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ABSTRACT |
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INTRODUCTION |
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This amoeba species is ubiquitous in nature and can be found in soil samples and probably in water sources.3,4 This organism infects the brain by hematogenous routes, after first infecting either the lungs after aspiration or the skin through cuts or abrasions. However, an olfactory nerve pathway into the CNS has recently been described.5 The clinical course of B. mandrillaris infection can be subacute or chronic, and the neurologic picture can be extremely variable.
Radiologic studies usually show one or more nonspecific enhancing lesions, but the gold standard diagnostic method is indirect immunofluorescence staining of brain tissue sections.6 In addition, immunofluorescence testing of serum can also be useful.7 Recently, a new tool for B. mandrillaris identification has been developed. The polymerase chain reaction (PCR) technique enables detection of mitochondrial 16S rRNA gene DNA from the amoeba in clinical specimens such as brain tissue and cerebrospinal fluid (CSF).8 However, amoebic meningoencephalitis diagnosis is rarely performed before death, and thus far only three such patients have survived. At present, no specific treatment is available, but if the infection is recognized early, empirical antimicrobial therapy can be offered.9,10
Dissemination of this amoeba species to organs other than the skin and CNS has rarely been described,11 perhaps because in most places necropsy is rarely performed. The aim of this study was to present the first case of disseminated B. mandrillaris infection in a Brazilian AIDS patient.
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CASE REPORT |
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At admission, he presented extreme cachexia, anemia, and dehydration. His blood pressure was 120/80 mm of Hg, his temperature was 37°C, and no remarkable neurologic abnormalities were observed. The laboratory test results were as follows: hemoglobin level, 8.8 g%; hematocrit, 29.3%; platelets, 69,000; white blood cells, 1700 cells - 4 bands; 81 neutrophils, 10 lymphocytes, and 5 monocytes; glucose level, 110 mg%; serum nitrogen level, 31 mg%; serum creatinine level, 1.1 mg%; cerebrospinal fluid analysis, 1 cell; glucose, 48 mg%; proteins, 108 mg%. Stains and cultures for bacteria, fungi, and acid-fast bacilli were negative. VDRL was negative, fluorescent treponemal antibody (FTA)-absorption (Abs) was positive, and Toxoplasma gondii IgG was 1:256. At that time, no CD4 count was available in the hospital.
A cranial computed tomography (CT) scan revealed a ring-enhanced lesion with edema and a mass effect in the right occipital lobe (Figure 1A
). The initial diagnosis was toxoplasmosis, and therefore, sulfadiazine, pyrimethamine, and folic acid were administered. Over the first days, his clinical state remained unchanged, but on the fifth day his condition abruptly worsened and progressed to death.
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). The microscopic findings included multifocal necrotizing hemorrhagic encephalitis and great numbers of amoeba trophozoites clustered around the vessels (Figure 1C). These structures measured 15–25 µm and presented light nuclei and central nucleoli. No granulomatous reaction was noticed. Furthermore, the kidneys, adrenal glands, thyroid gland, and liver also showed the presence of amoeba trophozoites and cysts (Figure 1, D–G).
Brain sections from this case were sent to the Centers for Disease Control and Prevention (Atlanta, GA) where B. mandrillaris was identified by an immunofluorescence test (Figure 1H). In addition, esophageal candidiasis, aspiration bronchopneumonia, and septic foci on the skin, tongue and kidneys were seen.
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DISCUSSION |
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In clinical practice, AIDS patients who are not receiving antiretroviral therapy or antitoxoplasma prophylaxis and who present acute or subacute neurologic symptoms, T. gondii IgG antibodies and CT scans or MRI showing multiple ring-enhancing lesions are highly likely to have Toxoplasma encephalitis (positive predictive value of 80%).15 In most treatment centers using these criteria, empirical therapy with sulfadiazine plus pyrimethamine is begun and such patients often improve within 10–14 days. If no improvement is seen or there is clinical worsening after 3 days of therapy, other diseases such as lymphoma, viral encephalitis, nocardiosis, endemic mycosis, or less common infections like free-living amoebae must be considered. In such cases, lumbar puncture and/or brain biopsy are indicated.
Nevertheless, with few exceptions, B. mandrillaris has only been shown postmortem.7,9 Although immunofluorescence and PCR techniques are available for diagnoses on tissues and fluids; unfortunately, no reference laboratories are available in most places where this disease occurs.6,8
The appearance of the structures seen in different organs makes it possible to suspect free-living amoeba infection, although absence of the characteristic cysts of B. mandrillaris hinders differentiation from Acanthamoeba spp. Otherwise, granulomatous encephalitis is the neuropathologic hallmark of both of these amoebic infections, although no granulomatous reaction was noticed in our case. Sometimes this may occur and it may be related to the intense lymphoid depletion that was observed in the spleen and lymph nodes. Despite the lack of CD4 count, this could explain the advanced immunodeficient state of our patient after long-duration HIV infection without therapy compliance.
In addition to the CNS involvement, B. mandrillaris dissemination to several organs was also shown. This feature has only rarely been described.13 Regrettably, necropsy is carried out less and less in teaching hospitals, which impedes better knowledge of the causes of mortality among AIDS patients and the real prevalence of free-living amoeba infection in these individuals.
Received April 23, 2007. Accepted for publication August 27, 2007.
Acknowledgments: We thank Ann M. Nelson of the Division of AIDS and Emerging Infectious Diseases, Armed Forces Institute of Pathology, Washington, DC, and the Centers for Disease Control and Prevention, Atlanta, GA, for amoeba identification.
Financial support: This study was supported by FAPEMIG.
* Address correspondence to Mario León Silva-Vergara, Avenida Getúlio Guaritá, s/n, Uberaba, Minas Gerais, Brazil 380001-970. E-mail: marioleon.dip{at}mednet.com.br 
Authors’ addresses: Mario León Silva-Vergara, Av. Getúlio Guarita, s/n Uberaba-MG 38001-970, Brazil, Telephone: 55-34-33185286, Fax: 55-34-33185279. Eduardo Rodrigues da Cunha Colombo and Travessa Coronel José Ferreira, 200 Apt. 1100 Uberaba-MG 38010-320, Brazil, Telephone: 55-34-33331578. Eduardo de Figueiredo, Vissotto Rua Vigário Silva, 389, Apt 301 Uberaba-MG 38010-130, Brazil, Telephone: 55-34-33322954. Ana Cristina Araújo Lemos Silva, Av. Getúlio Guarita, s/n Uberaba-MG 38001-970, Brazil, Telephone: 55-34-33185644. Javier Emilio Lazo Chica, Av. Frei Paulino, 30 Uberaba-MG 38025-180, Brazil, Telephone: 55-34-33185644. Renata Margarida Etchebehere and Sheila Jorge Adad, Av. Getúlio Guarita, s/n Uberaba-MG 38001-970, Brazil, Telephone: 55-34-33185644.
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