide in freshwater, bottom freshwater and soil sediment, and soil Cases reported 180-200 [less than or equal worldwide to] 200 Seasonal Summertime or warmest Year round occurrence seasons High-risk groups Immunocompetent Immuncompromised children and young children and adults adults, especially (acquired males with histories immunodeficiency of freshwater syndrome, cancer or exposures (skiing, chemo, organ or bone wakeboarding) within marrow transplant, two weeks liver or renal failure); rarely in the immunocompetent Pathology Trophozoites Hematogenous penetrate nasal dissemination from mucosa and cribriform granulomatous skin plate and migrate via ulcers or lung olfactory nerves to granulomas, across olfactory bulbs and blood-brain barrier tracts along basilar to CNS brain to cerebellum Incubation period Mean 5-7 days (range Weeks to months 1-16 days) following indolent draining skin ulcers, sinusitis, or pneumonia Clinical features Fever, headache, Same as PAM, early stiff neck mental status (meningismus), changes, visual loss, nausea, specific CN photophobia dysfunction (altered senses of smell and taste, anisocoria), seizures, disorientation, coma Laboratory Trophozoites in CSF Both cysts and studies wet mounts, stained trophozoites in CSF sediment or brain fixed, stained brain tissues enhanced by tissue enhanced by IIF or IFA; N. IIF or IFA; fowleri DNA by PCR on Acanthamoeba DNA by CSF or unfixed brain PCR on CSF or unfixed brain Imaging studies Nonspecific: basilar Nonspecific: multiple by computed leptomeningeal space-occupying tomography or enhancement, lesions, with or magnetic intraparaenchymal without ring- resonance imaging lesions and-or enhancing effects hemorrhagic necrosis; evidence of ICP- cerebral edema, midline shift, cisternal and ventricular compression Treatment IV and IT: IV and IT: azoles IV: amphotericin B, azoles, flucytosine, azoles: fluconazole, pentamidine, itraconazole, rifampin, miconazole trimethoprim-sulfa- Synergistic methoxazole antibiotics: Experimental: azithromycin po, miltefosine rifampin Experimental: chlorpromazine or other phenothiazines Outcomes (CFRs) Death within 3-7 days Usually fatal in (>95%) immunocompromised (90%-94%); immunocompetent children most likely to survive Infections Granulomatous amebic encephalitis (GAE) caused by either Acanthamoeba species or Balamuthia mandrillaris) Pathogens Balamuthia mandrillaris Distribution Worldwide in freshwater and soil; more common in the US South and South America Cases reported Approximately 150 worldwide Seasonal Year round occurrence High-risk groups Immunocompetent children and adults, most often males with soil exposures (dirt/biking, agriculture) and/or Hispanic origin; less common in immunocompromised with acquired immunodeficiency syndrome or intravenous drug use Pathology Hematogenous dissemination from granulomatous skin ulcers, often facial, or lung granulomas across blood-brain barrier to CNS Incubation period Mean 8.5 days (Range 1-30 days) following indolent pneumonia or draining granulomas on the face or upper arms Clinical features Same as PAM and GAE with early confusion and disorientation, nonspecific CN dysfunction Laboratory IFA staining of fixed brain tissue; PCR studies for Balmuthia DNA in CSF or brain tissue Imaging studies Nonspecific: cerebral edema, by computed hydrocephalus, multiple space-occupying tomography or and ring-enhancing in cortex and magnetic cerebellum resonance imaging Treatment IV: azoles-albendazole, fluconazole, itraconazole, pentamidine, flucytosine, sulfadiazine Synergistic macrolides: azithromycin, clarithromycin Experimental: phenothiazines- thioridazine, trifluoperazine Outcomes (CFRs) Usually fatal ([greater than or equal to] 90%) CFR: case fatality rate; CN: cranial nerve; CSF: cerebrospinal fluid; PCR: polymerase chain reaction nucleic acid assay; IFA: immunofluorescent assay; IIF: indirect immunofluorescence; DNA: deoxyribonucleic acid; ICP: intracranial pressure; IV: intravenous; IT: intrathecal Table 2. Selected demographic and presenting clinical features of 25 male cases of Balamuthia amebic encephalitis in the US, 1980-2010. State Age of Case in Residence, Race/Ethnicity Number years Year Reported 1 2.5 FL, 1980 Caucasian 2 0.3 SC, 1980 Caucasian 3 1.5 NC, 1993 Caucasian 4 0.75 CA, 1994 Not reported (NR) 5 2.25 AZ, 1994 NR 6 5 TX, 1993 Caucasian 7 15 TX, 1993 Hispanic 8 38 TX, 2000 Hispanic 9 32 CA, 2002 Caucasian 10 64 CA, 2003 Caucasian 11 7 CA, 2003 Hispanic 12 2.5 TX, 2003 Hispanic 13 89 TX, 2004 Caucasian 14 1.5 CA, 1999-2007 Hispanic 15 7 CA, 1999-2007 Hispanic 16 12 CA, 1999-2007 Hispanic 17 19 CA, 1999-2007 Hispanic 18 35 CA, 1999-2007 Hispanic 19 43 CA, 1999-2007 Caucasian 20 72 CA, 1999-2007 Pacific Islander 21 4 MS, 2009 Caucasian 22 27 MS, 2009 Not Hispanic, otherwise NR 23 27 AZ, 2010 Hispanic 24 56 AZ, 2010 Not Hispanic, otherwise NR 25 24 AZ, 2010 Not Hispanic, otherwise NR Age Case in Immune status Exposure status Number years 1 2.5 Within normal limits None 2 0.3 Within normal limits None 3 1.5 Within normal limits Bathed in lake 1 month prior 4 0.75 Within normal limits None 5 2.25 Within normal limits None 6 5 Within normal limits None 7 15 Within normal limits None 8 38 Within normal limits Puncture wound on thigh 9 32 Within normal limits Alcohol-drug abuse 10 64 Steroid therapy Nodular lesion-rose thorn, forearm 11 7 +cysticercosis titer, None otherwise within normal limits 12 2.5 Within normal limits None 13 89 Within normal limits Lived on cattle ranch and had chronic nasal ulcer 14 1.5 Within normal limits None 15 7 Steroid therapy None 16 12 Within normal limits Frequent desert motorcycling 17 19 Within normal limits Former drug abuser 18 35 Within normal limits None 19 43 Within normal limits Occupational soil exposure 20 72 Within normal limits Garden and yard soil exposures 21 4 Within normal limits Outdoor wading pool and soil exposures 22 27 Kidney transplant None recipient, anti- rejection therapy 23 27 Within normal limits Chronic skin ulcer on back post insect bite 24 56 Liver transplant None recipient, anti- rejection therapy 25 24 Kidney-pancreas None transplant recipient, anti-rejection therapy Age Case in Confirmed diagnosis Outcome Reference Number years number 1 2.5 +IFF on brain biopsy Died 14 2 0.3 Same Died 15 3 1.5 Same Died 16 4 0.75 Same Died 17 5 2.25 Same Died 17 6 5 Same Died 18 7 15 Same Died 18 8 38 Same Died 19 9 32 Same Died 20 10 64 +serology and brain Lived 21 biopsy by IIF 11 7 +serology by IIF Died 22 12 2.5 +brain biopsy by Died 22 microscopy and IIF 13 89 +IFF on nasal lesion Died 23 biopsy 14 1.5 +brain biopsy by Died 13 microscopy and IIF 15 7 +serology and brain Died 13 biopsy by IIF and PCR 16 12 +serology by IIF, + Died 13 brain biopsy by IIF and PCR 17 19 +brain biopsy by IIF Died 13 and PCR 18 35 +serology by PCR Lived 13 19 43 +brain biopsy by IIF Died 13 and PCR 20 72 +brain biopsy by IIF Died 13 and PCR 21 4 +brain biopsy by IIF Died 24 and PCR; organ donor 22 27 +organ donor by IIF Lived 24 and PCR on brain biopsy 23 27 Organ donor; suspected Died 25 by +IIF and PCR on 2 organ recipients 24 56 +IIF and PCR on brain Died 25 biopsy 25 24 Same Died 25 FL: Florida; SC: South Carolina; AZ: Arizona; TX: Texas; CA California; MS: Mississippi; IIF: indirect immunofluorescence; PCR: polymerase chain reaction nucleic acid assay Table 3. Selected demographic and presenting clinical features of 10 female cases of Balamuthia amebic encephalitis in the US, 1988-2009. State Age of Case in Residence, Race/Ethnicity Immune status Number years Year Reported 1 11 TX, 1988 Hispanic +cysticercosis titer, otherwise within normal limits 2 0.4 AZ, 1992 Caucasian Within normal limits 3 13 AZ, 1994 Hispanic Within normal limits 4 52 MA, 2000 Caucasian Chronic neutropenia 5 5 CA, 2002 Hispanic Within normal limits 6 5 CA, 2003 Hispanic Within normal limits 7 3 CA, 2003 Hispanic Within normal limits 8 2 CA, 2003 Hispanic Within normal limits 9 72 NY, 2004 Caucasian Within normal limits 10 31 MS, 2009 Non-Hispanic, Kidney recipient from a otherwise not brain biopsy +donor; reported anti-rejection therapy Age Case in Exposure status Confirmed diagnosis Number years 1 11 None +brain biopsy by IIF 2 0.4 None Same 3 13 Frequent travel to Same Mexico 4 52 None Same 5 5 None Same 6 5 Frequent travel to Same Mexico 7 3 Contact with potting +brain biopsy by IIF and soil culture 8 2 Frequent travel to +brain biopsy by IIF Mexico 9 72 Frequent travel to +brain biopsy by IIF Arizona and Texas 10 31 None +brain biopsy by IIF and PCR Age Case in Outcome Reference number Number years 1 11 Died 26 2 0.4 Died 27 3 13 Died 17 4 52 Died 28 5 5 Lived 20 6 5 Lived 21 7 3 Died 22 8 2 Died 22 9 72 Lived 29 10 31 Died 24 TX: Texas; AZ: Arizona; MA: Massachusetts ; CA: California; NY: New York; MS: Mississippi; IIF: indirect immunofluorescence; PCR: polymerase chain reaction nucleic acid assay Table 4. A comparative analysis of US cases of Balamuthia amebic encephalitis stratified by gender, N=35. Males Females Number 25 10 Mean age [+ or -] 23.49 [+ or -] 25.01 19.44 [+ or -] 24.58 standard deviation Age significance t=0.435; p=0.667 test Age range (years) 0.3-89 0.4-72 Hispanic ethnicity 10 (40%) 5 (50%) (%) Immunocompetent (%) 21 (84%) 8 (80%) Immunosuppressed (%) 4 (16%) 2 (20%) Reside in southern 23 (92%) 8 (80%) tier US state ** (%) Soil exposures (%) 6 (24%) 2 (20%) Deaths (case 22 (88%) 7 (70%) fatality rate [%]) * Immunosuppressed=steroid therapy, organ transplant anti-rejection therapy, pre-existing immunodeficiency disorder. ** Southern tier US state=Arizona, California, Florida, Mississippi, and Texas. Table 5. A comparative analysis of US cases of Balamuthia amebic encephalitis stratified by age, N=35. Children (< 18 years Adults (age 18 years of age) and older) Number 20 10 Mean age [+ or -] 5.035 [+ or -] 4.454 19.44 [+ or -] 24.58 standard deviation Age significance t=8.369; p < 0.0001 test Age range (years) 0.3-15 19-89 Hispanic ethnicity 11 (55%) 4 (27%) (%) Immunocompetent (%) 19 (95%) 9 (60%) Immunosuppressed (%) 1 (5%) 6 (40%) Reside in southern 18 (90%) 13 (87%) tier US state ** (%) Soil exposures (%) 2 (10%) 4 (27%) Deaths (case 18 (90%) 11 (73%) fatality rate [%]) * Immunosuppressed=steroid therapy, organ transplant anti-rejection therapy, pre-existing immunodeficiency disorder. ** Southern tier US state=Arizona, California, Florida, Mississippi, and Texas.
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|Author:||Diaz, James H.|
|Publication:||The Journal of the Louisiana State Medical Society|
|Date:||Jul 1, 2011|
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