Cryptococcal infections in patients with acquired immune deficiency syndrome

Eng, Robert H. K.; Bishburg, Eliahou; Smith, Sharon; Kapila, Rajendra

doi:10.1016/0002-9343(86)90176-2

Cited by 282 publications

(129 citation statements)

References 9 publications

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“…Inadequate T cell (CD4+/CD8+) response against C. neoformans infection leads to the death of patients suffering from AIDS [14,10]. C. neoformans is the most common fatal mycosis in AIDS patients, but is less common in non-cell-mediated immunodeficiency [15,16], which suggest that CMI is an important immune mechanism in the clearance of C. neoformans. In the present case report, it appears that the low CD4+ lymphocyte count supports the opportunistic condition to establish mixed fungal infections caused by C. neoformans and C. tropicalis.…”

Section: Discussionmentioning

confidence: 99%

Disseminated cryptococcosis and fluconazole resistant oral candidiasis in a patient with acquired immunodeficiency syndrome (AIDS)

Kothavade¹,

Oberai

Valand

et al. 2010

J Infect Dev Ctries

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Disseminated cryptococcosis and recurrent oral candidiasis was presented in a-heterosexual AIDS patient. Candida tropicalis (C.tropicalis) was isolated from the oral pseudomembranous plaques and Cryptococcus neoformans (C. neoformans) was isolated from maculopapular lesions on body parts (face, hands and chest) and body fluids (urine, expectorated sputum, and cerebrospinal fluid). In vitro drug susceptibility testing on the yeast isolates demonstrated resistance to fluconazole acquired by C. tropicalis which was a suggestive possible root cause of recurrent oral candidiasis in this patient. Case ReportA 34-year-old heterosexual HIV-I positive male developed mucopurulent productive cough, recurrent oral plaques, occasional syncope, and neurological symptoms that included headache and dizziness. Physical examination revealed discrete erythematous maculopapular lesions on his face (Figure 1), neck, chest, and both hands. There were not any significant enlargement of the cervical lymph nodes, and oral examination revealed pseudo-membranous plaques (Figure 1). He was previously treated with antifungal drugs (fluconazole and amphotericin-B), primary anti-tuberculous drugs (isoniazid, rifampin, ethambutol, and streptomycin), and an antigiardial drug (tinidazole) for giardiasis, caused by, Giardia lamblia. The CD4+ lymphocyte count for this patient was 40 cells/μl with a CD4+/CD8+ ratio of 1:72. Despite a history of multiple unprotected sexual exposures, the patient tested negative for venereal disease.The skin biopsies and body fluids, such as, cerebrospinal fluid (CSF), urine, and mucopurulent expectorated sputum, showed encapsulated yeasts in India-ink-wet-mount preparation. The cultures for acid-fast bacilli (AFB) on Lowenstein-Jenson and non-selective Middle-brook 7H12 agar media were negative. Periodic-acid-Schiff and Grocott-Gomorimethylamine-silver-stained smears were negative for Pneumocystis carinii. Serum and CSF tested positive for capsular Cryptococcal polysaccharide antigen using the latex agglutination test with a titer of 1:1015. Skin sections revealed gelatinous troma ( Figure 2) filled with numerous encapsulated yeast cells (Figure 3). Biopsied specimens of skin and other body fluids (CSF, urine, and sputum) yielded the growth of C. neoformans on Sabouraud's dextrose agar (SDA) medium. The resultant mucoid-creamcolored colonies were negative for germ tube and positive for urease test. Colonies failed to grow on Cyclohexamide-supplemented SDA. Colonic growth at 37 o C on plain SDA was weakly positive. Microscopic examination of the Gram-stain preparation from a portion of scraped oral lesions showed Gram-positive yeasts and pseudo-hyphal forms. The remaining portion the scraped oral lesions were inoculated on SDA which then showed a typical growth of C. tropicals. Identification of C. tropicalis was further confirmed by the germ tube test; morphological characteristics were determined on cornmeal tween-80-agar and Vitek-32 and API 20C

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Section: Discussionmentioning

confidence: 99%

Disseminated cryptococcosis and fluconazole resistant oral candidiasis in a patient with acquired immunodeficiency syndrome (AIDS)

Kothavade¹,

Oberai

Valand

et al. 2010

J Infect Dev Ctries

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“…The hearing loss observed in HIV-infected patients has been attributed to a number of sources including a neurotrophism of the virus (Moazzez and Alvi 1998), neurological complications of AIDS-related opportunistic infections (Eng et al 1986), direct invasion of the cochlea from local opportunistic infections or malignancies (Michaels et al 1994), and drug use due to the accompanying infections (Nadol 1993). It can be hypothesized that a relatively significant percentage of the hearing loss observed in HIV+ patients is due to the use of ototoxic drugs such as the antibiotics commonly used to treat opportunistic infections that complicate the disease (e.g., aminoglycoside compounds and amphotericin B).…”

Section: Introductionmentioning

confidence: 99%

Noise-induced hearing loss in mice treated with antiretroviral drugs

et al. 2008

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The results reported here for CBA/CaJ mice describe the effects of regular dosing with a common antiretroviral drug combination on outer hair cell (OHC) function using measures of 2f 1 -f 2 distortion product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs). Specifically, experimental mice were treated daily over a 3-mo period with the nucleoside reverse transcriptase inhibitors (NRTIs), zidovudine (ZDV) and lamivudine (3TC), dissolved in their drinking water, while their control counterparts received untreated water. DPOAE levels and ABR detection thresholds prior to and after 12 wk of NRTI treatment did not differ between experimental and control groups. To assess whether NRTI treatment potentiates the adverse effects of noise overexposure on OHC function, both experimental and control mice were exposed 1 wk later, while still on the drug regimen, to a 10-kHz octave-band noise (OBN) at 105 dB SPL for 1 h. A major outcome of the sound overexposure episode was that the NRTI-pretreated mice showed significantly greater permanent OBNinduced reductions in DPOAE levels at 2 wk postexposure than were observed for the untreated control animals. These findings support the notion that a synergistic relationship exists between certain NRTIs and intense sounds in that such preexposure drug treatments produced greater noiseinduced decreases in DPOAE activity than did noise exposure alone. This drug/noise interaction is consistent with the known harmful effects of NRTIs on cellular mitochondrial activity.

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“…After inhalation of spores into the lung, infection spreads by the bloodstream to the brain where it causes lifethreatening infection of the central nervous system [21]. Cryptococcosis is the fourth most common cause of mortality in patients with AIDS [22,23]. Currently, 4% of AIDS patients in the United Kingdom [24], 5ϳ10% of AIDS patients in the United States [25], and an increasing percentage in the developing countries have cryptococcosis [26].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of β-1,3-Glucan Synthase and Cell Growth of Cryptococcus species by Recombinant Single-chain Anti-idiotypic Antibodies

et al. 2006

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Recombinant single-chain fragment variable (scFv) anti-idiotypic antibodies were produced to represent the internal image of a HM-1 killer toxin, which is characterized by a wide spectrum of anti-fungal activity through inhibiting b-1,3-glucan synthase (GS). We examined if scFv antibodies are active against Cryptococcus species, a human pathogen of increasing medical importance. The anti-cryptococcal activity of scFv antibodies and HM-1 were assessed by MIC analysis for C. neoformans IFM 40215 and C. albidus NBRC 0612 cells. The scFv antibodies had strong anti-cryptococcal activity in vitro with IC 50 at 1.07ϫ10 Ϫ7 to 2.60ϫ10 Ϫ7 M for C. neoformans and C. albidus. Furthermore, the scFv antibodies potentially inhibited GS of C. neoformans with IC 50 at 1.27ϫ10 Ϫ7 to 2.27ϫ10 Ϫ7 M. Both the anti-fungal and anti-GS activities of the scFv antibodies were markedly neutralized by the monoclonal antibody that neutralizes HM-1 killer toxin.

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Cryptococcal infections in patients with acquired immune deficiency syndrome

Cited by 282 publications

References 9 publications

Disseminated cryptococcosis and fluconazole resistant oral candidiasis in a patient with acquired immunodeficiency syndrome (AIDS)

Disseminated cryptococcosis and fluconazole resistant oral candidiasis in a patient with acquired immunodeficiency syndrome (AIDS)

Noise-induced hearing loss in mice treated with antiretroviral drugs

Inhibition of β-1,3-Glucan Synthase and Cell Growth of Cryptococcus species by Recombinant Single-chain Anti-idiotypic Antibodies

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