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Previous Volume 336:474-478 February 13, 1997 Number 7 Next

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Microsporidia are obligate, intracellular, spore-forming protozoa that are parasitic in every major animal group.¹ Cerebral microsporidial infection was first described in 1922 in rabbits with granulomatous encephalitis,² and the organism was named Encephalitozoon cuniculi.³ In 1959 and 1984, two cases of infection in children with seizure disorders were attributed to E. cuniculi.^4,5 The diagnosis was based on light-microscopical detection of microsporidial spores in cerebrospinal fluid and urine samples, but the identification of the species remained inconclusive, because immunologic and molecular techniques to distinguish among encephalitozoon-like microsporidia were not available at that time. In recent years, three distinct encephalitozoon species (E. hellem, E. intestinalis, and E. cuniculi) with most of the morphologic features of E. cuniculi of animal origin have been detected in persons with human immunodeficiency virus (HIV) infection who had hepatitis, peritonitis, keratoconjunctivitis, nephritis, cystitis, bronchiolitis, sinusitis, or diarrhea.⁶

In preliminary reports, we and Orenstein and colleagues have described HIV-infected patients with central nervous system E. cuniculi infection.^7,8 In this report, we describe an HIV-infected patient with multiple cerebral lesions in whom the rabbit strain of E. cuniculi was detected in cerebrospinal fluid, sputum, urine, and stool samples.

Case Report

A 29-year-old HIV-infected man with a history of intravenous drug use was referred to a hospice in December 1995, after eight weeks of unsuccessful treatment for multiple small, contrastenhanced brain lesions. HIV seroconversion had been documented in 1989, and his CD4 cell count had been 0 per cubic millimeter since November 1994. He was receiving methadone and trimethoprim–sulfamethoxazole as chemoprophylaxis but had declined antiretroviral therapy. Previous infections included hepatitis B and C and oropharyngeal candidiasis, as well as Mycobacterium haemophilum infection, which was diagnosed in February 1995 and treated with antimycobacterial agents (initially isoniazid, rifampin, pyrazinamide, and ethambutol, with a subsequent switch to ciprofloxacin, clarithromycin, and rifabutin). An evaluation of diarrhea in July 1995 revealed microsporidial spores in stool specimens, but the diarrhea ceased without treatment.

In October 1995, the patient was hospitalized because of headache, visual impairment, cognitive impairment, nausea, and vomiting. He was afebrile, and a clinical examination was normal except for anisocoria. His visual acuity and visual field were normal, as were the results of funduscopy, and there was no keratoconjunctival inflammation.

His hematocrit was 32 percent, his leukocyte count was 1800 per cubic millimeter, and his platelet count was 191,000 per cubic millimeter. The serum alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, and creatinine concentrations were normal. Serologic tests for toxoplasma and syphilis were negative. A computed tomographic (CT) scan of the brain showed multiple, hypodense lesions up to 2 cm in diameter. Examination of the cerebrospinal fluid showed 3 cells per cubic millimeter, 0.061 g of protein per deciliter, and 68.5 mg of glucose per deciliter (3.80 mmol per liter). Blood and cerebrospinal fluid cultures for bacteria, mycobacteria, and fungi were negative, as was a test for cryptococcal antigen. The results of molecular studies to detect Epstein–Barr virus, Toxoplasma gondii, and cytomegalovirus in cerebrospinal fluid were negative.

Empirical antitoxoplasma treatment was started. Because of signs and symptoms of increased intracranial pressure, corticosteroids were added. The patient's condition improved intermittently but deteriorated during the following weeks. Four consecutive CT scans of the brain showed an increasing number of lesions with ring enhancement, each less than 1 cm in diameter. The antimycobacterial therapy, which had been continued even though the M. haemophilum infection appeared to be cured, was extended, with the combination of isoniazid, rifampin, pyrazinamide, ethambutol, clarithromycin, and ciprofloxacin.

On admission to the hospice in December 1995, the patient was somnolent and had intermittent fever. No focal neurologic deficits were found. The C-reactive protein concentration was 100 mg per liter, and the creatinine concentration was 1.78 mg per deciliter (157 µmol per liter). The urinary sediment was normal, and a dipstick test was positive (+) for protein. The chest film was normal. Magnetic resonance imaging (MRI) showed right maxillary sinusitis and multiple small, contrast-enhanced lesions, most of which were ring-like and some of which were micronodular, in the hippocampal, mesencephalic, and intracortical regions, with slight edema (Figure 1A and Figure 1B). Examination of the cerebrospinal fluid showed 83 cells per cubic millimeter (90 percent neutrophils and 10 percent mononuclear cells), with intracellular and extracellular microsporidial spores (Figure 2A and Figure 2B), and the cytomegalovirus genome was detected with the use of the polymerase chain reaction. Microsporidial spores were also detected in sputum, urine, and stool specimens.

View larger version (84K): [in this window] [in a new window]   Figure 1. Axial T1-Weighted, Contrast-Enhanced MRI Scans Obtained before and after Treatment with Albendazole in an HIV-Infected Patient with Cerebral E. cuniculi Infection. The scan in Panel A, obtained before treatment, shows multiple small, contrast-enhanced lesions in the hippocampal, mesencephalic, and intracortical regions, with slight edema. Most of the lesions are ring-like, and some are micronodular. There is congestion of the right maxillary sinus. In Panel B, which shows an MRI scan obtained after four weeks of treatment with albendazole, the lesions are substantially reduced in number and size, and the maxillary sinusitis is improved.

 

View larger version (56K): [in this window] [in a new window]   Figure 2. Specimens of Urinary Sediment (Panel A) and Cerebrospinal Fluid (Panel B) Containing Intracellular Clusters of Pink-Stained Microsporidial Spores 2 to 3 µm in Diameter (Chromotrope Stain, x400).

 
Antimycobacterial therapy was stopped, and treatment with albendazole (400 mg orally twice a day) was initiated on December 28, 1995. Trough levels of albendazole in serum ranged from 3.11 to 3.93 µmol per liter during treatment. The patient's clinical condition improved, and the C-reactive protein and serum creatinine values returned to normal. After four weeks of treatment, repeated MRI showed that most of the brain lesions had disappeared; the remaining lesions were smaller, and the maxillary sinusitis was improved (Figure 1A and Figure 1B). The average number of microsporidial spores detected in smears of urinary sediment decreased from 305 per visual field at a magnification of 1000 (range, 168 to 518) to 7 (range, 1 to 18). Urinary excretion of spores, however, did not cease completely.

Despite continued treatment with albendazole, the patient's condition deteriorated in March 1996. MRI showed the reappearance of multiple contrast-enhanced brain lesions in the same locations where they had been observed initially. The patient declined a reexamination of the cerebrospinal fluid. In vitro cultivation of microsporidial spores from a urine specimen obtained on March 13, 1996, remained negative. The patient died on March 28. Permission for an autopsy was denied.

Results

Smears of cerebrospinal fluid obtained by cytocentrifugation were subjected to Gram's, Giemsa, and acid-fast staining and examined by light microscopy at magnifications of 400 and 1000 (with an oil-immersion lens). A few gram-labile intracellular and extracellular spore-like bodies (one to five per slide), approximately 2.5 µm in diameter, were detected. They were assumed to be microsporidial spores because of their oval shape, the intracellular location of most, the size, and the staining pattern.^9,10 Subsequently, smears of cerebrospinal fluid specimens, washed sputum specimens, and urinary sediment obtained by centrifugation at 1500xg, as well as stool specimens, were stained with a chromotrope-based stain and examined by light microscopy.^9,10 A few cells (1 to 3 per slide) containing clusters of pink microsporidial spores were detected in cerebrospinal fluid, a few (1 to 10 per slide) in stool specimens, and abundant numbers in sputum and urine (Figure 2A and Figure 2B). The presence of spores with the ultrastructural characteristics of microsporidia was confirmed by electron-microscopical examination of urinary sediment (Figure 3A and Figure 3B).^9,10,11

View larger version (78K): [in this window] [in a new window]   Figure 3. Transmission Electron Micrographs of Urinary Sediment. Panel A shows intracellular clusters of microsporidial spores (arrow) (x7250). Panel B shows an individual spore characterized by polar tubes (arrowheads), an electron-lucent endospore layer (long arrow), and a dense outer coat (short arrow) (x54,300).

 
In vitro cultivation of microsporidial spores was performed with human embryonic lung fibroblasts (MRC-5 cells).^11,12,13 Spores were detected in cerebrospinal fluid specimens after six weeks of cultivation and in urine and sputum specimens within seven days. The isolates were characterized by Western blot analysis with the use of antibodies to spores of E. cuniculi,¹² by riboprinting, and by determining the intergenic transcribed spacer sequence of ribosomal DNA, as previously described.^12,13,14,15 All isolates were identical to E. cuniculi isolates from rabbits in the area of Zurich, Switzerland.^12,13 The presence of E. cuniculi–specific DNA in stool specimens was confirmed.¹⁶

Discussion

The microsporidian E. cuniculi infects epithelial and endothelial cells, fibroblasts, and macrophages in numerous mammals, including rabbits, rodents, carnivores, monkeys, and humans.^1,4,12,17,18 It usually causes a chronic infection that is latent or mildly symptomatic, but interstitial nephritis and severe neurologic disease may develop as a result of central nervous system vasculitis and granulomatous encephalitis.¹

In humans, encephalitozoon species were first recognized as the etiologic agent of a neurologic disorder in a nine-year-old boy with fever, loss of consciousness, headache, vomiting, and spastic convulsions⁴ and in a two-year-old boy with convulsive seizures.⁵ HIV-infected patients with E. cuniculi infection have presented with renal failure, pneumonitis, sinusitis, and keratopathy^17,18; granulomatous liver necrosis¹⁹; or peritonitis.²⁰ In a recent report, autopsy findings in a patient with the acquired immunodeficiency syndrome showed disseminated E. cuniculi infection involving the brain.⁸ We have followed six patients with E. cuniculi infection¹²: three asymptomatic carriers with spores in urine specimens and three patients with pneumonitis, renal insufficiency, conjunctivitis, sinusitis, or seizures of unknown origin.^12,13

The patient described here was evaluated because of diarrhea six months before cerebral and disseminated microsporidiosis was diagnosed. Microsporidial spores had been detected in stool specimens at that time, but no treatment had been initiated, probably because the diarrhea ceased spontaneously. Reviewing these stool specimens by light microscopy, we found microsporidial spores similar to those found in subsequent stool specimens, as well as in urine, sputum, and cerebrospinal fluid specimens. These findings suggest that our patient acquired E. cuniculi by the oral route, with the subsequent development of disseminated infection. Oral transmission of microsporidia has been documented in studies in animals.¹ However, airborne transmission is also possible, because spores have been found repeatedly in respiratory specimens from patients with encephalitozoon infection.^7,8,12,17 It is not known whether the infection in our patient had been acquired recently or was a reactivation of a latent infection acquired before he became immunosuppressed.

E. cuniculi infection is considered a zoonosis.^12,13 Three different strains of E. cuniculi (the so-called rabbit, mouse, and canine strains) have recently been identified phenotypically, by Western blot analysis of spore antigens, and genetically, by random amplification of polymorphic DNA and determination of differences in the ribosomal DNA intergenic spacer region.^13,14,15,21 So far, infections with the canine strain of E. cuniculi have been identified in two patients from the United States^8,15,17 and in one patient who had lived in Mexico.¹³ No infections with the mouse strain, which was found in mice and blue foxes, have been reported in humans.^14,21 The rabbit strain, which is highly prevalent in Swiss rabbits,^7,13 was previously isolated from five HIV-infected patients from Switzerland and has also been identified in the patient described in this report. He was exposed to animals, including rabbits, between 1986 and 1989, when he was living on a farm.

Albendazole, an anthelmintic drug that is also effective against various protozoa, has been found to partly or entirely eradicate encephalitozoon species propagated in cell cultures.^22,23,24 There has been little experience with treatment of microsporidiosis in humans, but case reports suggest that treatment of encephalitozoon infection with albendazole may be curative.^{12,17,25,26,27} The successful use of albendazole in the treatment of cerebral cysticercosis suggests that the drug may diffuse across the blood–brain barrier, but no data on drug levels in cerebrospinal fluid are available. In our patient, albendazole therapy appeared to be successful initially, as indicated by a decrease in the number and size of brain lesions and the substantial reduction of spore shedding. Nevertheless, urinary excretion of spores persisted, and cerebral E. cuniculi infection was the most probable cause of death. The small number of spores that continued to be excreted appeared to be intact but were not viable, because spores could not be propagated in cell cultures. Nevertheless, we assume that infection with viable parasites persisted, because spores were shed over a period of three months. Some in vitro studies have shown that albendazole does not destroy mature microsporidial spores, which may account for the persistent infection in our patient.^23,24

E. cuniculi should be included in the expanding spectrum of potentially life-threatening opportunistic pathogens that infect the brain. Detection of the parasite in cerebrospinal fluid may be difficult, since the number of spores may be low. Microscopical examination of urinary sediment, however, appears to be a simple method for the diagnosis of disseminated encephalitozoonosis.^6,10,12

Supported by a grant (3237399.93) from the Swiss National Science Foundation.

We are indebted to Johannes Eckert, Isabelle Tanner, Ruth Keller, Thomas Bächi, Werner Wichmann, Richard Cone, and the staff of the Institute for Clinical Pharmacology of the University of Bern, Switzerland, for their consultative and technical assistance.

Source Information

From the Division of Infectious Diseases and Hospital Epidemiology, Department of Medicine, University Hospital (R.W., M.F., B.S., H.K., R.L.); the Institute of Parasitology, University of Zurich (P.D., A.M.); and the Anker-Huus, Diakoniewerk Bethanien (R.B.) — all in Zurich, Switzerland.

Address reprint requests to Dr. Weber at the Division of Infectious Diseases and Hospital Epidemiology, University Hospital, CH-8091 Zurich, Switzerland.

References

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Cerebral Microsporidiosis Due to Encephalitozoon cuniculi
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