| Abstract|| |
Central Nervous System complications are the most dreaded complications in patients of HIV. CNS aspergillosis in HIV is a rare complication. The primary risk-factors for invasive aspergillosis are profound neutropenia and glucocorticoid use; risk increases with longer duration of these conditions. In our case report, the HIV patient was treated with Anti Tubercular Treatment and steroids for CNS tuberculosis previously. Use of steroids might have predisposed him for aspergillosis. Physicians should be aware that the CNS might be the only site of Aspergillus involvement and should include CNS aspergillosis in the differential diagnosis of HIV-infected patients presenting with focal neurologic signs and symptoms, especially, when the head Computed Tomography reveals hypodense lesions.
Keywords: CNS aspergillosis, HIV, neutropenia, steroid use
|How to cite this article:|
Reddy H, Saraf S, Singh MM. Invasive aspergillosis in a HIV patient on prolonged steroid therapy. Ann Trop Med Public Health 2013;6:245-7
|How to cite this URL:|
Reddy H, Saraf S, Singh MM. Invasive aspergillosis in a HIV patient on prolonged steroid therapy. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Feb 18];6:245-7. Available from: http://www.atmph.org/text.asp?2013/6/2/245/116493
| Introduction|| |
CNS complications are the most dreaded complications in patients of HIV. CNS aspergillosis in HIV is a rare complication. Case reports of CNS aspergillosis in a HIV patient are rare. The authors report a rare case of CNS aspergillosis in a HIV patient presenting with headache and vomiting along with mild to moderate grade fever followed by altered sensorium. No neurological deficit was detected. He was treated with ATT and steroids for CNS tuberculosis previously. Use of steroids might have predisposed him for aspergillosis.
| Case Report|| |
A 30-year-old male presented to our department on 12 January 2010 with a 25 days history of moderate grade fever, headache, along with generalized weakness. Physical examination revealed glasgow coma scale of 10/15, a temperature of 39.2°C, a blood pressure of 110/70 mm Hg, a pulse rate of 76/min, and a respiratory rate of 22/min. No neurological deficit was detected. Even after taking antibiotics and paracetamol, there was no improvement, later on the basis of chest X-ray he was diagnosed pulmonary tuberculosis for which he took anti-tubercular treatment for 5 months (standard five drug regimen).
By the end of June 2010 patient started having oral ulcers and episodes of loose stools, then he was diagnosed to be HIV reactive. He was put on anti-retroviral therapy (stavudine-lamivudine-efavirenz) regimen.
Subsequently, a month later he started having headache, generalized tonic seizures, followed by left sided hemiparesis.
Again he was admitted from 23/7/10 to 16/8/10. Then, Cerebro Spinal Fluid analysis was done which revealed Total Leucocyte Count-30 cells Differential Leucocyte Count -Neutrophils 15 Lymphocytes 85 , protein-516, Adenosine Deaminase -46.5, India Ink-negative, Cryptococcal antigen positive.
Considering his raised ADA and Cryptococcal antigen positive and positive HIV status, he was given both anti-tubercular treatment (T. Isoniazid 300 mg, T. Ethambutol 800 mg, T. Levofloxacin 750 mg, Note: patient showed rifampicin induced hepatitis) and added amphotericin-B. His CD-4 count (9/8/10) was 126. CT scan was within normal limits. On discharge (16/8/10), his power was 4/5 in both left upper and lower limb, which gradually improved in 2 months.
Again after 6 months, he was admitted (10/12/10-17/12/10) with the complaints of mild to moderate fever along with headache for 7 days. On admission, his CSF analysis was again repeated (TLC-80, DLC-N 20 L 80 , protein-108.1 mg/dl sugar-25, India Ink-negative, CSF Venereal Disease Research Laboratory-negative). After 7 days of admission he was discharged on T. Isoniazid 300 mg, T. Pyrizinamide 1000 mg, T. Levofloxacin 750 mg. CT head was not done. His ATT was stopped in early February 2011.
In the middle of August 2011, patient developed headache and vomiting along with mild to moderate grade fever for 10 days followed by altered sensorium for the past 4 days. CT Head was done, which revealed non-communicating hydrocephalus with obstruction at the level of 3 rd ventricle but there were no sign of raised Intra cranial tension. CSF analysis was done (TLC-70, DLC-N 10 L 90 , protein-760, sugar-8, India Ink-negative, ADA-14.7). ATT was started again, 10 days after treatment CSF analysis was repeated which revealed TLC-28, DLC-N 97 L 3 , protein-44 mg/dl, sugar-5 mg/dl, India Ink-negative, CSF for fungal culture revealed-Aspergillus fumigatus.
| Investigation|| |
| Differential Diagnosis|| |
Tuberculous meningitis, CNS toxoplasmosis.
| Treatment|| |
By the end of June 2010, he was put on anti-retroviral therapy (stavudine-lamivudine-efavirenz) regimen.
Again he was admitted from 23/7/10 to 16/8/10. Considering his raised ADA and Cryptococcal antigen positive and positive HIV status, he was given both anti-tubercular treatment (T. Isoniazid 300 mg, T. Ethambutol 800 mg, T. Levofloxacin 750 mg, Note: patient showed rifampicin induced hepatitis) and added amphotericin-B.
His ATT was stopped in early February 2011.
In the middle of August 2011, ATT was started again.
| Discussion|| |
CNS complications are the most dreaded complications in patients of HIV. It can be due to primary HIV infection itself or secondary to opportunistic infections. Some common opportunists that involve CNS are toxoplasmosis, cryptococcosis, progressive multifocal leukoencephalopathy, and primary CNS lymphoma.  Other less common problems include mycobacterial infections; syphilis; and infection with Cytomegalo Virus, Human T Lymphotrophic Virus-I, Trypanosoma cruzi, or Acanthamoeba. CNS aspergillosis in HIV is a rare complication. The primary risk-factors for invasive aspergillosis are profound neutropenia and glucocorticoid use; risk increases with longer duration of these conditions.  Neutrophil and/or phagocyte dysfunction is also an important risk-factor, as evidenced by aspergillosis in chronic granulomatous disease, advanced HIV infection, and relapsed leukemia.  Aspergillus infection is rare in HIV disease because of relatively intact phagocytic cell function.  Hematogenous dissemination to the brain is a devastating complication of invasive aspergillosis. Single or multiple lesions may develop. In acute disease, hemorrhagic infarction is most typical, and cerebral abscess is common. Rarer manifestations include meningitis, mycotic aneurysm, and cerebral granuloma.  Local spread from cranial sinuses also occurs. Post-operative infection occurs rarely and is exacerbated by glucocorticoids, which are often given after neurosurgery. The presentation can be either acute or subacute, with mood changes, focal signs, seizures, and decline in mental status. Cerebral granuloma can mimic a primary or secondary tumor. Magnetic Resonance Imaging is the most useful immediate investigation; unenhanced CT of the brain is usually non-specific, and contrast is often contraindicated because of poor renal function.  More than half of the patients with AIDS who develop Invaive Aspergillosis have either neutropenia, usually secondary to ganciclovir, or corticosteroid treatment as additional risk factors.  Nevertheless, some patients with Invasive AspergillosisA have no such risk factors, and this observation, combined with the fact that aspergillosis typically occurs in the setting of advanced HIV infection with < 50 CD4 cells/μL, indicates that HIV infection may represent an independent risk-factor for IA. ,,
In our case report, patient was treated with ATT and steroids for CNS tuberculosis previously. Use of steroids might have predisposed him for aspergillosis.
| References|| |
|1.||Lanska DJ. Epidemiology of human immunodeficiency virus infection and associated neurologic illness. Semin Neurol 1999;2:105-11. |
|2.||Walsh TJ, Hier DB, Caplan LR. Fungal infections of the central nervous system: Comparative analysis of risk factors and clinical signs in 57 patients. Neurology 1985;35:1654-7. |
|3.||Bodey GP, Vartivarian S. Aspergillosis. Eur J Clin Microbiol Infect Dis 1989;8:413-37. |
|4.||Minamoto GY, Barlam TF, Vander Els NJ. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1992;14:66-74. |
|5.||Woods GL, Goldsmith JC. Aspergillus infection of the central nervous system in patients with acquired immunodeficiency syndrome. Arch Neurol 1990;47:181-4. |
|6.||Boes B, Bashir R, Boes C, Hahn F, McConnell JR, McComb R. Central nervous system aspergillosis. Analysis of 26 patients. J Neuroimaging 1994;4:123-9. |
|7.||Khoo SH, Denning DW. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1994;19:S41-8. |
|8.||Holding KJ, Dworkin MS, Wan PC, Hanson DL, Klevens RM, Jones JL, et al. Aspergillosis among people infected with human immunodeficiency virus: Incidence and survival. Adult and Adolescent Spectrum of HIV Disease Project. Clin Infect Dis 2000;31:1253-7. |
|9.||Lortholary O, Meyohas MC, Dupont B, Cadranel J, Salmon-Ceron D, Peyramond D, et al. Invasive aspergillosis in patients with acquired immunodeficiency syndrome: Report of 33 cases. French Cooperative Study Group on Aspergillosis in AIDS. Am J Med 1993;95:177-87. |
Department of Medicine, King George Medical University, Lucknow, Uttar Pradesh
Source of Support: None, Conflict of Interest: None