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Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV

Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV
Literature review current through: Jan 2024.
This topic last updated: Jun 29, 2023.

INTRODUCTION — Disseminated Cryptococcus neoformans infection is a serious opportunistic infection that occurs in patients with untreated AIDS [1]. Although cryptococcal infection begins in the lungs, meningitis is the most frequently encountered manifestation of cryptococcosis among those with advanced immunosuppression. However, the infection is more properly characterized as "meningoencephalitis" rather than meningitis since the brain parenchyma is almost always involved on histologic examination [2,3].

The clinical manifestations and diagnosis of C. neoformans meningoencephalitis in persons living with AIDS will be reviewed here. Treatment and monitoring of patients with HIV who have cryptococcal meningoencephalitis is found elsewhere. The microbiology, clinical manifestations, and treatment of this infection in other patient populations, such as transplant patients, are discussed elsewhere. Cryptococcus gattii infection is also presented separately. (See "Cryptococcus neoformans meningoencephalitis in persons with HIV: Treatment and prevention" and "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV" and "Microbiology and epidemiology of Cryptococcus neoformans infection" and "Clinical manifestations and diagnosis of Cryptococcus neoformans meningoencephalitis in patients without HIV" and "Cryptococcus neoformans: Treatment of meningoencephalitis and disseminated infection in patients without HIV" and "Cryptococcus neoformans infection outside the central nervous system" and "Cryptococcus gattii infection: Microbiology, epidemiology, and pathogenesis" and "Cryptococcus gattii infection: Clinical features and diagnosis" and "Cryptococcus gattii infection: Treatment".)

EPIDEMIOLOGY — The vast majority (90 percent) of cases of cryptococcal meningoencephalitis are seen among patients with AIDS and a CD4 count <100 cells/microL [4]. Patients who present with cryptococcosis can be antiretroviral therapy (ART) naïve or can be prescribed ART but have drug resistance or poor adherence to their prescribed regimen.

In 2008, it was estimated that approximately 957,900 cases of cryptococcal meningoencephalitis occurred worldwide each year, resulting in more than 600,000 deaths [5,6]. The regions with the highest number of estimated cases in 2006 were sub-Saharan Africa (720,000 cases; range, 144,000 to 1.3 million), followed by South and Southeast Asia (120,000 cases; range, 24,000 to 216,000) [5].

The incidence of cryptococcal meningoencephalitis has dropped with the widespread availability of antiretroviral drugs [7-9]. In one report, there was an estimated 223,100 cases per year worldwide, resulting in 181,100 annual deaths in 2014 [8]. In this report, cryptococcal disease caused approximately 15 percent of AIDS-related mortality globally [8]. Even with the increased availability of potent ART, the rates of cryptococcal diseases seem to have stabilized at a relatively high level in sub-Saharan Africa [10].

Early diagnosis and treatment may help reduce cryptococcal meningitis-related mortality. One way to diagnose cryptococcal infection early in the course of disease is through the detection of serum cryptococcal antigen (CrAg), which can be detected at least three weeks prior to the onset of neurologic symptoms. The prevalence of antigenemia has been found to vary depending upon the geographical area. As an example, in the United States, the prevalence of cryptococcal antigenemia among patients with a CD4 count <100 cells/microL was reported to be approximately 3 percent, whereas in Uganda the prevalence among such patients was 8.2 percent [11,12]. A detailed discussion of the use of CrAg screening and early therapy to preemptively manage meningoencephalitis is found elsewhere. (See "Cryptococcus neoformans meningoencephalitis in persons with HIV: Treatment and prevention", section on 'Screening and treatment of early infection'.)

CLINICAL MANIFESTATIONS

Symptoms — Symptoms of cryptococcal meningoencephalitis typically begin indolently over a period of one to two weeks. The most common symptoms are fever, malaise, and headache [2]. Stiff neck, photophobia, and vomiting are seen in one-fourth to one-third of patients. Occasionally, patients can present with coma and fulminant death in days.

Other symptoms suggesting disseminated disease include cough, dyspnea, and skin rash [13]. Visual and hearing loss can also occur [14,15].

Physical examination — The initial physical examination may be notable for lethargy or confusion in association with fever. In one report, 24 percent of patients had altered mentation on presentation, and 6 percent presented with focal neurologic deficits, such as cranial neuropathies [2]. Other manifestations of disseminated disease may be evident, including tachypnea and skin lesions resembling molluscum contagiosum (picture 1) [13]. Increased diastolic hypertension may be reflective of increased intracranial pressure.

Laboratories — General laboratory studies are nonspecific. Patients with advanced immunosuppression may have leukopenia, anemia, hypoalbuminemia, and an increased gamma globulin antibody fraction.

DIAGNOSIS — We have a high index of suspicion for cryptococcal meningoencephalitis in patients with advanced HIV infection (CD4 cell count <100 cells/microL) who have isolated fever and headache. Initial evaluation includes a careful history, neurologic exam, and serum cryptococcal antigen (CrAg). Evaluation should also include a lumbar puncture (LP) to assess for increased intracranial pressure and culture of cerebrospinal fluid (CSF) to confirm the diagnosis in those with symptoms and/or a positive serum CrAg. (See 'Importance of neuroimaging' below and 'Lumbar puncture' below.)

A more detailed discussion on the diagnosis of cryptococcal meningoencephalitis in resource-limited settings is found below. (See 'Special considerations in resource-limited settings' below.)

Importance of neuroimaging — Prior to an LP, patients suspected of having increased intracranial pressure and/or central nervous system (CNS) mass lesions must have neuroimaging (eg, computed tomography [CT] scan or magnetic resonance imaging [MRI]). Discussions of when to perform neuroimaging prior to LP and considerations in resource-limited settings are presented separately. (See 'Special considerations in resource-limited settings' below and "Lumbar puncture: Technique, contraindications, and complications in adults", section on 'Cerebral herniation'.)

Imaging can detect the presence of mass lesions, increased intracranial pressure, and/or hydrocephalus, all of which impact treatment decisions.

Imaging may suggest possible increased ICP with or without mass/space occupying lesions in patients with cryptococcal meningoencephalitis. While LP and removal of CSF may be beneficial for both diagnostic and therapeutic purposes, the risks and benefits of the procedure must be discussed with the patient and/or health care proxy given the very small, but possible chance of cerebral herniation in the setting of raised intracranial pressure. Consultation with neurology and/or neurosurgery can be obtained to help guide this discussion. A more detailed discussion on the risks of lumbar punctures is found elsewhere. (See "Lumbar puncture: Technique, contraindications, and complications in adults", section on 'Cerebral herniation'.)

If mass lesions are identified, we typically consider an alternative diagnosis (eg, toxoplasmosis, lymphoma, tuberculosis) (see "Approach to the patient with HIV and central nervous system lesions"). Mass lesions due to C. neoformans are rarely seen in patients with HIV who are not receiving ART [16,17]; however, they can occur with unmasking cryptococcosis in the setting of an immune reconstitution inflammatory syndrome [12] and in patients with C. gattii infection. (See "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV", section on 'Immune reconstitution inflammatory syndrome' and "Cryptococcus gattii infection: Clinical features and diagnosis".)

If imaging is consistent with cryptococcal-associated hydrocephalus, placement of a ventricular shunt may be required. (See "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV", section on 'Monitoring of intracranial pressure'.)

Lumbar puncture — A lumbar puncture (LP) is required to obtain CSF for confirmatory testing to make the diagnosis of cryptococcal meningoencephalitis. The CSF profile classically demonstrates a low white blood cell count in the CSF (eg, <50 cells/microL) with a mononuclear predominance [18]. The CSF protein may be slightly elevated, while the glucose concentrations are commonly low or normal [15]. Approximately 25 to 30 percent of patients with culture-proven cryptococcal meningoencephalitis have a normal CSF profile [19,20].

An LP is also important for determining the patient's intracranial pressure (ICP), which can be associated with significant morbidity and mortality [2,15]. The management of increased ICP is discussed elsewhere. (See "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV", section on 'Monitoring of intracranial pressure'.)

Cryptococcal culture — CSF should be sent for cryptococcal culture; cream-colored mucoid colonies are seen on agar plates generally within three to seven days.

India ink staining — Since the burden of organisms is usually high in patients with AIDS, an India ink preparation of the CSF may demonstrate typical round encapsulated yeast organisms consistent with Cryptococcus in 60 percent of patients [21]. However, India ink can miss low burden infections; in one report, the sensitivity of India ink was only 42 percent when the culture burden was <1000 colony forming units (CFU)/mL [21].

The advantage of the India ink preparation is that a diagnosis of cryptococcal infection can be made rapidly while confirmatory testing is being performed (eg, CSF culture or antigen). India ink stains should be reviewed by a microbiologist who is familiar with the physical characteristics of the organism.

Regardless of India ink results, a CrAg test should also be performed to confirm the diagnosis. The antigen titer measurement can also provide an estimate of fungal burden and prognosis. (See 'Prognosis' below.)

Cryptococcal antigen (CrAg) — CrAg can be detected in serum and CSF through immunodiagnostic techniques, such as latex agglutination or sandwich enzyme-linked immunosorbent assay (ELISA). The lateral flow assay (LFA) is an alternative approach to detecting cryptococcal antigen. It is a simple dipstick test that is inexpensive to perform and can be used on blood, serum, CSF, or plasma samples. The LFA compares favorably with the latex agglutination and ELISA, and is used in both resource-limited and resource-available areas [21,22]. In resource-limited settings, the LFA improves access to diagnostic testing and time to diagnosis. The analytical sensitivity of LFA is approximately fourfold higher than latex agglutination, thus CrAg titers by LFA and latex agglutination are not comparable.

Spinal fluid — A positive CrAg in the CSF strongly supports the diagnosis of cryptococcal meningoencephalitis and is sufficient evidence to initiate treatment in patients with symptoms and/or risk factors that are consistent with infection. Results of the CrAg test can be obtained immediately after the LP is performed; thus, a positive CrAg test can suggest the presence of infection well before the cultures become positive.

The CrAg is very sensitive and specific in the CSF and has been commonly detected by latex agglutination. In a study of four latex agglutination assays and one enzyme linked immunoassay, all performed well with sensitivities ranging from 93 to 100 percent and specificities from 93 to 98 percent [23]. With latex agglutination, diagnostic false-positive tests can result from infection due to the fungus Trichosporon asahii (formerly T. beigelii) or bacteria of the Stomatococcus and Capnocytophaga genera [24-26]. These positive results are usually present with low titers. False-positive CSF cryptococcal antigen results have been reported rarely following exposure of samples to disinfectants or soap, or after samples were placed into an anaerobic transport vial [27-29]. (See "Infections due to Trichosporon species and Blastoschizomyces capitatus (Saprochaete capitata)".)

The lateral flow assay (LFA) has become the primary approach for detecting CrAg worldwide. The LFA is easier to use and less expensive than latex agglutination. In addition, the LFA appears to perform equally well as or better than other tests. As an example, in a study of 832 HIV-infected individuals from sub-Saharan Africa, LFA was shown to have >99 percent sensitivity and specificity among persons with suspected meningoencephalitis [21]. In this study, LFA had the best test performance when compared with latex agglutination, culture, or India ink microscopy.

Serum/plasma — Serum/plasma testing can have a role in diagnosing patients with both symptomatic and asymptomatic disease.

Symptomatic patients – In patients with AIDS and suspected cryptococcal meningoencephalitis, the sensitivity of serum CrAg testing is comparable to CSF testing and is a useful diagnostic modality in patients who cannot undergo lumbar puncture [30]. Antigenemia in peripheral blood can even precede development of meningitis.

CrAg titers generally correlate with initial organism burden and prognosis. However, following titers are not helpful in management of acute disease in patients with HIV since changes in titer do not precisely correlate with clinical response [31]. Also, the slope of decline is not helpful in predicting those patients who may relapse [32]. (See "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV", section on 'Laboratory monitoring for fungal infection'.)

Asymptomatic patients – In asymptomatic patients with advanced immunosuppression, screening with serum CrAg can identify those with early infection. The use of CrAg screening and preemptive therapy to prevent symptomatic disease is discussed in detail elsewhere. (See "Cryptococcus neoformans meningoencephalitis in persons with HIV: Treatment and prevention", section on 'Screening and treatment of early infection'.)

Cryptococcal PCR — Multiplex polymerase chain reaction (PCR) systems for CNS infections (eg, BioFire FilmArray), which screen for the presence of C. neoformans and C. gattii, are increasingly being used in clinical practice. In one study from Africa, this test detected Cryptococcus in the CSF of patients diagnosed with a first episode of cryptococcal infection with >90 percent sensitivity and excellent specificity. PCR was particularly help to distinguish persistent culture-positive relapse from paradoxical immune reconstitution inflammatory syndrome (IRIS) [33]. (See "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV", section on 'Immune reconstitution inflammatory syndrome'.)

However, clinicians should be cautioned that PCR sensitivity decreases to less than 50 percent with low fungal burdens (<100 CFU/mL CSF) [33]. In addition, this test is expensive and is not commonly used in low and middle income countries. More studies are needed to better understand the sensitivity and specificity of this test for cryptococcal infections, as well as the clinical value in patients without HIV [34].

Extraneural cultures — The diagnosis of cryptococcal disease is occasionally made only after C. neoformans is recovered from another body site, such as blood, urine, or sputum. Routine blood cultures may be positive for Cryptococcus in up to one-third of AIDS-associated cases with meningoencephalitis [2]. If cryptococcemia is suspected, fungal isolator tubes can be ordered for improved sensitivity, although most standard automated blood culture systems are able to detect cryptococcemia.

The prostate gland is recognized as an extraneural site from which Cryptococcus can reside, leading to relapse with systemic dissemination after discontinuation of treatment. Detection of Cryptococcus on urine culture can be improved with prostatic massage. Prior to the era of potent antiretroviral therapy (ART), persistent prostatic sequestration of Cryptococcus was described in patients who were treated for six weeks with amphotericin B with or without flucytosine, with subsequent relapse after treatment discontinuation [35].

Special considerations in resource-limited settings — In resource-limited settings, especially in areas where the prevalence of cryptococcal disease is high, the diagnostic approach may be modified.

Prompt LP with measurement of CSF opening pressure and rapid CSF CrAg assays (or India ink testing if CrAg is not available) remains the preferred diagnostic approach. However, obtaining a diagnosis can be challenging in some settings because of limited access to LP and/or neuroimaging. When this occurs, the risks and benefits favor performing LP without prior neuroimaging, rather than in high-income country settings where the prevalence of cryptococcal meningoencephalitis is lower.

If an individual does not have immediate access to LP, or if an LP is clinically contraindicated, we support the recommendations of the World Health Organization (WHO) that recommend serum or plasma CrAg testing be performed if the results can be delivered in <24 hours [36]. The results of serum/plasma CrAg testing can be used to determine if antifungal treatment should be administered pending further work-up.

If testing for CrAg is positive, treatment with antifungal therapy should be initiated. (See "Cryptococcus neoformans meningoencephalitis in persons with HIV: Treatment and prevention".)

If rapid serum or plasma CrAg is negative or not available, empiric therapy should generally not be administered. Instead, the patient should undergo further diagnostic evaluation, in an appropriate setting, as soon as possible.

A preemptive strategy involving serum CrAg screening and antifungal therapy may reduce the risk of developing cryptococcal meningoencephalitis in asymptomatic patients who are at high risk for developing disease, and may allow earlier therapy for those with CNS involvement. A detailed discussion on the prevention of cryptococcal disease is found elsewhere. (See "Cryptococcus neoformans meningoencephalitis in persons with HIV: Treatment and prevention", section on 'Screening and treatment of early infection'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis in the advanced AIDS patient with fever and headache includes toxoplasmosis, tuberculosis meningitis, lymphoma, syphilis, and progressive multifocal leukoencephalopathy. Patients with toxoplasmosis may also have focal findings, such as specific hand weakness, while patients with cryptococcal meningoencephalitis usually have cranial neuropathies, particularly cranial nerve VI. Patients with tuberculous meningitis may also have other clues to the diagnosis, such as cough, hemoptysis, and an abnormal chest x-ray. Patients with secondary syphilis with aseptic meningitis usually have normal mentation and a disseminated maculopapular rash. Those with central nervous system (CNS) lymphoma may have focal neurologic deficits with abnormal neuroimaging reflecting an intracranial tumor. (See "Toxoplasmosis in patients with HIV" and "Progressive multifocal leukoencephalopathy (PML): Epidemiology, clinical manifestations, and diagnosis".)

PROGNOSIS — The prognosis for patients with AIDS-associated central nervous system (CNS) cryptococcosis has improved dramatically with antifungal treatment coupled with potent antiretroviral therapy (ART), which leads to effective viral suppression and immunologic recovery [37,38]. However, early treatment with ART during the first two weeks of induction antifungal therapy for CNS cryptococcosis should be avoided since higher mortality occurred in comparison with delayed ART [39]. The treatment of cryptococcal meningoencephalitis and the timing of ART initiation are discussed elsewhere. (See "Cryptococcus neoformans meningoencephalitis in persons with HIV: Treatment and prevention" and "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV".)

Acute mortality from cryptococcal meningoencephalitis with underlying HIV infection ranges from 6 to 16 percent in high-income countries [18,37,40-42] and approximately 25 percent in controlled research studies conducted in resource-limited health care systems [43,44]. In one report, the mortality for those diagnosed with cryptococcal meningoencephalitis was as high as 32 percent over a median follow-up of 2.6 years, even in resource-available health care systems [9].

Significant clinical and laboratory predictors of death during the initial few weeks of treatment include [40]:

Abnormal mental status (due to encephalitis and/or increased intracranial pressures)

Cerebrospinal fluid (CSF) antigen titer >1:1024 by latex agglutination or >1:4000 by lateral flow assay (LFA) (high burden of yeasts)

CSF white blood cell count <20/microL (poor host response)

Abnormal mental status on baseline examination or a deterioration of mental status can reflect increased intracranial pressure (ICP). Raised ICP should be considered an urgent medical issue requiring prompt intervention. (See "Clinical management and monitoring during antifungal therapy for cryptococcal meningoencephalitis in persons with HIV", section on 'Monitoring of intracranial pressure'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cryptococcosis" and "Society guideline links: Opportunistic infections in adults with HIV".)

SUMMARY AND RECOMMENDATIONS

Epidemiology – Cryptococcosis is an invasive fungal infection, most commonly caused by Cryptococcus neoformans. The incidence of cryptococcal meningoencephalitis in persons with HIV has declined in those who have access to antiretroviral therapy (ART). However, cryptococcal disease remains a leading cause of mortality in resource-limited settings. (See 'Epidemiology' above.)

Clinical manifestations – Meningoencephalitis is the most frequently encountered manifestation of cryptococcosis in patients with HIV. Symptoms typically begin indolently over a period of one to two weeks. The most common symptoms are fever, malaise, and headache. Other neurologic findings (eg, cranial neuropathies), may also be present. Symptoms suggesting disseminated disease include cough, dyspnea, and skin rash. (See 'Clinical manifestations' above.)

Evaluation and diagnosis – A definitive diagnosis of cryptococcal meningoencephalitis is made by culture of the organism from the cerebrospinal fluid (CSF). A positive cryptococcal polysaccharide antigen in the CSF or serum strongly suggests the presence of infection well before the cultures become positive in high-risk patients. (See 'Diagnosis' above.)

Radiographic imaging of the brain must be performed prior to lumbar puncture if there is a concern for increased intracranial pressure and/or other space-occupying lesions. (See 'Importance of neuroimaging' above.)

Prognostic factors – The significant clinical and laboratory predictors of death during initial induction therapy include an abnormal mental status, a CSF antigen titer of >1:1024 by latex agglutination or >1:4000 by lateral flow assay (LFA), and a pleocytosis of <20 CSF white blood cells/microL. (See 'Prognosis' above.)

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Topic 3757 Version 29.0

References

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