Next Article in Journal
Interference of Small RNAs in Fusarium graminearum through FgGMTV1 Infection
Next Article in Special Issue
Diagnosis and Treatment of Invasive Aspergillosis Caused by Non-fumigatus Aspergillus spp.
Previous Article in Journal
Genome Organization and Copy-Number Variation Reveal Clues to Virulence Evolution in Coccidioides posadasii
Previous Article in Special Issue
The Changing Landscape of Invasive Fungal Infections in ICUs: A Need for Risk Stratification to Better Target Antifungal Drugs and the Threat of Resistance
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:

Invasive Fungal Diseases in Africa: A Critical Literature Review

Department of Medical Microbiology and Immunology, Faculty of Medicine, Gulu University, Gulu P.O. Box 166, Uganda
Department of Medical Microbiology and Parasitology, University of Calabar Teaching Hospital, Calabar P.O. Box 540281, Nigeria
Department of Medicine, School of Medicine, Makerere University, Kampala P.O. Box 7072, Uganda
Department of Medicine, School of Medicine, Kabale University, Kabale P.O. Box 317, Uganda
Department of Medicine, St. Francis’s Hospital Nsambya, Kampala P.O. Box 7176, Uganda
Department of Internal Medicine, University of Calabar Teaching Hospital, Calabar P.O. Box 540281, Nigeria
Department of Microbiology and Parasitology, Faculty of Science, University of Buea, Buea P.O. Box 63, Cameroon
Department of Reproductive Health, Faculty of Medicine, Gulu University, Gulu P.O. Box 166, Uganda
Department of Medical Microbiology and Parasitology, Olabisi Onabanjo University Teaching Hospital, Sagamu P.O. Box 121102, Nigeria
Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 4114 McGavran-Greenberg, 135 Dauer Drive, Chapel Hill, NC 27599, USA
Division of Evolution, Infection and Genomics, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK
Translational Research Laboratory, Department of Research, Infectious Diseases Institute, College of Health Sciences, Makerere University, Kampala P.O. Box 22418, Uganda
Division of Pulmonology, Kiruddu National Referral Hospital, Kampala P.O. Box 7178, Uganda
Makerere Lung Institute, College of Health Sciences, Makerere University, Kampala P.O. Box 22418, Uganda
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
J. Fungi 2022, 8(12), 1236;
Submission received: 20 October 2022 / Revised: 15 November 2022 / Accepted: 18 November 2022 / Published: 22 November 2022
(This article belongs to the Special Issue Current Epidemiological Trends of Invasive Fungal Infections)


Invasive fungal diseases (IFDs) are of huge concern in resource-limited settings, particularly in Africa, due to the unavailability of diagnostic armamentarium for IFDs, thus making definitive diagnosis challenging. IFDs have non-specific systemic manifestations overlapping with more frequent illnesses, such as tuberculosis, HIV, and HIV-related opportunistic infections and malignancies. Consequently, IFDs are often undiagnosed or misdiagnosed. We critically reviewed the available literature on IFDs in Africa to provide a better understanding of their epidemiology, disease burden to guide future research and interventions. Cryptococcosis is the most encountered IFD in Africa, accounting for most of the HIV-related deaths in sub-Saharan Africa. Invasive aspergillosis, though somewhat underdiagnosed and/or misdiagnosed as tuberculosis, is increasingly being reported with a similar predilection towards people living with HIV. More cases of histoplasmosis are also being reported with recent epidemiological studies, particularly from Western Africa, showing high prevalence rates amongst presumptive tuberculosis patients and patients living with HIV. The burden of pneumocystis pneumonia has reduced significantly probably due to increased uptake of anti-retroviral therapy among people living with HIV both in Africa, and globally. Mucormycosis, talaromycosis, emergomycosis, blastomycosis, and coccidiomycosis have also been reported but with very few studies from the literature. The emergence of resistance to most of the available antifungal drugs in Africa is yet of huge concern as reported in other regions. IFDs in Africa is much more common than it appears and contributes significantly to morbidity and mortality. Huge investment is needed to drive awareness and fungi related research especially in diagnostics and antifungal therapy.

1. Introduction

Invasive fungal diseases (IFDs) are a major cause of morbidity and mortality, especially in immunocompromised individuals, such as those with human immunodeficiency virus (HIV), haematological malignancies, organ transplant recipients, as well as prolonged immunosuppressive therapy [1,2,3]. The majority of IFDs occur as opportunistic infections and are defined as the presence of fungal elements in deep tissues of biopsy or needle aspirates identified on culture or histopathological investigations [4]. IFDs still trammel developing countries, with high burden of HIV, tuberculosis, and poverty being the three main drivers [5].
In addition, timely diagnosis of IFDs is a challenge in Africa due to unavailability of reliable point-of-care tests (POCTs), with barriers, such as high cost of tests, lack of awareness among healthcare providers, delays, and low sensitivity of confirmatory blood cultures [5,6]. Early diagnosis and initiation of appropriate antifungal therapy is important in the eradication of IFDs with eventual reduction in morbidity and mortality due to IFDs [7,8].
However, there is a paucity of data on the burden of invasive fungal diseases in Africa. Therefore, the overarching aim of this critical review is to highlight the current state of the burden of invasive fungal diseases in Africa through comprehensive literature review of published cases of IFDs, including cryptococcosis, histoplasmosis, aspergillosis, pneumocystis pneumonia, candidaemia, mucormycosis, talaromycosis, emergomycosis, blastomycosis, coccidiodomycosis, paracoccidiodomycosis, chromoblastomycosis, and sporotrichosis, in the continent.

2. Methods

We conducted a literature search using PubMed, Google Scholar, and African Journal Online to identify published papers on invasive fungal infections from Africa. No date limitation or any other search criteria were applied, to avoid the exclusion of articles on IFDs in Africa. The following search terms were used: ‘histoplasmosis and Africa’, ‘cryptococcosis and Africa’, ‘aspergillosis and Africa’, ‘blastomycosis and Africa’, ‘pneumocystis pneumonia and Africa’, ‘candidiasis and Africa’, ‘mucormycosis and Africa’, ‘emergomycosis and Africa’, ‘talaromycosis and Africa’, ‘blastomycosis and Africa’, ‘sporothricosis and Africa’, ‘coccidiodomycosis and Africa’, and ‘paracoccidiodomycosis and Africa’. All authors were involved in initial data curation, thereafter 3 authors (FB, BEE, WK) screened publications for eligibility. We included retrospective studies, prospective studies, and case series predominantly. Case reports were included for IFDs with scant reports. References in all relevant papers were also reviewed for additional publications (‘snow balling’) on IFDs that may not have been published in the searched databases. Publications without patients’ country of origin were excluded. Publications on IFDs outside Africa were excluded. Data extracted from each case included: age, gender, disease type (single focus vs. multiple foci), sites of infection, clinical features, diagnostic test, treatment, and patient outcome.

3. Results

3.1. Cryptococcosis

Cryptococcosis is an opportunistic fungal infection caused by the fungal species Cryptococcus neoformans and Cryptococcus gattii [9,10]. It is the leading cause of morbidity and mortality in AIDS patients worldwide, affecting one million people annually [9,10]. The invasive form of the disease, cryptococcal meningitis (CM) kills more than 180,000 HIV-positive patients annually, with over 70% in low-income countries, including sub-Saharan African (SSA) countries [11,12]. Rare forms of extra-neuromeningococcal cryptococcosis exist in Africa [13]. The rate of CM is higher than tuberculosis meningitis [14]. Typical signs and symptoms associated with the disease are headaches, neck stiffness, and altered consciousness [15,16,17,18]. Low body mass index, low haemoglobin, and low CD4 cell count (<200 cells/mm3) are significant predictors for CM [19,20,21,22,23,24,25]. The burden of cryptococcosis has previously been estimated across Africa, and it remains extremely high [26]. It was estimated at 720,000 (144,000–1.3 million) and 162500 (113,000–193,000) cases annually in 2009 and 2014, respectively, in patients with CD4 count < 100 cells/mm3 in SSA [27,28], Table 1. A review carried out in 2020 based on cross-sectional studies estimated the magnitude of cryptococcosis in SSA countries at 8.3% (6.1–10.5%) [29].
A recent global burden of cryptococcosis estimated CrAg positivity and cryptococcal meningitis at 75,000 (55,000–95,000) and 63,000 (45,000–80,000) cases, respectively, in Eastern and Southern Africa, and at 22,000 (19,000–26,000) and 19,000 (16,000–22,000) cases, respectively, in Western and Central Africa. The burden of CM in some African countries has been estimated over the years, with the lowest rate in Algeria (35 cases/year) and the highest in Nigeria (57,866 cases/year) [30]. These estimates are based on studies carried out in these countries and usually in HIV-positive patients with low CD4 count [6,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46] (Table 1). The availability of studies and data on cryptococcal antigenemia and CM varies from one country to the other (Table 2). A multicenter study estimated the prevalence of cryptococcal antigenemia in four regions of Nigeria at 2.3% (1.8–3%) in HIV patients with CD4 < 200 cells/mm3 [47]. However, this prevalence significantly differs from one region to another [47], with a prevalence from 1.4% (4/290) to 19.67% (59/300) for cryptococcal antigenemia [9,14,23,24,25,48,49,50,51], and from 16.8% (31/184) to 36% (36/100) for CM [10,52]. In Uganda, a prospective study found 32 (5.7%) HIV-infected patients with cryptococcal antigen (CrAg) positivity from 2009 to 2010 [53]. Still in Uganda, in two cross-sectional studies in HIV-positive patients, prevalence of 5.7% and 19% were obtained [22,53]. Jacinta et al. (2012) also found 6.5% cases of CM [22]. A large screening program in South Africa from 2017 to 2019 among HIV patients with low CD4 count found a cryptococcal antigenemia rate of 5.8% (35,000/600,000) [54]. A prevalence of 23.1% (43/186) for cryptococcal antigenemia and 21.7% (5/23) for CM were obtained from a similar study in Cameroon [55]. Little is known about the prevalence of cryptococcosis in Ethiopia. This prevalence ranges from 4% to 11.43% with CD4 < 100 cells/mm3 as a common factor [56,57,58,59] and sometimes co-infection with other diseases [56,57]. More data on cryptococcosis are available in Mali, Democratic Republic of Congo (DRC), Togo, Kenya, Ghana, Nigeria, Burkina Faso, Botswana, Senegal, Tanzania, South Africa, Cameroon, and Mozambique, sometimes with a high mortality rate [13,16,17,18,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75]. Data on cryptococcosis in HIV negative patients and children is rare. Then, rates of 18.8% (22/117), 2.5% (1/150), 7% (16/228), and 1.47% (3/204) for CM and cryptococcal antigenemia in HIV-negative patients were obtained from studies in Nigeria and Mali [10,49,51,76]. Two studies in Cameroon determined a prevalence in children of 6.12% (9/147) and 3.6% (12/331) for cryptococcal antigenemia and CM, respectively [67,69]. Data in some countries are available only in form of case reports [77], Table 2.
Table 1. Estimated burden of cryptococcosis in some African countries.
Table 1. Estimated burden of cryptococcosis in some African countries.
Country Pub YearBurdenRate/100KPrevalence Used for EstimationGroup at RiskReferences
Senegal 2015366NA7% HIV/AIDS Badiane et al. [31]
Burkina Faso20184592.53.4% HIV/AIDSBamba et al. [39]
Ethiopia 201999009.411.7%HIV/AIDSTufa and Denning [40]
Togo 2021134218.526.12%HIV/AIDSDorkenoo et al. [41]
Namibia 201954321.83.3%HIV/AIDSDunaiski and Denning [42]
Mozambique 201818,64070.519.4%AIDSSacarlal and Denning [43]
Ghana 2019627521.712.7%HIV/AIDSOcansey et al. [45]
Morocco 20221600.432.9%AIDSLmimouni et al. [46]
Côte d’Ivoire2020459018.2212.7HIV/AIDSKoffi et al. [36]
Algeria 2016360.095.6%HIV/AIDS, CancerTalbi and Denning [6]
Egypt 2017380.0NAHIV/AIDSZaki and Denning [32]
Cameroon 201867203011%HIV/AIDSMandengue and Denning [33]
Nigeria 20145786637.410% of new adults AIDS
cases 12.7% of
adults with CD4 < 200
10% cases in children
HIV/AIDSOladele and Denning [36]
Uganda 20132783NA5.8%HIV/AIDSParkes-Ratanshi and
Denning [34]
South Africa2019835714.8NAHIV/AIDSSchwartz and Denning [37]
Kenya 201611,900297%HIV/AIDSGuto et al. [44]
Zimbabwe 2021608641NAHIV/AIDSPfavayi et al. [35]
NA: not available.

3.2. Histoplasmosis

Histoplasmosis is a serious fungal disease endemic in the Ohio and Mississippi river valleys in the United States, as well as Central, South America, Western Africa, Southern Africa, Eastern Africa, Central Africa, and Southeast Asia [79,80,81,82]. The classical form of the disease is caused by Histoplasma capsulatum var. capsulatum (Hcc), while the African type is caused by Histoplasma capsulatum var. duboisii (Hcd) [79,80]. Histoplasma infection is commonly acquired via the inhalation of microconidia. Its greatest attributable risk factor in the adult population is HIV/AIDS and was classified as an AIDS-defining illness in 1987 [79]. However, retrospectively, several cases of histoplasmosis were also recorded in Africa prior to HIV/AIDS pandemic [79]. On the contrary, in the paediatric population, histoplasmosis is predominantly associated with risk factors other than HIV, including environmental exposures and toxins, autoimmune diseases, childhood malignancies, as well as their treatment, lung diseases, immunosuppressive therapies, pancytopenia, T-cell deficiency, and malnutrition [83,84]. Clinical features are non-specific and mimic other clinical entities, including tuberculosis, malignancies, tropical splenomegaly syndrome, leishmaniasis, amongst others [85,86,87]. The classical form usually presents as a pulmonary disease, while the African-type presents with extrapulmonary manifestations, including bone lesions and ulcers [79,80]. Diagnosis of histoplasmosis often requires a high index of clinical suspicion otherwise may lead to delayed or misdiagnosis. The gold standard for diagnosis is culture, however most cases are diagnosed by histopathology, as fungal cultures are not routinely available in many African countries. Other diagnostic modalities include Histoplasma antigen assay, antibody detection, molecular techniques, direct examination, and the use of peripheral blood smear [79,80].
Despite the apparent increase in reported cases, the true burden of histoplasmosis in Africa is yet unclear due to several reasons: (1) poor awareness on the part of clinicians with some cases diagnosed post mortem [85,86,87]; (2) a low index of suspicion on the part of clinicians resulting in several cases being misdiagnosed as other clinical entities [79,85,86,87]; (3) inadequate or the lack of diagnostic capacity across African countries [88,89]; (4) data on the incidence and prevalence, as well as information on its morbidity and mortality in most African countries are fragmentary and perhaps not available in some African countries [79]. Be that as it may, some studies have described cases in some specific countries in Africa and across Africa generally. One review by Oladele et al. that spanned six decades (1952–2017) identified 470 cases of histoplasmosis with HIV-infected patients consisting of 38% (178) of the cases. West Africa had the highest number of recorded cases with 179; the majority (n = 162 cases) were caused by Histoplasma (H) capsulatum var. dubuosii (Hcd). In total, 150 cases were reported from the Southern African region, and the majority (n = 119) were caused by H. capsulatum var. capsulatum (Hcc). Hcc was found to be the most predominant infective agent in Africa, while Hcd was primarily found in Central and West Africa and Madagascar. Most of the reported cases from Africa were diagnosed by culture and histology; only in five countries (Tanzania, Benin, South Africa, Egypt, and Uganda) was serology reported as being used to make a diagnosis, and in three of the cases, the samples were processed in Western countries [79]. A more recent review focused on African histoplasmosis in the context of HIV/AIDS by Develoux et al. identified 94 well documented cases (1993 to 2019) of Hcd infection, with 30.1% of the patients under 18 years old. HIV coinfection rate was 20.8% with fever, lymphadenopathies, and absence of bone infection being the differentiating elements from patients living without HIV [90]. With regard to the paediatric population in Africa, a global review (1939–2021) mentioned 65 cases with most of the cases reported from the Republic of Congo (n = 26) and Nigeria (n = 13) [83]. Another review (1950–2021) yet focused on histoplasmosis in the paediatric population in Africa described 44 selected cases distributed across Western Africa (38.6%, n = 17), Eastern Africa (9.1%, n = 4), Southern Africa (9.1%, n = 4), and Central Africa (43.2%, n = 19). No case report was found from Northern Africa. The age range was 1–17 years, with a mean of 9.2. Of the 44 case reports, 8 cases (18.2%, 8/44) were caused by Histoplasma capsulatum var. capsulatum, 33 cases (75%, 33/44) were caused by Histoplasma capsulatum var. duboisii, and specie identification was not found in 3 cases. Only three (6.8%) cases were HIV positive; 56.8% (25/44) were disseminated histoplasmosis, pulmonary histoplasmosis accounted for just one case (2.3%, 1/44) [86]. Findings from more recent studies and other reviews focused on specific countries in Africa are as summarized in Table 3 [83]. None of the studies indicated case fatality rates.

3.3. Invasive Aspergillosis

Invasive aspergillosis (IA) is a life-threatening infection that affects those with impaired immune systems [99]. It is caused by Aspergillus species, which are saprophytic fungi that belong to the class ascomycetes and produce conidia that are easily dispersed into the air [100]. There are more than 300 species of Aspergillus, and 90% of human infection is caused by A. fumigatus with the other implicated species being A. flavus, A. terreus, A. niger, and A. nidulans [101]. The lungs are the common site of infection and the conidia when inhaled results in a diverse clinical spectrum namely, allergic, chronic, and invasive aspergillosis [101].
Globally, IA affects more than 300,000 people annually and the fatality rate ranges from 30 to 80% [102]. The incidence rises with an increase in immunosuppression [102] because the phagocytic and neutrophilic functions of the immune system that prevent conidia germination are impaired [103]. Hence, IA is commonly found in those with neutropenia, recipient of transplantation, steroid therapy, and chronic granulomatous disease. Other people that could be affected are those who recently underwent surgery; are in intensive care units; those with HIV/AIDS, coronavirus disease 2019 (COVID-19), influenza virus, diabetic mellitus, chronic obstructive pulmonary disease, and cytomegalovirus; and those on newer immunosuppressive agents, such as tumour necrosis factor-alpha inhibitors [104]. The most common form is invasive pulmonary aspergillosis (IPA). Diagnosing IA is challenging because it involves culture of the respiratory specimen, histology of biopsy tissue, non-culture-based methods using Aspergillus antigen, imaging with computer tomography, magnetic resonance imaging, and molecular techniques with polymerase chain reaction [105].
In Africa, the burden of IA was estimated as 0.05 to 10.9 per 100,000 population. However, most of these estimates do not take into consideration the “at-risk population” and the clinical spectrum of invasive aspergillosis. The estimates per 100,000 population were 4.8 to 16 in Southern Africa, 0.05 to 10.9 in Northern Africa, and 0.3 to 6.25 in Western Africa while it ranges from 7.1 to 10.7 and 3.2 to 6.9 in Northern Africa and Central Africa, respectively [106].
The few cases published in Africa are listed in Table 4 below. These include six case reports, and four prospective and one retrospective study. Of the case reports, the underlying risks were HIV, recipients of renal transplant, antibiotic use, cytomegalovirus, diabetics mellitus, renal failure, and chronic granulomatous disease, while none was specified from the cases reported from Sudan. From Nigeria, a case in an immunocompetent elderly woman in whom the diagnosis was made with computer tomography (CT) was reported. In all the cases reported below, galactomannan assay in combination with CT and/or culture was only performed in the cases reported from Tunisia. Concerning the observational studies, IPA was the only clinical spectrum reported and the underlying risk were Hodgkin lymphoma; HIV; haematological malignancies, such as acute myeloid leukemia (AML), acute lymphoid leukemia (ALL), and neutropenia; broad-spectrum antibiotics; severe combined immunodeficiency; and bronchiectasis. In three of the cases, the diagnosis was established by histopathology of biopsy specimen after post-mortem.
The data on invasive aspergillosis are limited in Africa, and this could have been because of the low level of clinicians’ awareness of invasive fungal infections (IFI) and the few numbers of medical mycologist specialists. Importantly, diagnostic tools, such as Aspergillus antigen assays are not readily available; also, the high prices involved in carrying out CT scans and polymerase chain reaction (PCR) are contributory factors that hamper diagnosis, leading to the underreporting of cases.

3.4. Pneumocystis Pneumonia

Pneumocystis jirovecii is a fungus belonging to the phylum Ascomycota and is famed for causing a fatal infection of pneumonia among immunocompromised individuals [117]. Initially classified as a protozoan, rRNA sequencing led its subsequent designation to the fungi kingdom [117]. The HIV epidemic brought P. jirovecii to the forefront as a cause of a severe form of pneumocystis pneumonia (PCP) among people with advanced HIV. As such, most epidemiological data available from Africa are among people living with HIV (PLWH). About 15% of new AIDS patients develop PCP.
The burden of PCP among PLWH in Africa is well described in two systematic reviews. In a meta-analysis of hospital-based studies from 18 countries in sub-Saharan Africa, the overall prevalence of PCP was 15.4% but it was higher among people with respiratory symptoms (18.8%), inpatients (22.4%), and inpatients with respiratory symptoms (24%) [118]. This meta-analysis demonstrated a decline in the prevalence of PCP among inpatients over the years: 28% in the 1990s, 27% between 2000 and 2004, and 9% after 2005 [118]. This trend correlated with the proportion of people initiated on anti-retroviral therapy (ART) and cotrimoxazole prophylaxis. The rate of respiratory co-infections (alongside P. jirovecii) was reportedly high (29.3%) and included pulmonary tuberculosis (14.8%), bacterial pneumonia (18.7%), pulmonary cytomegaly virus (3.9%), and pulmonary cryptococcosis (1.4%) [118]. In most African countries, PCP is diagnosed clinically and managed with high dose cotrimoxazole without laboratory confirmation. Radiology is non-specific. PCR is considered the gold standard for diagnosis. However, the low diagnostic accuracy of clinical and radiological features for PCP limits an accurate estimation of the true burden of PCP in Africa where laboratory confirmation by microscopy and polymerase chain reaction (PCR) on bronchoalveolar lavage is largely inaccessible in many places. A more recent meta-analysis of studies from 15 African countries reported an overall prevalence of laboratory-confirmed P. jirovecii of 19% on any respiratory sample from adult PLWH with respiratory symptoms [119]. The prevalence varied from 15% among studies that utilised microscopy to 22% among studies that used PCR. Interestingly, the prevalence of laboratory-confirmed P. jirovecii has remained relatively level in the pre-ART era (1995–2005) and the ART era (2006–2020) at 21% and 18%, respectively [119]. The case fatality rate from PCP among PLWH has been estimated to be 18.8% [118].
With regard to P. jirovecii colonisation (a positive P. jirovecii PCR test in the absence of respiratory symptoms), three small studies from Tanzania, Guinea-Bissau, and Cameroon reported a prevalence of 0.3%, 3%, and 42.9% (18.9% among HIV-negative individuals), respectively, among PLWH [120,121,122]. Although the clinical relevance of P. jirovecii colonisation is not very apparent, colonisation could increase transmission of P. jirovecii and disease progression among at-risk individuals and has been implicated in chronic obstructive pulmonary disease exacerbations [123].
There is a paucity of data on the burden of P. jirovecii among HIV-uninfected individuals in Africa. HIV-negative people with haematological malignancies, long-term steroid use, people on treatment for solid cancers with chemo-radiotherapy, recipients of organ transplants and people with rheumatological conditions are at risk of PCP [124]. However, systematic reviews on P. jirovecii in non-HIV populations report no studies from Africa [125,126]. Nonetheless, a few studies among children exist. The prevalence of P. jirovecii was 12.8% in one study among HIV-negative children admitted with hypoxic pneumonia in South Africa [127]. In another multi-centre study, the proportion of severe pneumonia caused by P. jirovecii requiring hospitalisation among children was reported to be 0.2% in The Gambia, 2.4% in Mali, 2.3% in Kenya, 4.1% in Zambia, and 2.1% in South Africa [128]. More studies are needed to characterise disease caused by P. jiroveciii among HIV-uninfected adults in Africa.

3.5. Candidemia

Candidaemia refers to the presence of Candida species in the blood stream and is among the most common blood-stream infections [129]. The most common Candida species that cause candidaemia include: C. albicans, C. auris, C. krusei, C. parapsilosis, C. tropicalis, and C. glabrata [130]. Diagnosis of candidaemia is by blood culture. A positive 1,3-beta –D-glucan (BDG) assay is suggestive but is, however, not specific, as it has been shown to be positive for other fungal diseases, including cryptococcosis and pneumocystis pneumonia. A study on the comparative sensitivity of 1,3 beta-D-glucan for common causes of candidaemia showed an overall sensitivity of 79% and per species sensitivity of 81%, 72%, 90%, 71%, and 100% for C. albicans, C. parapsilosis, C. glabrata, C. auris, and C. krusei, respectively [131]. In a recent study, Lockhart et al. showed that C. auris consisting of clades (I to IV) is an emerging healthcare associated pathogen with high mortality due to limited treatment options as a result of resistance to antifungal drugs, as well as hygiene and infection control measures, such as hospital chlorine-based disinfectants [132,133]. In fact, the high nosocomial transmission of C. auris has been attributed to the antifungal and disinfectant resistance, use of reusable skin surface temperature monitoring probes, and prior exposure to systemic fluconazole [133,134]. A recent publication by Parak et al. revealed 45 cases of C. auris caused candidaemia in South Africa, all of which were susceptible to amphotericin B and micafungin however, patients treated with amphotericin B only had a higher mortality rate than those treated with an echinocandin [135].
C. albicans has been shown to have higher mortality than C. auris (36% and 29%, respectively) [136]. A rising number of cases of antifungal resistance by Candida species has been registered with the most recent retrospective study conducted in South Africa showing an overall rise in the proportion of azole resistant candidaemia cases from 39.6% in 2016 to 69.5% in 2020 [137]. However, only 0.2% and 0.3% of C. albicans and, 0.9% and 6.6% of non-albicans isolates were resistant to amphotericin B and echinocandin, respectively [137].
Recent publication from South Africa showed through laboratory based surveillance that neonates were the most affected age group (49%) followed by infants (27%) with C. parapsilosis (42%) and C. albicans (36%) as the commonest causative agents of single species candidaemia [138]. Moreover, the highest 30-day in-hospital mortality was identified to be highest in neonates (43%) and adolescents (43%) [138]. Hegazi et al. in a study conducted in Egypt showed a slightly lower mortality (16.7%) due to candidaemia among patients aged 6 months to 15 years [139]. A five-year retrospective descriptive study conducted in South Africa by Hussain et al., showed a high overall mortality associated with candidaemia with 55% of the participants dying from candidaemia and its complications [129].
Surveillance studies in South Africa, Algeria, and Kenya, reports C. parapsilosis, C. tropicalis, and C. auris as the most commonly isolated species, respectively [136,138,140]. Other surveillance-based studies conducted in 2009 and 2010 in South Africa, and retrospective hospital-based studies in South Africa and Nigeria, found C. albicans to be the most cause of candidaemia (23.8%, 73%, and 77%, respectively) [134,141,142]. As evidenced by results from a prospective case–control study in Cairo, Egypt, neutropenia is highly associated with a diagnosis of candidaemia for which, 56% and 16% of premature neonates with neutropenia and without neutropenia, respectively, were diagnosed with candidaemia based on blood culture results [143]. Table 5 summarizes published cases of candidaemia in Africa.

3.6. Mucormycosis

Mucormycosis is an opportunistic invasive disease predominantly found in immunocompromised individuals [148]. The sequelae is severe and often life threatening [149,150].
These fungi are members of the genera Mucor, Rhizopus, Rhizomucor, Syncephalostrum, and Lichtheimia in the order Mucorales [149]. They are widely distributed in the environment as airborne spores which may result in skin and respiratory infections in susceptible individuals [149]. They are also seen as bread mold, laboratory contaminant, and is a common inhabitant of soil and decaying vegetation [151].
Immunocompromised states which result in invasive fungal diseases are: diabetes mellitus, recipients of haematopoietic stem cells or solid organ transplants, patients infected with HIV, and those receiving chemotherapy for cancer [148]. Penetrating trauma, steroid use, deferoxamine therapy, burns, and complications as a result of healthcare procedures are also implicated [152].
There are varied sites of involvement of mucormycosis infection with rhino–sino–orbital–cerebral, pulmonary, cutaneous, and gastrointestinal involvement being the most common sites of involvement reported [148,151,153]. There is a great need for a high index of suspicion to aid in early identification and treatment of this disease condition as it is associated with high mortality rate with survival rate as low as 3% reported in the absence of treatment [154]. Prompt commencement of treatment is required to reduce the mortality rate even though in the presence of appropriate medical management, mortality is still high [152]. Treatment involves a combination of surgery to completely remove the infected tissues and first line antifungal therapy, which are amphotericin B, Isavuconazole, and Posaconazole [155]. In addition to this, identification and treatment of a predisposing factor is essential in order to further reduce mortality rate [156].
In Africa, Mucormycosis infection has been documented to span across all age groups. A case series performed in Egypt by El-Mahallawy et al. [157], documented mucormycosis in the paediatric age group with patients age ranging from 1.5 years to 12 years on treatment for haematological malignancies: acute lymphoblastic leukaemia and acute myeloid leukaemia, and a high mortality recorded at 60% [157]. Mucormycosis has also been recorded in a 10-month-old baby in South Africa attributed to underdeveloped immunity [151]. Its presentation as recorded in case series of rhinocerebral mucormycosis by Bodenstein et al. [158], Hauman et al. in South Africa [151]; Zaki et al. [152], Alfishawy et al. [159], Alloush et al. in Egypt [160]; and Anane et al. [161] in Tunisia. Its presentation as gastrointestinal mucormycosis was recorded by Thomson et al. [162] and Kahn et al. [163] in South Africa. Its presentation as pulmonary mucormycosis was recorded by Feki et al. [164] in Tunisia; and Madeney et al. [165] and El Mahallawy et al. [157] in Egypt. In addition, there are also case reports in this regard [166,167,168,169].
There is a notable increase in the occurrence of murcormycosis in Africa which corresponds to the increase global prevalence of diabetes mellitus and immunocompromised patients [148,153] and also the emergence of the COVID-19 pandemic. Case series from Egypt, performed by Abd El-hameed et al. [166], Alfishaway et al. [159], and Alloush et al. [160] revealed the bidirectional relationship between COVID-19 and diabetes mellitus with increased risk of mucormycosis, while new onset diabetes (NOD) and the exacerbation of pre-existing diabetes mellitus had been identified in COVID-19 patients [159,166].
In Tunisia, Trabelsi et al. reported 11 cases (3.4%) out of 321 renal transplant recipients with a high mortality rate of 72% [108]. This reiterates the need for heightened suspicion of this fungal disease entity in renal transplant patients as Africa currently has 46 countries involved in renal transplant [168]. A 70-year retrospective study conducted in Uganda also revealed four cases of mucormycosis due to unidentified fungi that were diagnosed by PAS stain and microscopy and affecting multiple body parts [98]. Diagnoses is mostly by histopathology [151,152,157,158,162,163,164,165]. Other modalities include microscopy [151,159,160,161], culture [152,157,159,164,165], and PCR [152], Table 6.
Problems faced across Africa in the diagnosis and management of mucormycosis infection include: late presentation of patients [151], its presumed rarity leading to delay in diagnosis [151], and the poor accessibility to antifungal medications for management of patients [169].
Based on widespread areas of involvement of invasive mucormycosis and associated increased mortality, a greater surveillance protocol set up is needed in African countries to prevent and reduce morbidity and mortality in affected individuals.

3.7. Talaromycosis

Talaromycosis, previously known as penicilliosis, is a fungal infection caused by the fungus Talaromyces marneffei (Penicillium marneffei). It is endemic in east and southeast Asia and considered a neglected tropical disease [170]. It may present with painless skin lesions on the face and neck, fever, anaemia, large lymph glands, and liver [171]. It typically occurs in immunocompromised patients, such as those with HIV, cancer, organ transplant, long-term steroid use, old age, malnutrition, or autoimmune disease. T. marneffei is the only thermally dimorphic fungus in the genus Talaromyces [172]. As most dimorphic fungi are, it exists as a mold in the environment but forms small round yeast cells in host tissue. Data are limited about its natural habitat. However, it has been isolated from soil [171]. There is evidence showing that heavy rainfall may provide favourable conditions for the growth and dissemination of the fungus [173]. Infection is thought to follow inhalation of fungal spores from unidentified environmental sources. Incubation period may vary, and the fungus can sometimes cause an asymptomatic dormant infection for long periods [174]. Diagnosis is usually made by the identification of the fungus from clinical specimens, either by microscopy or culture. Biopsies of skin lesions, lymph nodes, and bone marrow demonstrate the presence of organisms on histopathology.
As seen in the table below, data are scant about the burden of talaromycosis in Africa. We found only two case reports [175,176], Table 7. From these reports, HIV and a travel history to Asia are the major risk factors. Cases are aged between 37 and 83 years. Most common clinical presentation includes multiple umbilicated papules associated with cough, fever, loss of appetite, loss of weight, urethral discharge, febrile pneumonia, dyspnoea, “molluscum contagiosum” such as lesions located on the face, arms, neck, and trunk. It is mainly diagnosed using culture-based methods in Africa. However, some sites employ molecular diagnostics, although these are rarely available in Africa. One case was managed with Itraconazole and responded well, while the other died within 12 h of admission.

3.8. Emergomycosis

Emergomycosis is a systemic fungal infection caused by the fungus Emergomyces (formerly called Emmonsia). Emergomyces is a dimorphic fungus and consists of five known species that have been reported globally [177]. These species are Es. Pasteurianus, Es. Africanus, Es. Canadensis, Es. Orientalis, and Es. Europaeus. Es. pasteurianus and Es. africanus are commonly isolated from Africa with South Africa having the highest number of cases [177]. Es. africanus is a newly discovered fungus within this group and, so far, has only been found in southern Africa. Emergomyces is also a thermally dimorphic fungus and is known to cause disease globally mostly in people with advanced HIV disease [178]. It is found in soil and human infection is through inhalation of fungal spores. So far, emergomycosis has been report on four continents: Asia, Europe, Africa, and North America. However, considering the increasing global burden of HIV, it is presumed that the disease must have a worldwide distribution with many cases going undetected [179]. Diagnosis is challenging and is confirmed by culture and/or histology. It should be considered in the differential diagnosis of histoplasmosis as there is considerable clinical and histopathological similarities between the two diseases. Currently, there are no consensus guidelines for the treatment of emergomycosis. Treatment requires antifungal medicines, such as amphotericin B for 1–2 weeks, followed by oral itraconazole for at least 12 months.
Data about Emergomycosis in Africa are limited and mostly reported in case reports/series, Table 8. The table below summarizes some of the published cases of Emergomycosis from Africa. Majority of the case were reported from South Africa. However, considering the burden of HIV in Africa, we believe that there are more cases across all Africa that go undetected due to low index of clinical suspicion and the lack of diagnostics. From these identified cases, the median age of patients is about 34 years. HIV is the major risk factor reported in all cases with majority having CD4 count less than 200 cells/mm3 and undetectable viral load. Most of the cases have skin lesions as the primary symptom. Other presentations include anaemia, pneumonia, gastroenteritis, herpes gingivostomatitis, and weight loss. Diagnosis was challenging and mainly performed using a combination of histology, culture, and molecular tests (mostly sequencing). These cases were mostly managed using amphotericin B and itraconazole. Some of the cases we identified in this article were managed with Fluconazole. However, in vitro susceptibility data from South Africa recommends the use of amphotericin B, followed by itraconazole, voriconazole, or posaconazole. Fluconazole was a relatively less potent agent [180].
Schwartz et al. summarized the geographic distribution, clinical characteristics, and management of 54 cases of disseminated emmonsiosis published across South Africa from January 2008 through to February 2015 [181]. Two more cases were described in South Africa by Heys et al. in 2014; one being immunocompetent and the other a renal-transplant patient receiving immunosuppressive therapy [182]. According to the authors, this one case of disseminated emmonsiosis in an apparently immunocompetent person raised the question of whether this was a more virulent strain or different species or whether the patient had exposure to a large amount inoculum or had an undiagnosed immune disorder.
Es. africanus has also been isolated from air samples from 34 days distributed over 11 weeks in Cape Town, South Africa [183]. It has also been isolated by PCR in 30% of soil samples from a wide range of habitats in South Africa [184].
Table 7. Published cases of Talaromycosis in Africa.
Table 7. Published cases of Talaromycosis in Africa.
AuthorsYear CountryStudy Type Number of CasesSexAgeRisk FactorsSymptomsDiagnostic ToolTreatmentOutcomes
Guiguemde et al., [175]2019Burkina FasoCase report1M83HIV,
CD4 = 240 cells/Ul
Poor ART adherence
Persistent itching skin lesions on the right foot,
>1 year
CultureItraconazole (400 mg/day) for 8 weeksFavourable
Govender et al., [176]2014South AfricaCase report1F37HIV,
Cd4 = 20 cells/Ul
travel to China

Skin lesions
Blood smear,
β-D-glucan assay,
Gene sequencing
NSThe patient died within 12 h of admission.
M, Male; F, Female; NS, Not stated.
Table 8. Studies published on emergomycosis in Africa.
Table 8. Studies published on emergomycosis in Africa.
AuthorsYear CountryStudy TypeNumber of CasesSexAgeRisk FactorsClinical presentationDiagnostic ToolCausative AgentTreatmentOutcomes
Kenyon et al., [185]2013South AfricaCase series13M = 8
F = 5
Median age = 34 yearsHIV, median CD4 count = 16 cells/UlAnemia
Skin lesions
DNA sequencingEmmonsia speciesamphotericin B
Death (n = 3), LTFU (n = 1), Favourable (n = 9)
Moodley et al., [186]2019South AfricaCase report1F31HIV,
CD4 count = 80 cells/Ul
Skin lesionsHistopathology, Culture, Molecular testing Emergomyces africanus
Fluconazole Favourable
Schwartz et al., [187]2017South AfricaCase series14NSMedian = 35HIVPlaques
scale crust
Histopathology, Culture,
Molecular testing
Emergomyces africanus
Amphotericin B,
Rooms et al., [188]2019UgandaCase report1F38HIV
CD4 = 140 cells/Ul
Skin lesionsHistopathology, Gene sequqencingE. pasteurianusFluconazole Favourable
Lochan et al., [189]2015South AfricaCase report1M3HIVpneumonia, gastroenteritis and herpes gingivostomatitisCulture and DNA sequencingEmmonsia speciesAmphotericin B,
Tulleken et al., [190]2014South AfricaCase series3M3HIV
CD4 < 5 cells/Ul
skin rash, pneumonia, anemia, and substantial weight lossHistopathology, CultureEmmonsia speciesAmphotericin B,
Death (n = 2), Favourable (n = 1)
M, Male; F, Female; LTFU, Lost to follow up.

3.9. Blastomycosis

Blastomycosis is a fungal infection caused by inhalation of spores of Blastomyces species found in soil [191,192]. In Africa, blastomycosis is commonly caused by Blastomyces percursus and mostly manifests as pulmonary followed by cutaneous disease, with other organs, such as the brain, being affected [191,192,193,194]. However, extra-pulmonary disease is the commonest manifestation of blastomycosis [195]. Pulmonary disease manifests radiologically with alveolar infiltrates, consolidation, and cavitation as seen on a plain chest radiograph [193]. Bonifaz et al., in their article showed that blastomycosis in middle and east Africa are caused by B. dermatitidis with middle and east Africa in the second place of the most endemic areas [191,193]. Blastomycosis is diagnosed using direct microscopy using potassium hydroxide (KOH), culture, histology, antibody test, as well as PCR identification using specimen such as wound secretion, sputum, or bronchial lavage [191]. Blastomycosis is treated using antifungal drugs, such as with amphotericin B for severe disease for at least 12 months and itraconazole, voriconazole, or posaconazole for about 6–12 months for mild to moderate disease [191,192,196,197].
In South Africa, a study involving 20 cases of blastomycosis revealed that most of the cases were caused by B. percursus (n = 12) and only 8 were caused by B. emzantsi [196]. The patients with B. percursus had extra-pulmonary disease (n = 7), pulmonary disease (n = 3), cutaneous disease (n = 4), vertebral disease (n = 1) and multisystem disease (n = 4) [198]. Whereas those with B. emzantsi had subcutaneous abscess (n = 1) and both pulmonary and vertebral disease (n = 2) [198]. The antifungals with the most in vitro potency for the isolates from all 20 cases included voriconazole, posaconazole, itraconazole, amphotericin B, and micafungin [198]. Several cases of cutaneous blastomycosis have been reported in South Africa, Tunisia, and Morocco with no pulmonary involvement [199,200,201,202,203]. B. dermatitidis has been implicated in several cases of pulmonary, subcutaneous, vertebral and paravertebral blastomycosis in Tunisia, Morocco, and Tanzania [194,204,205,206]. An earlier case report by Ibrahim et al. described a case of a 37-year-old from Nigeria who was diagnosed with pulmonary blastomycosis with right-sided pleural effusion, was managed with ketoconazole and saline pleural lavage with eventual clinical improvement [207]. In a 70-year retrospective study conducted in Uganda, Kwizera et al. revealed that blastomycosis took up 1.6% of the deep mycoses identified using histology [98], Table 9.

3.10. Coccidioidomycosis

Coccidioidomycosis (Valley Fever) is a disease caused by the soil inhabiting spores of the fungi coccidioides. Fisher et al., 2002, isolated Coccidioides immitis and Coccidioides posadasii as two separate pathogenic species causing Valley Fever. The two are morphologically identical but epidemiologically and genetically varied species [208].
Coccidioides posadasii is a soil fungus that is native to certain arid to semi-arid areas of southwestern United States, northern parts of Mexico and South America, while C. immitis is endemic to the San Joaquin Valley of California [209,210]. With a geographic overlap between the two species in Southern California [210].
Coccidioidomycosis is transmitted via inhalation of the airborne spores of the dimorphic fungi Coccidioides (C. immitis and C. posadasii) from the soil. The fungus is most frequently acquired in summer or late fall seasons. These dry months are when soil is disturbed by wind and storms. Exposure to contaminated balls of cotton or other fomites can result in infection beyond the endemic region, although rarely [210].
It has an extremely low prevalence outside America, and the few cases reported from Asia and Europe have been seen in travellers to these endemic areas and become clinically significant when they return home or the disease many be transported through contaminated materials [211]. It is also hypothesized that cases of coccidioidomycosis exist in Africa, but had not yet been reported because of failure in diagnosis and misdiagnosis because of its similarity with other pulmonary infections [212]. Person to person transmission of pulmonary infection has not been reported.
Coccidioidomycosis is usually asymptomatic in healthy patients. This occurs in about 60–65% of the patients. The primary infection is in the lungs. The disease can have an acute, chronic, or disseminated form. Acute pulmonary coccidioidomycosis is usually mild, with few or no symptoms, such as fever, sore throat, cough fatigue, etc. It has an incubation period of 7–21 days and is self-limiting in immunocompetent individuals [208].
Chronic pulmonary coccidioidomycosis can develop 20 or more years after initial infection and may present as lung abscess, empyema, bronchopleural fistula, or scarring (fibrosis). While extrapulmonary disseminated infections result of hematogenous spread and are common in, but not limited to, individuals with compromised immune status [213]. Immunosuppressive conditions, such as HIV infection, diabetes mellitus, or malignancy. It may develop weeks, months, or years after the primary infection. It may involve any body organ but has a predilection for dissemination to skin, soft tissue, joints, and the central nervous system. Cutaneous coccidioidomycosis may from puncture with a contaminated object [212,213].
Diagnostic workup for coccidioidomycosis requires detailed history and physical examination, followed by imaging studies with a chest X-ray finding of primary pulmonary disease, including variable nonspecific infiltrates, hilar adenopathy, and pleural effusions. Findings such as cavities and nodules demonstrate progression towards the complicated or residual stage of pulmonary coccidioidomycosis. Confirmation of coccidioidomycosis relies on isolation of fungus in culture, identification upon histopathology or serologic testing [214,215]. Pathological diagnosis requires the demonstration of endosporulating spherules or endospores.
Patients with coccidioidomycosis are usually asymptomatic and only require supportive care. Management of symptomatic patients is according to clinical syndrome [216,217]. The mainstay of antifungal treatment generally consists of amphotericin B deoxycholate or azoles. Amphotericin B is for the severe form of coccidioidomycosis, while azoles, e.g., Ketoconazole, Fluconazole, and Itraconazole, are for mild form of the disease. The duration of therapy is long and may take months to years in certain patients [217].
Only four cases of coccidioidomycosis were identified using histology in Africa. All four cases were caused by unidentified Coccidioides species. None of the cases had a correct clinical diagnosis [98]. Yoo and colleagues [212], described a case of a 23-year-old HIV seronegative Ugandan man with a 10-month history of haemoptysis and difficulty breathing, and a 6-month history of localized swellings on the extremities, associated weight loss, and drenching sweats. He reported no history of travel out of Uganda. Bronchoscopic examination showed two masses occluding the right main bronchus. Bronchoscopic biopsy showed findings consistent with coccidioidomycosis. The patient improved with antifungal treatment and was discharged [212], Table 10. Details of other cases were not found by these authors.

3.11. Paracoccidioidomycosis

Paracoccidioidomycosis is a systemic mycosis caused by thermally dimorphic fungi: Paracoccidioides brasiliensis and Paracoccidioides lutzii. It occurs in the subtropical humid areas of most of the countries in Latin America (Brazil, Argentina, Colombia, and Venezuela) and parts of Central America [218,219,220].
The lungs are the primary site of infection, this is transmitted by inhalation of conidia and mycelial fragments. Infection is usually asymptomatic, however, there are two forms of paracoccidioidomycosis: an acute/subacute form, this is also known as juvenile paracoccydioidomycosis and chronic form or adult paracoccidioidomycosis [221].
The acute or subacute clinical forms, representing 10% of the clinical cases, are prevalent in children and adolescents (younger than 16 years), affecting both sexes equally. Clinical features usually include lymphadenopathy, hepatosplenomegaly, fever, weight loss, malaise, and multiple skin lesions. Mucous membranes and respiratory symptoms are unusual [221].
The chronic form is prevalent in adults (older than 16 years), with a male to female ratio of 20:1, and this difference might be secondary to inhibition of mycelial-to-yeast conversion by oestrogens. They have: primary lung infection, cough, dyspnoea, fever, weight loss, sequelae of chronic pulmonary disease, fibrosis, bullae, and emphysematous changes. Other features include: mucous membrane involvement, oral lesions, cutaneous lesions, and cervical lymphadenopathy. The risk factors for paracoccidiodomycosis include agricultural work, malnutrition, smoking, and alcoholism [221].
Diagnosis of paracoccidioidomycosis is made by microscopy. Rounded, thick-walled yeast cells (typically 15–30 μm in diameter, and up to 60 μm in some cases) with multiple buds (ship wheel-like, pilot wheel-like, or Mickey Mouse ear-like cells) are diagnostic features. Most patients in endemic areas are diagnosed using non-invasive testing, such as serological testing. Immunodiffusion assays (IMMY, Norman, OK, USA) are the most widely used reference assay. This assay is inexpensive and has a high specificity (>95%) and sensitivity (around 80%) [221,222].
Itraconazole has largely been used for patients with (trimethoprim–sulfamethoxazole) has shown itraconazole to be formulation, maintenance treatment with an azole derivative or co-trimoxazole is required [223,224]. Itraconazole (200 mg daily for 9–12 months) is the therapy of choice for patients with mild-to-moderate forms of paracoccidioidomycosis, with co-trimoxazole (for 18–24 months) being the main therapeutic alternative to itraconazole. A short (2–4 weeks) induction therapy with amphotericin B is reserved for severe cases, or for patients who are immunocompromised. Induction therapy with amphotericin B should be followed by 200–400 mg of itraconazole. Surgical management includes relive of granuloma induced spinal cord compression to alleviate fibrotic sequelae [223,224].
A case of a 35-year-old Hausa female from Kano area presented with infiltrated and enormously enlarged and unevenly eroded lips with regional adenopathy. No visceral affection was found. Paracoccidioides brasiliensis was cultured and characteristic spherule budding cells were also found in sections taken from the lip and from a cervical lymph node. The patient responded to long acting Sulphormethoxine (Fanasil) [225].

3.12. Chromoblastomycosis

Chromoblastomycosis is a subcutaneous mycoses caused by several dematiaceous fungi and was classified together with mycetoma by the WHO as a neglected tropical disease. It is more prevalent in tropical and sub-tropical areas and often associated with poverty. The main etiological agents are Fonsecaea spp., Cladophialophora spp., and Phialophora spp. Chromoblastomycosis is also an implantation mycosis and transmitted via transcutaneous inoculation of spores of the fungi. The causative pathogens are common in the soil and vegetation. Activities that tamper with ecological niche of the fungi, including farming and gardening increases the risk of exposure to infection. Most patients affected by chromoblastomycosis dwell in rural settings. The clinical manifestation is appearance of cutaneous or subcutaneous lesions on the limbs, face, and neck.
Chromoblastomycosis has been reported from every continent, but majority of cases are from South and Central America, Asia, and Africa. In Africa, the present epidemiological data mainly comprise case reports and series. The hotspot on the African continent is Madagascar, where beyond large number of case studies, prospective, and surveillance studies have been undertaken, including recent studies [226,227,228]. In a recent survey evaluating the global burden of chromoblastomycosis from 1947 to 2018, Africa had the second largest number of reported cases after South America, recording 1875 cases from 22 countries [229]. Subsequently, over 80 more cases have been described in Madagascar, Ethiopia and Uganda [98,228,230]. Details on cases of chromoblastomycosis from Africa are summarized in Table 11.
Madagascar had the largest burden of chromoblastomycosis in Africa, followed by South Africa. The disease was noted to be rare in desert areas and the West African sub-region had the least number of cases. The causative pathogen varied depending on geographical location but F. pedrosoi predominates, followed by Cladophialophora spp. and Phialophora spp. However, new studies in Madagascar reported F. nubica as the predominate cause of chromoblastomycosis. Like other implantation mycoses, males were more affected than females. Laboratory diagnosis mostly involves traditional direct microscopy, histology, and/or culture. In a recent surveillance study in Madagascar, molecular and MALDI-TOF techniques were employed in confirming diagnosis in suspected cases [227]. The treatment of chromoblastomycosis was not completely documented and absent in most cases. However, treatment was observed to comprise a combination of antifungal therapy, surgical excision, and physical methods. The common antifungal used was itraconazole and occasionally fluconazole, ketoconazole, and potassium iodide. Follow-up information was rarely available. In a current study with substantial treatment and follow-up data in Madagascar, patients were treated with for 4–26 months depending on disease severity and although complete cure or healing was not achieved there was either a major or minor clinical improvement.

3.13. Sporotrichosis

Sporotrichosis is a sub-acute to chronic infection caused by the thermal dimorphic fungi of the genera Sporothrix. It is more common in tropical and sub-tropical areas. It is usually transmitted through traumatic implantation facilitating the entry of spores into a host and known as an implantation mycosis. The clinical manifestation is broadly classified into skin, mucosal, systemic, and immunoreactive forms [231]. Cutaneous/subcutaneous and lymph node lesions are the commonest manifestations and was observed in disseminated cases. Sporotrichosis is rarely life threatening but may be associated with significant morbidity and reduced quality of life. The ecological niche of the fungus in the environment is mostly in soil and decaying vegetation. Infection is generally initiated during activities such as farming, gardening, animal husbandry, and mining activities [232,233,234]. Zoonotic transmission is common. Sporotrichosis was recently adopted as one of the deep mycoses listed as a neglected tropical disease. The ecology and epidemiology of sporotrichosis vary across different geographical regions or continent. In Africa, the epidemiology of sporotrichosis is not extensively studied except in few countries, such as South Africa and Madagascar [226,234,235]. In South Africa, undocumented cases are estimated to be over 3300, and have been associated with outbreaks among workers in mining settings during the 20th century [236]. In other African countries, there have been sporadic cases reports or series. Details of cases of sporotrichosis in Africa are shown in Table 12. Experts suggest many cases are misdiagnosed and many other cases are undocumented or unpublished. Emerging concerns presently are the effect of climate change on the dynamics of deep fungal infections, such as sporotrichosis [237].
Table 12. Published cases of sporotrichosis in Africa.
Table 12. Published cases of sporotrichosis in Africa.
YearCountryManifestationsNo. of Case(s)AetiologyDiagnostic ToolTreatmentOutcomesAuthors
2015South AfricaCutaneous17Sporothrix schenckiiCulture, Histopathology--Govender et al. [234]
1927South AfricaAbscess, Ulcer14Sporothrix beurmanniCulture--Pijper et al. [238]
1963South Africa 5Sporothrix schenckii---Lurie et al. [236]
1965EgyptSuperficial, Lymphocutaneous, Disseminated 7Sporothrix schenckiiCulturePotassium iodide, saline, Lugol’s iodineFavourable (n = 6), Death (n = 1)El-mofty et al. [239]
1969South AfricaDisseminated 1Sporothrix schenckiiCulture--Brandt et al. [240]
1977MalawiPulmonary1Sporothrix schenckiiHistopathology, Culture--Berson et al. [241]
1978SudanLymphocutaneous2Sporothrix schenckiiHistopathologyPotassium iodideFavourableGumaa et al. [242]
1978Zimbabwe-3----Ross et al. [243]
1992South AfricaCutaneous, Lymphocutaneous5Sporothrix schenckiiCultureTerbinafineFavourableHull et al. [244]
2002TanzaniaLymphocutaneous1-HistopathologyPotassium iodideFavourablePonnighaus et al. [245]
2008MoroccoLymphocutaneous1----Benchekroun et al. [246]
2020Uganda-1Sporothrix spp. Histopathology--Kwizeraet al [98]
2016MadagascarCutaneous, Lymphocutaneous34Sporothrix schenckiiHistopathology, Microscopy, Culture, PCR--Rasamoelina et al. [226]
2016ZambiaDisseminated, Cutaneous1-HistopathologyItraconazoleFavourablePatel et al. [247]
2019MadagascarCutaneous63Sporothrix schenckiiCulture, Molecular testing--Rasamoelina et al. [235]
1981NigeriaLympho-cutaneous2Sporothrix schenckiiCulture--Jacyk et al. [248]
2021South AfricaCutaneous, Dissemination1Sporothrix schenckiiCulture, Histopathology, MALDI-TOFFluconazole, ItraconazoleFavourableTshisevhe et al. [249]
Sporotrichosis in Africa was largely predominant in South Africa and Madagascar. It affects all age groups but was mostly reported among young adults. Males were the most affected, probably due to occupational and environmental risks of exposure which may be mainly associated with males. The common manifestation recorded was lymphocutaneous lesions that are nodular and frequently ulcerating that mostly affected limbs and faces. Other unusual manifestations do occur, including appearance of muscular, osteoarticular, and visceral lesions [235]. Systemic cases are rarely reported. Sporotrichosis generally occurred in immunocompetent patients, but few cases in immunocompromised patients, such as one in an HIV patient was reported in South Africa [249]. Diagnosis was broadly made by culture and/or histology, and occasionally by direct examination of clinical specimen. The common isolated fungi were Sporothrix schenckii, now identified collectively as S. schenckii sensu stricto with other closely related variants. In the recent case report from South Africa, MALDI-TOF was employed to confirm culture reports [249]. Potassium iodide was the common treatment option prior to the 20th century. In the past few decades, itraconazole has been the frequently used drug for treatment, but fluconazole or terbinafine is occasionally used when the latter is not available. Outcomes are mostly non-fatal.

4. Limitations

Our review focused on commonly encountered IFDs in Africa. Other fungal diseases, including dermatophytosis, pityriasis, tinea nigra, piedra, and mycetoma, were not discussed in this review.

5. Conclusions and Future Perspective

In this critical literature review, we exclusively describe the epidemiology of IFDs in Africa, with particular emphasis on the most described IFDs. Cryptococcosis is the most common IFD in Africa, contributing significantly to HIV-related deaths, especially in the high-burden sub-Saharan Africa. Though mostly undiagnosed, invasive aspergillosis is increasingly being reported, mostly in the setting of pulmonary tuberculosis, with a similar predilection towards people living with HIV. Similarly, histoplasmosis previously considered to be non-endemic in Africa, is increasingly being reported, particularly in PLWH. The burden of PCP has significantly reduced owing to increased uptake of anti-retroviral therapy among people living with HIV both in Africa, and globally. Other rare IFDs, such as mucormycosis, talaromycosis, emergomycosis, blastomycosis, and coccidiomycosis have also been described. It is significant to note that there is emerging resistance to most of the available antifungal drugs that are available in Africa.
Our review continues to affirm that IFDs are much more common than expected and contribute to significant mortality and morbidity in Africa. A lot of investments have been made on cryptococcal meningitis, a leading cause of mortality in people living with HIV/AIDS in Africa, yet other invasive fungal diseases, such as invasive aspergillosis and histoplasmosis, are still neglected. We recommend a considerable investment into clinical research, diagnostics, and management of these fungal diseases, that cause significant morbidity and mortality. Important areas of research include diagnosis and therapeutics, tailored to the low- and middle-income nature of most African countries.

Author Contributions

Authors’ contribution F.B. and B.E.E. were involved in the conception, design of the study and initial draft. F.B, B.E.E., W.K., L.N., R.O., A.I.-E., M.P.N.K., F.P.P., A.A.D., M.M., B.O., R.K., and J.B.B.: literature review, writing of manuscript and review. All authors have read and agreed to the published version of the manuscript.


This manuscript received no external funding.

Institutional Review Board Statement

Not applicable

Informed Consent Statement

Not applicable.

Data Availability Statement

All underlying data have been included in the main text of the manuscript.

Conflicts of Interest

All authors declare that they have no competing interests.


  1. Kamwiziku, G.K.; Makangara, J.C.C.; Orefuwa, E.; Denning, D.W. Serious fungal diseases in Democratic Republic of Congo—Incidence and prevalence estimates. Mycoses 2021, 64, 1159–1169. [Google Scholar] [CrossRef] [PubMed]
  2. Vallabhaneni, S.; Walker, T. The Global Burden of Fungal Diseases. Infect. Dis. 2016, 30, 30329. [Google Scholar] [CrossRef] [PubMed]
  3. Firacative, C. Invasive fungal disease in humans: Are we aware of the real impact? Mem. Inst. Oswaldo Cruz 2020, 115, e200430. [Google Scholar] [CrossRef]
  4. Ascioglu, S.; Rex, J.H.; De Pauw, B.; Bennett, J.E.; Bille, J.; Crokaert, F.; Denning, D.W.; Donnelly, J.P.; Edwards, J.E.; Erjavec, Z.; et al. Defining opportunistic invasive fungal infections in immunocompromised patients with cancer and hematopoietic stem cell transplants: An international consensus. Clin. Infect. Dis. 2003, 34, 7–14. [Google Scholar] [CrossRef] [PubMed]
  5. Bongomin, F.; Kibone, W.; Okot, J.; Nsenga, L.; Olum, R.; Baluku, J.B. Fungal diseases in Africa: Epidemiologic, diagnostic and therapeutic advances. Ther. Adv. Infect. Dis. 2022, 9, 20499361221081440. [Google Scholar] [CrossRef]
  6. Chekiri-Talbi, M.; Denning, D.W. Burden of fungal infections in Algeria. Eur. J. Clin. Microbiol. Infect. Dis. Off. Publ. Eur. Soc. Clin. Microbiol. 2017, 36, 999–1004. [Google Scholar] [CrossRef]
  7. Odukoya-Maijeh, O.O.; Ekeng, B.E.; Oladele, R.O. Fatal Disseminated histoplasmosis in a Nigerian woman: A Case report. Microbes Infect. Dis. 2022, in press. [Google Scholar]
  8. Gullo, A. Invasive Fungal Infections. Drugs 2009, 69, 65–73. [Google Scholar] [CrossRef]
  9. Balogun, T.M.; Okokon, M.; Dasola, F.; Oyetubosun, E.J.; Abimbola, A.; Bonaventure, B. Cryptococcal antigenaemia among treatment-naïve Adult HIV-infected Nigerian patients. World J. AIDS 2016, 6, 1. [Google Scholar] [CrossRef] [Green Version]
  10. Okolo, M.O.; Onyedibe, K.I.; Dabe, F.; Obishakin, E.F.; Envuladu, E.A.; Egah, D.Z. Cryptococcal Meningitis amomg HIV-Infected and HIV-Uninfected Patients in Jos, North Central Nigeria. J. Biomed. Res. Clin. Pract. 2021, 4, 1–7. [Google Scholar] [CrossRef]
  11. Lakoh, S.; Rickman, H.; Sesay, M.; Kenneh, S.; Burke, R.; Baldeh, M.; Jiba, D.F.; Tejan, Y.S.; Boyle, S.; Koroma, C.; et al. Prevalence and mortality of cryptococcal disease in adults with advanced HIV in an urban tertiary hospital in Sierra Leone: A prospective study. BMC Infect. Dis. 2020, 20, 141. [Google Scholar] [CrossRef]
  12. Ocansey, B.K.; Otoo, B.; Asamoah, I.; Ganu, V.; Berko, K.P.; Oladele, O.; Amankwa, E.A.; Opoku-Asare, B.; Agyei, M.; George, L.; et al. Cryptococcal and Histoplasma Antigen Screening Among People with Human Immunodeficiency Virus in Ghana and Comparative Analysis of OIDx Histoplasma Lateral Flow Assay and IMMY Histoplasma Enzyme Immunoassay. Open Forum Infect. Dis. 2022, 9, ofac277. [Google Scholar] [CrossRef]
  13. Minta, D.K.; Dolo, A.; Dembele, M.; Kaya, A.S.; Sidibe, A.T.; Coulibaly, I.; Maiga, I.I.; Diallo, M.; Traore, A.M.; Maiga, M.Y.; et al. Neuromeningeal cryptococcosis in Mali. Med. Trop. 2011, 71, 591–595. [Google Scholar]
  14. Oladele, R.O.; Akanmu, A.S.; Nwosu, A.O.; Ogunsola, F.T.; Richardson, M.D.; Denning, D.W. Cryptococcal Antigenemia in Nigerian Patients with Advanced Human Immunodeficiency Virus: Influence of Antiretroviral Therapy Adherence. Open Forum Infect. Dis. 2016, 3, ofw055. [Google Scholar] [CrossRef] [Green Version]
  15. Millogo, A.; Ki-Zerbo, G.A.; Andonaba, J.B.; Lankoandé, D.; Sawadogo, A.; Yaméogo, I.; Sawadogo, A.B. La cryptococcose neuroméningée au cours de l’infection par le VIH au centre hospitalier de Bobo Dioulasso (Burkina Faso). Bull. Soc. Pathol. Exot. 2004, 97, 119–121. [Google Scholar]
  16. Bamba, S.; Barro-Traoré, F.; Sawadogo, E.; Millogo, A.; Guiguemdé, R.T. Retrospective study of cases of neuromeningeal cryptococcosis at the University Hospital of Bobo Dioulasso since accessibility to antiretroviral in Burkina Faso. J. Mycol. Med. 2012, 22, 30–34. [Google Scholar] [CrossRef]
  17. Wajanga, B.M.; Kalluvya, S.; Downs, J.A.; Johnson, W.D.; Fitzgerald, D.W.; Peck, R.N. Universal screening of Tanzanian HIV-infected adult inpatients with the serum cryptococcal antigen to improve diagnosis and reduce mortality: An operational study. J. Int. AIDS Soc. 2011, 14, 48. [Google Scholar] [CrossRef] [Green Version]
  18. Mdodo, R.; Brown, K.; Omonge, E.; Jaoko, W.; Baddley, J.; Pappas, P.; Kempf, M.C.; Aban, I.; Odera, S.; Suleh, A.; et al. The prevalence, clinical features, risk factors and outcome associated with cryptococcal meningitis in HIV positive patients in Kenya. East Afr. Med. J. 2010, 87, 481–487. [Google Scholar]
  19. Manga, N.M.; Cisse-Diallo, V.M.P.; Dia-Badiane, N.M.; Diop-Nyafouna, S.A.; Yengo, D.E.; Ndour, C.T. Prevalence and factors associated with positive cryptococcal antigenemia among HIV infected adult hospitalized in Senegal. J. HIV Retrovir. 2016, 2. [Google Scholar] [CrossRef] [Green Version]
  20. Derbie, A.; Mekonnen, D.; Woldeamanuel, Y.; Abebe, T. Cryptococcal antigenemia and its predictors among HIV infected patients in resource limited settings: A systematic review. BMC Infect. Dis. 2020, 20, 407. [Google Scholar] [CrossRef]
  21. Assogba, K.; Belo, M.; Wateba, M.I.; Gnonlonfoun, D.D.; Ossou-Inguiet, P.M.; Tsanga, B.B.; Ndiaye, M.; Grunitzky, E.K. Neuromeningeal cryptococcosis in sub-Saharan Africa: Killer disease with sparse data. J. Neurosci. Rural Pract. 2015, 6, 221–224. [Google Scholar] [CrossRef] [PubMed]
  22. Oyella, J.; Meya, D.; Bajunirwe, F.; Kamya, M.R. Prevalence and factors associated with cryptococcal antigenemia among severely immunosuppressed HIV-infected adults in Uganda: A cross-sectional study. J. Int. AIDS Soc. 2012, 15, 15. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  23. Mohammed, Y.; Olayinka, A.T.; Giwa, F.J.; Abubakar, A.A. Prevalence and factors associated with cryptococcosis among human immunodeficiency virus-infected patients of a tertiary hospital in Northwestern Nigeria. Ann. Trop. Pathol. 2019, 10, 52. [Google Scholar] [CrossRef]
  24. Goni, B.; Kida, I.; Saidu, I.; Yusuph, H.; Brown, M.; Bakki, B. Cryptococcal neorformans Antigenemia among HIV-Infected Patients in North Eastern Nigeria. J. Transm. Dis. Immun. 2017, 1, 1–8. [Google Scholar]
  25. Egbe, C.A.; Omoregie, R.; Alex-Ighodalo, O. Cryptococcus neoformans infection among human immunodeficiency virus patients on highly active antiretroviral therapy in Benin City, Nigeria. N. Z. J. Med. Lab. Sci. 2015, 69, 21. Available online: = anon~757af4d&sid = googleScholar&xid = 40145fe4 (accessed on 19 October 2022).
  26. Okwir, M.; Link, A.; Rhein, J.; Obbo, J.S.; Okello, J.; Nabongo, B.; Alal, J.; Meya, D.; Bohjanen, P.R. High Burden of Cryptococcal Meningitis Among Antiretroviral Therapy-Experienced Human Immunodeficiency Virus-Infected Patients in Northern Uganda in the Era of “Test and Treat”: Implications for Cryptococcal Screening Programs. Open Forum Infect. Dis. 2022, 9, ofac004. [Google Scholar] [CrossRef]
  27. Park, B.J.; Wannemuehler, K.A.; Marston, B.J.; Govender, N.; Pappas, P.G.; Chiller, T.M. Estimation of the current global burden of cryptococcal meningitis among persons living with HIV/AIDS. AIDS 2009, 23, 525–530. [Google Scholar] [CrossRef]
  28. Rajasingham, R.; Smith, R.M.; Park, B.J.; Jarvis, J.N.; Govender, N.P.; Chiller, T.M.; Denning, D.W.; Loyse, A.; Boulware, D.R. Global burden of disease of HIV-associated cryptococcal meningitis: An updated analysis. Lancet Infect. Dis. 2017, 17, 873–881. [Google Scholar] [CrossRef] [Green Version]
  29. Alemayehu, T.; Ayalew, S.; Buzayehu, T.; Daka, D. Magnitude of Cryptococcosis among HIV patients in sub-Saharan Africa countries: A systematic review and meta-analysis. Afr. Health Sci. 2020, 20, 114–121. [Google Scholar] [CrossRef]
  30. Rajasingham, R.; Govender, N.P.; Jordan, A.; Loyse, A.; Shroufi, A.; Denning, D.W.; Meya, D.B.; Chiller, T.M.; Boulware, D.R. The global burden of HIV-associated cryptococcal infection in adults in 2020: A modelling analysis. Lancet Infect. Dis. 2022, in press. [Google Scholar] [CrossRef]
  31. Badiane, A.S.; Ndiaye, D.; Denning, D.W. Burden of fungal infections in Senegal. Mycoses 2015, 58 (Suppl. S5), 63–69. [Google Scholar] [CrossRef]
  32. Zaki, S.M.; Denning, D.W. Serious fungal infections in Egypt. Eur. J. Clin. Microbiol. Infect. Dis. Off. Publ. Eur. Soc. Clin. Microbiol. 2017, 36, 971–974. [Google Scholar] [CrossRef]
  33. Mandengue, C.E.; Denning, D.W. The Burden of Serious Fungal Infections in Cameroon. J. Fungi 2018, 4, 44. [Google Scholar] [CrossRef] [Green Version]
  34. Parkes-Ratanshi, R.; Achan, B.; Kwizera, R.; Kambugu, A.; Meya, D.; Denning, D.W. Cryptococcal disease and the burden of other fungal diseases in Uganda; Where are the knowledge gaps and how can we fill them? Mycoses 2015, 58 (Suppl. S5), 85–93. [Google Scholar] [CrossRef]
  35. Pfavayi, L.T.; Denning, D.W.; Baker, S.; Sibanda, E.N.; Mutapi, F. Determining the burden of fungal infections in Zimbabwe. Sci. Rep. 2021, 11, 13240. [Google Scholar] [CrossRef]
  36. Oladele, R.O.; Denning, D.W. Burden of serious fungal infection in Nigeria. West Afr. J. Med. 2014, 33, 107–114. [Google Scholar]
  37. Schwartz, I.S.; Boyles, T.H.; Kenyon, C.R.; Hoving, J.C.; Brown, G.D.; Denning, D.W. The estimated burden of fungal disease in South Africa. SAMJ South Afr. Med. J. 2019, 109, 885–892. [Google Scholar] [CrossRef]
  38. Koffi, D.; Bonouman, I.; Toure, A.; Kouadjo, F.; N’Gou, M.; Sylla, K.; Dosso, M.; Denning, D. Estimates of serious fungal infection burden in Côte d’Ivoire and country health profile. J. Med. Mycol. 2021, 31, 101086. [Google Scholar] [CrossRef]
  39. Bamba, S.; Zida, A.; Sangaré, I.; Cissé, M.; Denning, D.W.; Hennequin, C. Burden of Severe Fungal Infections in Burkina Faso. J. Fungi 2018, 4, 35. [Google Scholar] [CrossRef]
  40. Tufa, T.B.; Denning, D.W. The Burden of Fungal Infections in Ethiopia. J. Fungi 2019, 5, 109. [Google Scholar] [CrossRef] [Green Version]
  41. Dorkenoo, A.M.; Adjetey-Toglozombio, A.K.; Ocansey, B.K.; Sossou, E.; Lack, F.; Denning, D.W. Estimated burden of serious fungal infections in Togo. Mycoses 2021, 64, 1535–1541. [Google Scholar] [CrossRef] [PubMed]
  42. Dunaiski, C.M.; Denning, D.W. Estimated Burden of Fungal Infections in Namibia. J. Fungi 2019, 5, 75. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  43. Sacarlal, J.; Denning, D.W. Estimated Burden of Serious Fungal Infections in Mozambique. J. Fungi 2018, 4, 75. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  44. Guto, J.A.; Bii, C.C.; Denning, D.W. Estimated burden of fungal infections in Kenya. J. Infect. Dev. Ctries. 2016, 10, 777–784. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  45. Ocansey, B.K.; Pesewu, G.A.; Codjoe, F.S.; Osei-Djarbeng, S.; Feglo, P.K.; Denning, D.W. Estimated Burden of Serious Fungal Infections in Ghana. J. Fungi 2019, 5, 38. [Google Scholar] [CrossRef] [Green Version]
  46. Lmimouni, B.E.; Hennequin, C.; Penney, R.O.S.; Denning, D.W. Estimated Incidence and Prevalence of Serious Fungal Infections in Morocco. J. Fungi 2022, 8, 414. [Google Scholar] [CrossRef]
  47. Ezeanolue, E.E.; Nwizu, C.; Greene, G.S.; Amusu, O.; Chukwuka, C.; Ndembi, N.; Smith, R.M.; Chiller, T.; Pharr, J.; Kozel, T.R. Geographical Variation in Prevalence of Cryptococcal Antigenemia among HIV-infected Treatment-Naïve Patients in Nigeria: A multicenter cross-sectional study. J. Acquir. Immune Defic. Syndr. 2016, 73, 117. [Google Scholar] [CrossRef]
  48. Chukwuanukwu, R.C.; Uchenna, N.; Mbagwu, S.I.; Chukwuanukwu, T.O.; Charles, O. Cryptococcus neoformans seropositivity and some haematological parameters in HIV seropositive subjects. J. Infect. Public Health 2020, 13, 1042–1046. [Google Scholar] [CrossRef]
  49. Osazuwa, F.; Dirisu, J.O.; Okuonghae, P.E.; Ugbebor, O. Screening for cryptococcal antigenemia in anti-retroviral naïve AIDS patients in benin city, Nigeria. Oman Med. J. 2012, 27, 228–231. [Google Scholar] [CrossRef]
  50. Ezenabike, C.; Ashaka, O.S.; Omoare, A.A.; Fadeyi, A.; Salami, A.K.; Agbede, O.O. Cryptococcal antigen among HIV1-infected individuals in north-central Nigeria. Curr. Med. Mycol. 2020, 6, 43–48. [Google Scholar] [CrossRef]
  51. Odegbemi, O.; Dada-Adegbola, H.; Adeoye, I.; Fayemiwo, S.A. Epidemiology of Cryptococcal antigenemia among HIV infected patients in South-western Nigeria. Int. J. Infect. Dis. 2020, 101, 387. [Google Scholar] [CrossRef]
  52. Gomerep, S.S.; Idoko, J.A.; Ladep, N.G.; Ugoya, S.O.; Obaseki, D.; Agbaji, O.A.; Agaba, P.; Akanbi, M.; Badung, B.P.; Otitoloju, O. Frequency of cryptococcal meningitis in HIV-1 infected patients in north central Nigeria. Niger. J. Med. 2010, 19, 395–399. [Google Scholar] [CrossRef]
  53. Andama, A.O.; Boon, S.D.; Meya, D.; Cattamanchi, A.; Worodria, W.; Davis, J.L.; Walter, N.D.; Yoo, S.D.; Kalema, N.; Haller, B.; et al. Prevalence and outcomes of cryptococcal antigenemia in HIV-seropositive patients hospitalized for suspected tuberculosis in Uganda. J. Acquir. Immune Defic. Syndr. 2013, 63, 189–194. [Google Scholar] [CrossRef] [Green Version]
  54. Greene, G.; Desanto, D.; Matlapeng, P.; Govender, N. Cryptococcal Antigen Screening Surveillance Report, South Africa, February 2017–July 2019; NICD Public Health Surveillance Bulletin: Johannesburg, South Africa, 2019. [Google Scholar]
  55. Temfack, E.; Kouanfack, C.; Mossiang, L.; Loyse, A.; Fonkoua, M.C.; Molloy, S.; Koulla-Shiro, S.; Delaporte, E.; Dromer, F.; Harrison, T.; et al. Cryptococcal antigen screening in asymptomatic HIV-infected antiretroviral naive patients in Cameroon and evaluation of the new semi-quantitative Biosynex CryptoPS test. Front. Microbiol. 2018, 9, 409. [Google Scholar] [CrossRef]
  56. Negash, M.; Wondmagegn, T.; Tajebe, F. Opportunistic Cryptococcal Antigenemia in the HAART Era at HIV Epidemic Settings of Northwest Ethiopia. Can. J. Infect. Dis. Med. Microbiol. 2020, 2020, 5017120. [Google Scholar] [CrossRef]
  57. Jemal, M.; Deress, T.; Belachew, T.; Adem, Y. Prevalence of Cryptococcal Antigenemia and Associated Factors among HIV/AIDS Patients at Felege-Hiwot Referral Hospital, Bahir Dar, Northwest Ethiopia. Int. J. Microbiol. 2021, 2021, 8839238. [Google Scholar] [CrossRef]
  58. Geda, N.; Beyene, T.; Dabsu, R.; Mengist, H.M. Prevalence of Cryptococcal Antigenemia and associated factors among HIV/AIDS patients on second-line antiretroviral therapy at two hospitals in Western Oromia, Ethiopia. PLoS ONE 2019, 14, e0225691. [Google Scholar] [CrossRef]
  59. Hailu, K.; Niguse, S.; Hagos, K.; Abdulkader, M. Cryptococcal antigenemia and associated risk factors among ART-naïve and ART-experienced HIV-infected peoples at selected health institutions of Mekelle, Northern Ethiopia. Microbiologyopen 2019, 8, e00746. [Google Scholar] [CrossRef] [Green Version]
  60. Sow, D.; Tine, R.C.; Sylla, K.; Djiba, M.; Ndour, C.T.; Dieng, T.; Ndiaye, J.L.; Faye, B.; Ndiaye, D.; Gaye, O.; et al. Cryptococcal meningitis in Senegal: Epidemiology, laboratory findings, therapeutic and outcome of cases diagnosed from 2004 to 2011. Mycopathologia 2013, 176, 443–449. [Google Scholar] [CrossRef]
  61. Wateba, I.M.; Balaka, A.; Bawe, A.L.; Kotosso, A. Cryptococcal meningitis of the HIV-infected Person in Lomé: About 102 cases over 10 years. World J. AIDS 2017, 7, 217. [Google Scholar] [CrossRef] [Green Version]
  62. Deiss, R.; Loreti, C.V.; Gutierrez, A.G.; Filipe, E.; Tatia, M.; Issufo, S.; Ciglenecki, I.; Loarec, A.; Vivaldo, H.; Barra, C.; et al. High burden of cryptococcal antigenemia and meningitis among patients presenting at an emergency department in Maputo, Mozambique. PLoS ONE 2021, 16, e0250195. [Google Scholar] [CrossRef] [PubMed]
  63. Katabwa, J.K.; Mukuku, O.; Lwamba, G.K.; Wembonyama, S.O. Neuromeningeal cryptococcosis in HIV-infected patients in Lubumbashi, Democratic Republic of the Congo. J. Neurol Stroke. 2021, 11, 73–77. [Google Scholar] [CrossRef]
  64. Govender, N.P.; Roy, M.; Mendes, J.F.; Zulu, T.G.; Chiller, T.M.; Karstaedt, A.S. Evaluation of screening and treatment of cryptococcal antigenaemia among HIV-infected persons in Soweto, South Africa. HIV Med. 2015, 16, 468–476. [Google Scholar] [CrossRef] [PubMed]
  65. Luma, H.N.; Temfack, E.; Halle, M.P.; Tchaleu, B.C.N.; Mapoure, Y.N.; Koulla-Shiro, S. Cryptococcal meningoencephalitis in human immunodeficiency virus/acquired immunodeficiency syndrome in douala, cameroon: A cross sectional study. N. Am. J. Med. Sci. 2013, 5, 486–491. [Google Scholar] [PubMed] [Green Version]
  66. Ngouana, T.K.; Dongtsa, J.; Kouanfack, C.; Tonfack, C.; Fomena, S.; Mallié, M.; Delaporte, E.; Boyom, F.F.; Bertout, S. Cryptoccocal meningitis in Yaoundé (Cameroon) HIV infected patients: Diagnosis, frequency and Cryptococcus neoformans isolates susceptibility study to fluconazole. J. Mycol. Med. 2015, 25, 11–16. [Google Scholar] [CrossRef] [PubMed]
  67. Kalla, G.C.M.; Mboumnyemb, J.F.; Assob, J.C.N.; Mandeng, M.N.E.; Noubi, N.K.; Assoumou, M.C.O.; Mbopi-Keou, F.-X.; Monebenimp, F. Cryptococcal antigen carriage among HIV infected children aged 6 months to 15 years at Laquintinie Hospital in Douala. PLoS ONE 2021, 16, e0253781. [Google Scholar] [CrossRef]
  68. Dzoyem, J.P.; Kechia, F.A.; Ngaba, G.P.; Lunga, P.K.; Lohoue, P.J. Prevalence of cryptococcosis among HIV-infected patients in Yaounde, Cameroon. Afr. Health Sci. 2012, 12, 129–133. [Google Scholar] [CrossRef]
  69. Nguefack, S.; Taguebue, J.; Wandji, Y.; Kago, D.; Bate, B.; Chelo, D.; Ndombo, P.O.K. Neuromeningeal Cryptococcosis in children: Clinical and prognostic aspects in a Pediatric hospital in Yaoundé-Cameroon. Pediatr. Oncall J. 2020, 17, 77–81. [Google Scholar] [CrossRef]
  70. Mullan, P.C.; Steenhoff, A.P.; Draper, H.; Wedin, T.; Bafana, M.; Anabwani, G.; Jibril, H.; Tshepo, M.; Schutze, G.E. Etiology of meningitis among patients admitted to a tertiary referral hospital in Botswana. Pediatr. Infect. Dis. J. 2011, 30, 620–622. [Google Scholar] [CrossRef]
  71. Tenforde, M.W.; Mokomane, M.; Leeme, T.; Tlhako, N.; Tsholo, K.; Ramodimoosi, C.; Dube, B.; Mokobela, K.O.; Tawanana, E.; Chebani, T.; et al. Epidemiology of adult meningitis during antiretroviral therapy scale-up in southern Africa: Results from the Botswana national meningitis survey. J. Infect. 2019, 79, 212–219. [Google Scholar] [CrossRef] [Green Version]
  72. Zono, B.; Kamangu, E.; Situakibanza, H.; Amaela, E.; Bepouka, B.; Mbula, M.; Kayembe, J.M.; Mvumbi, G.; Hayette, M.P. Epidemiological, clinical and biological profile of neuromeningeal cryptococcosis among people living with HIV in Kinshasa, Democratic Republic of Congo. Pan Afr. Med. J. 2020, 37, 302. [Google Scholar] [CrossRef]
  73. Owusu, M.; Nguah, S.B.; Boaitey, Y.A.; Badu-Boateng, E.; Abubakr, A.-R.; Lartey, R.A.; Adu-Sarkodie, Y. Aetiological agents of cerebrospinal meningitis: A retrospective study from a teaching hospital in Ghana. Ann. Clin. Microbiol. Antimicrob. 2012, 11, 28. [Google Scholar] [CrossRef] [Green Version]
  74. Otedo, A.E.O.; Otieno, C.F.; Jowi, J.; Oyoo, G.O.; Omonge, E.O. Cryptococcus Meningitis in a Cohort of HIV Positive Kenyan Patients: Outcome after Two Weeks of Therapy. East Afr. Med. J. 2013, 90, S33–S39. [Google Scholar]
  75. Ngoy, D.K.; Kange, D.M.; Kakwaba, S.K.; Mutombo, C.T.; Takulilwe, A.K.; Nsambi, V.M.; Ilunga, W.K.J.-M.; Ilunga, Y.I.; Masangu, M.S.; Mbuyu, G.K.K.H.; et al. Mortalité liée à la Cryptococcose chez les Personnes Vivant avec l ’infection à VIH/SIDA à Lubumbashi. Rev. L’infirmier Congo. 2021, 5, 56–62. [Google Scholar]
  76. Oumar, A.A.; Dao, S.; Ba, M.; Poudiougou, B.; Diallo, A. Aspects épidémiologique, clinique et pronostique de la cryptococcose neuroméningée en milieu hospitalier de Bamako, Mali. Rev. Med. Brux. 2008, 29, 149. [Google Scholar]
  77. Ellabib, M.S.; Krema, Z.A.; Allafi, A.A.; Cogliati, M. First report of two cases of cryptococcosis in Tripoli, Libya, infected with Cryptococcus neoformans isolates present in the urban area. J. Mycol. Med. 2017, 27, 421–424. [Google Scholar] [CrossRef]
  78. Mamoojee, Y.; Shakoor, S.; Gorton, R.L.; Sarfo, S.; Appiah, L.T.; Norman, B.; Balakrishnan, I.; Phillips, R.; Chadwick, D. Short Communication: Low seroprevalence of cryptococcal antigenaemia in patients with advanced HIV infection enrolling in an antiretroviral programme in Ghana. Trop. Med. Int. Health 2011, 16, 53–56. [Google Scholar] [CrossRef]
  79. Oladele, R.O.; Ayanlowo, O.O.; Richardson, M.D.; Denning, D.W. Histoplasmosis in Africa: An emerging or a neglected disease? PLoS Negl. Trop. Dis. 2018, 12, e0006046. [Google Scholar] [CrossRef]
  80. Ekeng, B.E.; Oladele, R.O.; Emanghe, U.E.; Ochang, E.A.; Mirabeau, T.Y. Prevalence of Histoplasmosis and Molecular Characterization of Histoplasma species in Patients with Presumptive Pulmonary Tuberculosis in Calabar, Nigeria. Open Forum Infect. Dis. 2022, 9, ofac368. [Google Scholar] [CrossRef]
  81. Kuate, M.P.N.; Nyasa, R.; Mandengue, C.; Tendongfor, N.; Bongomin, F.; Denning, D.W. Screening for acute disseminated histoplasmosis in HIV disease using urinary antigen detection enzyme immunoassay: A pilot study in Cameroon. J. Microbiol. Methods 2021, 185, 106226. [Google Scholar] [CrossRef]
  82. Oladele, R.O.; Osaigbovo, I.I.; Akanmu, A.S.; Adekanmbi, O.A.; Ekeng, B.E.; Mohammed, Y.; Alex-Wele, M.A.; Okolo, M.O.; Ayanbeku, S.T.; Unigwe, U.S.; et al. Ascertaining the current prevalence of Histoplasmosis in Nigeria’s Advanced HIV disease population. EID 2022, 28, 2261–2269. [Google Scholar]
  83. Ekeng, B.E.; Edem, K.; Amamilo, I.; Panos, Z.; Denning, D.; Oladele, R.O. Histoplasmosis in Children; HIV/AIDS Not a Major Driver. J. Fungi 2021, 7, 530. [Google Scholar] [CrossRef] [PubMed]
  84. MacInnes, R.; Warris, A. Paediatric Histoplasmosis 2000–2019: A Review of 83 Cases. J. Fungi 2021, 7, 448. [Google Scholar] [CrossRef] [PubMed]
  85. Mandengue, C.E.; Ekeng, B.E.; Oladele, R.O. Disseminated histoplasmosis; a threat in advanced HIV disease population in sub-Saharan Africa. J. Adv. Med. Med. Res. 2021, 33, 115–144. [Google Scholar] [CrossRef]
  86. Ekeng, B.E.; Edem, K.; Akintan, P.; Oladele, R.O. Histoplasmosis in African children: Clinical features, diagnosis and treatment. Ther. Adv. Infect. Dis. 2022, 9, 20499361211068590. [Google Scholar] [CrossRef]
  87. Ekeng, B.E.; Davies, A.A.; Osaigbovo, I.I.; Warris, A.; Oladele, R.O.; Denning, D.W. Pulmonary and Extrapulmonary Manifestations of Fungal Infections Misdiagnosed as Tuberculosis: The Need for Prompt Diagnosis and Management. J. Fungi 2022, 8, 460. [Google Scholar] [CrossRef]
  88. Osaigbovo, I.I.; Oladele, R.O.; Orefuwa, E.; Akanbi, O.A.; Ihekweazu, C. Laboratory Diagnostic Capacity for Fungal Infections in Nigerian Tertiary Hospitals: A Gap Analysis Survey. West Afr. J. Med. 2021, 38, 1065–1071. [Google Scholar] [CrossRef]
  89. Driemeyer, C.; Falci, D.R.; Oladele, R.O.; Bongomin, F.; Ocansey, B.K.; Govender, N.P.; Hoenigl, M.; Gangneux, J.P.; Lass-Flörl, C.; Cornely, O.A.; et al. The current state of clinical mycology in Africa: A European Confederation of Medical Mycology and International Society for Human and Animal Mycology survey. Lancet Microbe. 2022, 3, e464–e470. [Google Scholar] [CrossRef]
  90. Develoux, M.; Amona, F.M.; Hennequin, C. Histoplasmosis Caused by Histoplasma capsulatum var. duboisii: A Comprehensive Review of Cases From 1993 to 2019. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2021, 73, e543–e549. [Google Scholar] [CrossRef]
  91. Lucas, A.O. Cutaneous manifestations of African histoplasmosis. Br. J. Dermatol. 1970, 82, 435–447. [Google Scholar] [CrossRef]
  92. Lofgren, S.M.; Kirsch, E.J.; Maro, V.P.; Morrissey, A.B.; Msuya, L.J.; Kinabo, G.D.; Saganda, W.; Diefenthal, H.C.; Ramadhani, H.O.; Wheat, L.J.; et al. Histoplasmosis among hospitalized febrile patients in northern Tanzania. Trans. R. Soc. Trop. Med. Hyg. 2012, 106, 504–507. [Google Scholar] [CrossRef]
  93. Mandengue, C.E.; Ngandjio, A.; Atangana, P.J.A. Histoplasmosis in HIV-Infected Persons, Yaoundé, Cameroon. Emerg. Infect. Dis. 2015, 21, 2094–2096. [Google Scholar] [CrossRef] [Green Version]
  94. Amona, F.M.; Denning, D.W.; Moukassa, D.; Develoux, M.; Hennequin, C. Histoplasmosis in the Republic of Congo dominated by African histoplasmosis, Histoplasma capsulatum var. duboisii. PLoS Negl. Trop. Dis. 2021, 15, e0009318. [Google Scholar] [CrossRef]
  95. Darré, T.; Saka, B.; Mouhari-Touré, A.; Dorkenoo, A.M.; Amégbor, K.; Pitche, V.P.; Napo-Koura, G. Histoplasmosis by Histoplasma capsulatum var. duboisii Observed at the Laboratory of Pathological Anatomy of Lomé in Togo. J. Pathog. 2017, 2017, 2323412. [Google Scholar] [CrossRef] [Green Version]
  96. Pakasa, N.; Biber, A.; Nsiangana, S.; Imposo, D.; Sumaili, E.; Muhindo, H.; Buitrago, M.J.; Barshack, I.; Schwartz, E. African Histoplasmosis in HIV-Negative Patients, Kimpese, Democratic Republic of the Congo. Emerg. Infect. Dis. 2018, 24, 2068–2070. [Google Scholar] [CrossRef]
  97. Khathali, L.C.; Nhlonzi, G.B.; Mwazha, A. Histoplasma capsulatum var. duboisii: A KwaZulu-Natal, South Africa public sector perspective. J. Cutan. Pathol. 2022, 49, 139–146. [Google Scholar] [CrossRef]
  98. Kwizera, R.; Bongomin, F.; Lukande, R. Deep fungal infections diagnosed by histology in Uganda: A 70-year retrospective study. Med. Mycol. 2020, 58, 1044–1052. [Google Scholar] [CrossRef]
  99. Dagenais, T.R.T.; Keller, N.P. Pathogenesis of Aspergillus fumigatus in Invasive Aspergillosis. Clin. Microbiol. Rev. 2009, 22, 447–465. [Google Scholar] [CrossRef] [Green Version]
  100. Ohba, H.; Miwa, S.; Shirai, M.; Kanai, M.; Eifuku, T.; Suda, T.; Hayakawa, H.; Chida, K. Clinical characteristics and prognosis of chronic pulmonary aspergillosis. Respir. Med. 2012, 106, 724–729. [Google Scholar] [CrossRef] [Green Version]
  101. Kosmidis, C.; Denning, D.W. The clinical spectrum of pulmonary aspergillosis. Thorax 2015, 70, 270–277. [Google Scholar] [CrossRef] [Green Version]
  102. Bongomin, F.; Gago, S.; Oladele, R.; Denning, D. Global and Multi-National Prevalence of Fungal Diseases—Estimate Precision. J. Fungi 2017, 3, 57. [Google Scholar] [CrossRef] [PubMed]
  103. Segal, B.H. Role of macrophages in host defense against aspergillosis and strategies for immune augmentation. Oncologist 2007, 12 (Suppl. S2), 7–13. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  104. Baddley, J.W. Clinical risk factors for invasive aspergillosis. Med. Mycol. 2011, 49 (Suppl. S1), S7–S12. [Google Scholar] [CrossRef] [PubMed]
  105. Ullmann, A.J.; Aguado, J.M.; Arikan-Akdagli, S.; Denning, D.W.; Groll, A.H.; Lagrou, K.; Lass-Flörl, C.; Lewis, R.E.; Munoz, P.; Verweij, P.E.; et al. Diagnosis and management of Aspergillus diseases: Executive summary of the 2017 ESCMID-ECMM-ERS guideline. Clin. Microbiol. Infect. Off. Publ. Eur. Soc. Clin. Microbiol. Infect. Dis. 2018, 24 (Suppl. S1), e1–e38. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  106. Yerbanga, I.W.; Diallo, S.N.; Rouamba, T.; Denis, O.; Rodriguez-Villalobos, H.; Montesinos, I.; Bamba, S. A systematic review of epidemiology, risk factors, diagnosis, antifungal resistance, and management of invasive aspergillosis in Africa. J. Med. Mycol. 2022, 33, 101328. [Google Scholar] [CrossRef]
  107. Bakhti, S.; Khoudir, W.; Terkmani, F.; Tighilt, N.; Djennas, M. Invasive Disseminated Aspergillosis with Multiple Intracranial Localizations Associated to Chronic Granulomatous Disease: Case Report. Afr. J. Neurol. Sci. 2015, 34, 69–74. [Google Scholar]
  108. Trabelsi, H.; Néji, S.; Sellami, H.; Yaich, S.; Cheikhrouhou, F.; Guidara, R.; Charffedine, K.; Makni, F.; Hachicha, J.; Ayadi, A. Invasive fungal infections in renal transplant recipients: About 11 cases. J. Mycol. Med. 2013, 23, 255–260. [Google Scholar] [CrossRef]
  109. Hakkouni, A.; El Mansouri, N. Invasive pulmonary aspergillosis in a patient with human immunodeficiency virus (HIV). Pan Afr. Med. J. 2018, 31, 40. [Google Scholar]
  110. El-Sayed, Z.A.; Hasan, Z.E.; Nasr, R.A.R. Real-Time PCR in the early detection of invasive fungal infection in immunodeficient infants and children. Egypt J. Pediatr. Allergy Immunol. 2012, 10, 67–74. [Google Scholar]
  111. Gheith, S.; Saghrouni, F.; Bannour, W.; Ben Youssef, Y.; Khelif, A.; Normand, A.-C.; Ben Saïd, M.; Piarroux, R.; Njah, M.; Ranque, S. Characteristics of invasive aspergillosis in neutropenic haematology patients (Sousse, Tunisia). Mycopathologia 2014, 177, 281–289. [Google Scholar] [CrossRef]
  112. Hadrich, I.; Makni, F.; Sellami, H.; Cheikhrouhou, F.; Sellami, A.; Bouaziz, H.; Hdiji, S.; Elloumi, M.; Ayadi, A. Invasive aspergillosis: Epidemiology and environmental study in haematology patients (Sfax, Tunisia). Mycoses 2010, 53, 443–447. [Google Scholar] [CrossRef]
  113. Ahmed, S.; Elseed, K.A. Presentation of invasive fungal rhinosinusitis in Sudanese children: A report of four cases. Sudan J. Med. Sci. 2018, 13, 125–131. [Google Scholar] [CrossRef] [Green Version]
  114. Onyekonwu, G.C.; Chuka-Okosa, C.M. Sino-Orbital aspergillosis with central nervous system complication: A case report. Niger J. Ophthalmol. 2005, 13, 62–66. [Google Scholar] [CrossRef]
  115. Aleksenko, A.; Gyasi, R.K. Disseminated invasive aspergillosis. Ghana Med. J. 2006, 40, 69. [Google Scholar] [CrossRef]
  116. Wong, E.B.; Omar, T.; Setlhako, G.J.; Osih, R.; Feldman, C.; Murdoch, D.M.; Martinson, N.A.; Bangsberg, D.R.; Venter, W.D.F. Causes of death on antiretroviral therapy: A post-mortem study from South Africa. PLoS ONE 2012, 7, e47542. [Google Scholar] [CrossRef] [Green Version]
  117. Skalski, J.H.; Kottom, T.J.; Limper, A.H. Pathobiology of Pneumocystis pneumonia: Life cycle, cell wall and cell signal transduction. FEMS Yeast Res. 2015, 15, fov046. [Google Scholar] [CrossRef] [Green Version]
  118. Wasserman, S.; Engel, M.E.; Griesel, R.; Mendelson, M. Burden of pneumocystis pneumonia in HIV-infected adults in sub-Saharan Africa: A systematic review and meta-analysis. BMC Infect. Dis. 2016, 16, 482. [Google Scholar] [CrossRef] [Green Version]
  119. Wills, N.K.; Lawrence, D.S.; Botsile, E.; Tenforde, M.W.; Jarvis, J.N. The prevalence of laboratory-confirmed Pneumocystis jirovecii in HIV-infected adults in Africa: A systematic review and meta-analysis. Med. Mycol. 2021, 59, 802–812. [Google Scholar] [CrossRef]
  120. Jensen, L.; Jensen, A.V.; Praygod, G.; Kidola, J.; Faurholt-Jepsen, D.; Changalucha, J.; Range, N.; Friis, H.; Helweg-Larsen, J.; Jensen, J.S.; et al. Infrequent detection of Pneumocystis jirovecii by PCR in oral wash specimens from TB patients with or without HIV and healthy contacts in Tanzania. BMC Infect. Dis. 2010, 10, 140. [Google Scholar] [CrossRef] [Green Version]
  121. Riebold, D.; Enoh, D.O.; Kinge, T.N.; Akam, W.; Bumah, M.K.; Russow, K.; Klammt, S.; Loebermann, M.; Fritzsche, C.; Eyong, J.E.; et al. Pneumocystis jirovecii colonisation in HIV-positive and HIV-negative subjects in Cameroon. Trop. Med. Int. Health 2014, 19, 643–655. [Google Scholar] [CrossRef]
  122. Hviid, C.J.; Lund, M.; Sørensen, A.; Eriksen, S.E.; Jespersen, B.; Dam, M.Y.; Dahlerup, J.F.; Benfield, T.; Jespersen, S.; Østergaard, L.; et al. Detection of Pneumocystis jirovecii in oral wash from immunosuppressed patients as a diagnostic tool. PLoS ONE 2017, 12, e0174012. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  123. Morris, A.; Norris, K.A. Colonization by Pneumocystis jirovecii and its role in disease. Clin. Microbiol. Rev. 2012, 25, 297–317. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  124. White, P.L.; Price, J.S.; Backx, M. Pneumocystis jirovecii pneumonia: Epidemiology, clinical manifestation and diagnosis. Curr. Fungal Infect. Rep. 2019, 13, 260–273. [Google Scholar] [CrossRef]
  125. Ding, L.; Huang, H.; Wang, H.; He, H. Adjunctive corticosteroids may be associated with better outcome for non-HIV Pneumocystis pneumonia with respiratory failure: A systemic review and meta-analysis of observational studies. Ann. Intensive Care 2020, 10, 1–15. [Google Scholar] [CrossRef] [PubMed]
  126. Cillóniz, C.; Dominedò, C.; Álvarez-Martínez, M.J.; Moreno, A.; García, F.; Torres, A.; Miro, J.M. Pneumocystis pneumonia in the twenty-first century: HIV-infected versus HIV-uninfected patients. Expert Rev. Anti-Infect. Ther. 2019, 17, 787–801. [Google Scholar] [CrossRef]
  127. Morrow, B.M.; Hsaio, N.-Y.; Zampoli, M.; Whitelaw, A.; Zar, H.J. Pneumocystis pneumonia in South African children with and without human immunodeficiency virus infection in the era of highly active antiretroviral therapy. Pediatr. Infect. Dis. J. 2010, 29, 535–539. [Google Scholar] [CrossRef]
  128. O’Brien, K.L.; Baggett, H.C.; Brooks, W.A.; Feikin, D.R.; Hammitt, L.L.; Higdon, M.M.; Howie, S.R.; Knoll, M.D.; Kotloff, K.L.; Levine, O.S.; et al. Causes of severe pneumonia requiring hospital admission in children without HIV infection from Africa and Asia: The PERCH multi-country case-control study. Lancet 2019, 394, 757–779. [Google Scholar] [CrossRef] [Green Version]
  129. Hussain, M.; Whitelaw, A.; Parker, A. A five-year retrospective descriptive study on the clinical characteristics and outcomes of candidaemia at a tertiary hospital in South Africa. IJID Reg. 2022, 3, 79–83. [Google Scholar] [CrossRef]
  130. Shoham, S.; Levitz, S.M. The immune response to fungal infections. Br. J. Haematol. 2005, 129, 569–582. [Google Scholar] [CrossRef]
  131. Chibabhai, V.; Fadana, V.; Bosman, N.; Nana, T. Comparative sensitivity of 1,3 beta-D-glucan for common causes of candidaemia in South Africa. Mycoses 2019, 62, 1023–1028. [Google Scholar] [CrossRef]
  132. Lockhart, S.R.; Etienne, K.A.; Vallabhaneni, S.; Farooqi, J.; Chowdhary, A.; Govender, N.P.; Colombo, A.L.; Calvo, B.; Cuomo, C.A.; Desjardins, C.A.; et al. Simultaneous Emergence of Multidrug-Resistant Candida auris on 3 Continents Confirmed by Whole-Genome Sequencing and Epidemiological Analyses. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2017, 64, 134–140. [Google Scholar] [CrossRef] [Green Version]
  133. Rhodes, J.; Fisher, M.C. Global epidemiology of emerging Candida auris. Curr. Opin. Microbiol. 2019, 52, 84–89. [Google Scholar] [CrossRef]
  134. Naicker, S.D.; Govender, N.; Patel, J.; Zietsman, I.L.; Wadula, J.; Coovadia, Y.; Kularatne, R.; Seetharam, S.; Govender, N.P.; TRAC-SA Group. Comparison of species-level identification and antifungal susceptibility results from diagnostic and reference laboratories for bloodstream Candida surveillance isolates, South Africa, 2009–2010. Med. Mycol. 2016, 54, 816–824. [Google Scholar] [CrossRef] [Green Version]
  135. Parak, A.; Stacey, S.L.; Chibabhai, V. Clinical and laboratory features of patients with Candida auris cultures, compared to other Candida, at a South African Hospital. J. Infect. Dev. Ctries. 2022, 16, 213–221. [Google Scholar] [CrossRef]
  136. Adam, R.D.; Revathi, G.; Okinda, N.; Fontaine, M.; Shah, J.; Kagotho, E.; Castanheira, M.; Pfaller, M.; Maina, D. Analysis of Candida auris fungemia at a single facility in Kenya. Int. J. Infect. Dis. IJID Off. Publ. Int. Soc. Infect. Dis. 2019, 85, 182–187. [Google Scholar]
  137. Chibabhai, V. Incidence of candidemia and prevalence of azole-resistant candidemia at a tertiary South African hospital—A retrospective laboratory analysis 2016–2020. South Afr. J. Infect. Dis. 2022, 37, 326. [Google Scholar] [CrossRef]
  138. Shuping, L.; Mpembe, R.; Mhlanga, M.; Naicker, S.D.; Maphanga, T.G.; Tsotetsi, E.; Wadula, J.; Velaphi, S.; Nakwa, F.; Chibabhai, V.; et al. Epidemiology of Culture-confirmed Candidemia Among Hospitalized Children in South Africa, 2012–2017. Pediatr. Infect. Dis. J. 2021, 40, 730–737. [Google Scholar] [CrossRef]
  139. Hegazi, M.; Abdelkader, A.; Zaki, M.; El-Deek, B. Characteristics and risk factors of candidemia in pediatric intensive care unit of a tertiary care children’s hospital in Egypt. J. Infect. Dev. Ctries. 2014, 8, 624–634. [Google Scholar] [CrossRef] [Green Version]
  140. Megri, Y.; Arastehfar, A.; Boekhout, T.; Daneshnia, F.; Hörtnagl, C.; Sartori, B.; Hafez, A.; Pan, W.; Lass-Flörl, C.; Hamrioui, B. Candida tropicalis is the most prevalent yeast species causing candidemia in Algeria: The urgent need for antifungal stewardship and infection control measures. Antimicrob. Resist. Infect. Control 2020, 9, 50. [Google Scholar] [CrossRef] [Green Version]
  141. Kreusch, A.; Karstaedt, A.S. Candidemia among adults in Soweto, South Africa, 1990–2007. Int. J. Infect. Dis. IJID Off. Publ. Int. Soc. Infect. Dis. 2013, 17, e621–e623. [Google Scholar] [CrossRef] [Green Version]
  142. Ezenwa, B.N.; Oladele, R.O.; Akintan, P.E.; Fajolu, I.B.; Oshun, P.O.; Oduyebo, O.O.; Ezeaka, V.C. Invasive candidiasis in a neonatal intensive care unit in Lagos, Nigeria. Niger Postgrad. Med. J. 2017, 24, 150–154. [Google Scholar] [CrossRef] [PubMed]
  143. Ramy, N.; Hashim, M.; Abou Hussein, H.; Sawires, H.; Gaafar, M.; El Maghraby, A. Role of Early Onset Neutropenia in Development of Candidemia in Premature Infants. J. Trop. Pediatr. 2018, 64, 51–59. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  144. Van Schalkwyk, E.; Iyaloo, S.; Naicker, S.D.; Maphanga, T.G.; Mpembe, R.S.; Zulu, T.G.; Mhlanga, M.; Mahlangu, S.; Maloba, M.B.; Ntlemo, G.; et al. Large Outbreaks of Fungal and Bacterial Bloodstream Infections in a Neonatal Unit, South Africa, 2012–2016. Emerg. Infect. Dis. 2018, 24, 1204–1212. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  145. Van Schalkwyk, E.; Mpembe, R.S.; Thomas, J.; Shuping, L.; Ismail, H.; Lowman, W.; Karstaedt, A.S.; Chibabhai, V.; Wadula, J.; Avenant, T.; et al. Epidemiologic Shift in Candidemia Driven by Candida auris, South Africa, 2016–2017. Emerg. Infect. Dis. 2019, 25, 1698–1707. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  146. Sellami, A.; Néji, S.; Makni, F.; Abbes, S.; Cheikhrouhou, F.; Chelly, H.; Bouaziz, M.; Hammami, B.; Ben Jemaa, M.; Khaled, S.; et al. Antifungal susceptibility of bloodstream Candida isolates in Sfax hospital: Tunisia. Mycopathologia 2011, 171, 417–422. [Google Scholar] [CrossRef]
  147. Saghrouni, F.; Ben Abdeljelil, J.; Nouri, S.; Gheith, S.; Fathallah, A.; Sboui, H. Double fungemia. Report of four Tunisian cases. J. Mycol. Med. 2012, 22, 192–196. [Google Scholar] [CrossRef]
  148. Stemler, J.; Hamed, K.; Salmanton-García, J.; Rezaei-Matehkolaei, A.; Gräfe, S.K.; Sal, E.; Zarrouk, M.; Seidel, D.; Khedr, R.A.; Ben-Ami, R.; et al. Mucormycosis in the Middle East and North Africa: Analysis of the FungiScope(®) registry and cases from the literature. Mycoses 2020, 63, 1060–1068. [Google Scholar] [CrossRef]
  149. Pan, J.; Tsui, C.; Li, M.; Xiao, K.; de Hoog, G.S.; Verweij, P.E.; Cao, Y.; Lu, H.; Jiang, Y. First Case of Rhinocerebral Mucormycosis Caused by Lichtheimia ornata, with a Review of Lichtheimia Infections. Mycopathologia 2020, 185, 555–567. [Google Scholar] [CrossRef]
  150. Petrikkos, G.; Skiada, A.; Lortholary, O.; Roilides, E.; Walsh, T.J.; Kontoyiannis, D.P. Epidemiology and clinical manifestations of mucormycosis. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2012, 54 (Suppl. 1), S23–S34. [Google Scholar] [CrossRef]
  151. Hauman, C.H.; Raubenheimer, E.J. Orofacial mucormycosis. Oral Surg. Oral Med. Oral Pathol. 1989, 68, 624–627. [Google Scholar] [CrossRef]
  152. Zaki, S.M.; Elkholy, I.M.; Elkady, N.A.; Abdel-Ghany, K. Mucormycosis in Cairo, Egypt: Review of 10 reported cases. Med. Mycol. 2014, 52, 73–80. [Google Scholar] [CrossRef] [Green Version]
  153. Prakash, H.; Chakrabarti, A. Global Epidemiology of Mucormycosis. J. Fungi 2019, 5, 26. [Google Scholar] [CrossRef] [Green Version]
  154. Roden, M.M.; Zaoutis, T.E.; Buchanan, W.L.; Knudsen, T.A.; Sarkisova, T.A.; Schaufele, R.L.; Sein, M.; Sein, T.; Chiou, C.C.; Chu, J.H.; et al. Epidemiology and outcome of zygomycosis: A review of 929 reported cases. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2005, 41, 634–653. [Google Scholar] [CrossRef] [Green Version]
  155. Riley, T.T.; Muzny, C.A.; Swiatlo, E.; Legendre, D.P. Breaking the Mold: A Review of Mucormycosis and Current Pharmacological Treatment Options. Ann. Pharmacother. 2016, 50, 747–757. [Google Scholar] [CrossRef]
  156. Spellberg, B.; Edwards, J.J.; Ibrahim, A. Novel perspectives on mucormycosis: Pathophysiology, presentation, and management. Clin. Microbiol. Rev. 2005, 18, 556–569. [Google Scholar] [CrossRef]
  157. El-Mahallawy, H.A.; Khedr, R.; Taha, H.; Shalaby, L.; Mostafa, A. Investigation and Management of a Rhizomucor Outbreak in a Pediatric Cancer Hospital in Egypt. Pediatr. Blood Cancer 2016, 63, 171–173. [Google Scholar] [CrossRef]
  158. Bodenstein, N.P.; McIntosh, W.A.; Vlantis, A.C.; Urquhart, A.C. Clinical signs of orbital ischemia in rhino-orbitocerebral mucormycosis. Laryngoscope 1993, 103, 1357–1361. [Google Scholar] [CrossRef]
  159. Alfishawy, M.; Elbendary, A.; Younes, A.; Negm, A.; Hassan, W.S.; Osman, S.H.; Nassar, M.; Elanany, M.G. Diabetes mellitus and Coronavirus Disease (Covid-19) Associated Mucormycosis (CAM): A wake-up call from Egypt. Diabetes Metab. Syndr. 2021, 15, 102195. [Google Scholar] [CrossRef]
  160. Alloush, T.K.; Mansour, O.; Alloush, A.T.; Roushdy, T.; Hamid, E.; El-Shamy, M.; Shokri, H.M. Rhino-orbito-cerebral mucormycosis during the COVID-19 third wave in 2021: An Egyptian preliminary report from a single tertiary hospital. Neurol. Sci. Off. J. Ital. Neurol. Soc. Ital. Soc. Clin. Neurophysiol. 2022, 43, 799–809. [Google Scholar] [CrossRef]
  161. Anane, S.; Kaouech, E.; Belhadj, S.; Ammari, L.; Abdelmalek, R.; Chaabane, T.B.; Lakhal, S.B.; Cherif, A.; Ammamou, M.; Fadhel, K.B.; et al. Rhino-orbito-cerebral mucormycosis in the diabetic: A better known pathology in Tunisia. Ann. Biol. Clin. 2009, 67, 325–332. [Google Scholar]
  162. Thomson, S.R.; Bade, P.G.; Taams, M.; Chrystal, V. Gastrointestinal mucormycosis. Br. J. Surg. 1991, 78, 952–954. [Google Scholar] [CrossRef] [PubMed]
  163. Kahn, L.B. Gastric Muucormycosis: Report of a case with a review of the literature. S. Afr. Med. J. 1963, 37, 1265–1269. [Google Scholar] [PubMed]
  164. Feki, W.; Sellami, S.; Charfi, S.; Ketata, W.; Msaad, S. Successful Medical Treatment of Pulmonary Mucormycosis in Diabetic Patients. J. Pulm. Respir. Med. 2018, 8, 2. [Google Scholar]
  165. Madney, Y.; Khedr, R.; Al-Mahellawy, H.; Adel, N.; Taha, H.; Zaki, I.; Youssef, A.; Taha, G.; Hassanain, O.; Hafez, H. “Mucormycosis” the Emerging Global Threat; Overview and Treatment Outcome Among Pediatric Cancer Patients in Egypt. Blood 2017, 130, 4830. [Google Scholar]
  166. El-Hameed, A.; Ayman, R.; Abdelsalam, N.M.; Saleh, A.M.A.; Awad, A.M.M.; ElShabrawy, A.M. COVID-19 associated mucormycosis and diabetes mellitus: An exploratory study. Microbes Infect. Dis. 2022, 3, 270–278. [Google Scholar] [CrossRef]
  167. Shabana, R.R.; Eldesouky, M.A.; Elbedewy, H.A. Exenterate or Not: A Simple Proposed Management Algorithm for Mucormycosis During the Era of COVID-19 in a Tertiary Eye Care Center in Egypt. Clin. Ophthalmol. 2022, 16, 1933–1940. [Google Scholar] [CrossRef]
  168. Ulasi, I.; Ijoma, C.; Ifebunandu, N.; Arodiwe, E.; Ijoma, U.; Okoye, J.; Onu, U.; Okwuonu, C.; Alhassan, S.; Onodugo, O. Organ Donation and Transplantation in Sub-Saharan Africa: Opportunities and Challenges. In Organ Donation and Transplantation; Mihaylov, V., Ed.; IntechOpen: Rijeka, Croatia, 2020. [Google Scholar] [CrossRef]
  169. Khaba, M.C.; Nevondo, L.M.; Moroatshehla, S.M.; Makhado, N.A. Disseminated mucormycosis presenting as a renal mass in an human immunodeficiency virus-infected patient: A case report. S. Afr. J. Infect. Dis. 2021, 36, 202. [Google Scholar] [CrossRef]
  170. Narayanasamy, S.; Dat, V.Q.; Thanh, N.T.; Ly, V.T.; Chan, J.F.-W.; Yuen, K.-Y.; Ning, C.; Liang, H.; Li, L.; Chowdhary, A.; et al. A global call for talaromycosis to be recognised as a neglected tropical disease. Lancet Glob. Health 2021, 9, e1618–e1622. [Google Scholar] [CrossRef]
  171. Vanittanakom, N.; Cooper, C.R.J.; Fisher, M.C.; Sirisanthana, T. Penicillium marneffei infection and recent advances in the epidemiology and molecular biology aspects. Clin. Microbiol. Rev. 2006, 19, 95–110. [Google Scholar] [CrossRef] [Green Version]
  172. LoBuglio, K.F.; Taylor, J.W. Phylogeny and PCR identification of the human pathogenic fungus Penicillium marneffei. J. Clin. Microbiol. 1995, 33, 85–89. [Google Scholar] [CrossRef] [Green Version]
  173. Chariyalertsak, S.; Sirisanthana, T.; Supparatpinyo, K.; Nelson, K.E. Seasonal variation of disseminated Penicillium marneffei infections in northern Thailand: A clue to the reservoir? J. Infect. Dis. 1996, 173, 1490–1493. [Google Scholar] [CrossRef] [Green Version]
  174. Stone, A.; Park, B.J. Penicillium marneffei infection: Knowledge, gaps, and future directions. Curr. Fungal Infect. Rep. 2011, 5, 193–198. [Google Scholar] [CrossRef]
  175. Guiguemde, K.T.; Sawadogo, P.M.; Zida, A.; Cisse, M.; Sangare, I.; Bamba, S. First case report of Talaromyces marneffei infection in HIV-infected patient in the city of Ouagadougou (Burkina Faso). Med. Mycol. Case Rep. 2019, 26, 10–12. [Google Scholar] [CrossRef]
  176. Govender, N.P.; Magobo, R.E.; Zulu, T.G.; Du Plooy, M.; Corcoran, C. Case Report: Disseminated fatal Talaromyces (Penicillium) marneffei infection in a returning HIV-infected traveller. S. Afr. J. HIV Med. 2014, 15, 154–155. [Google Scholar] [CrossRef] [Green Version]
  177. Schwartz, I.S.; Govender, N.P.; Sigler, L.; Jiang, Y.; Maphanga, T.G.; Toplis, B.; Botha, A.; Dukik, K.; Hoving, J.C.; Muñoz, J.F.; et al. Emergomyces: The global rise of new dimorphic fungal pathogens. PLoS Pathog. 2019, 15, e1007977. [Google Scholar] [CrossRef] [Green Version]
  178. Reddy, D.L.; Nel, J.; Govender, N.P. Emergomycosis. J. Med. Mycol. 2022, 33, 101313. [Google Scholar] [CrossRef]
  179. Samaddar, A.; Sharma, A. Emergomycosis, an emerging systemic mycosis in immunocompromised patients: Current trends and future prospects. Front. Med. 2021, 8, 670731. [Google Scholar] [CrossRef]
  180. Maphanga, T.G.; Britz, E.; Zulu, T.G.; Mpembe, R.S.; Naicker, S.D.; Schwartz, I.S.; Govender, N.P. In vitro antifungal susceptibility of yeast and mold phases of isolates of dimorphic fungal pathogen Emergomyces africanus (formerly Emmonsia sp.) from HIV-infected South African patients. J. Clin. Microbiol. 2017, 55, 1812–1820. [Google Scholar] [CrossRef] [Green Version]
  181. Schwartz, I.S.; Govender, N.P.; Corcoran, C.; Dlamini, S.; Prozesky, H.; Burton, R.; Mendelson, M.; Taljaard, J.; Lehloenya, R.; Calligaro, G.; et al. Clinical characteristics, diagnosis, management, and outcomes of disseminated emmonsiosis: A retrospective case series. Clin. Infect. Dis. 2015, 61, 1004–1012. [Google Scholar] [CrossRef] [Green Version]
  182. Heys, I.; Taljaard, J.; Orth, H. An emmonsia species causing disseminated infection in South Africa. New Engl. J. Med. 2014, 370, 283–428. [Google Scholar]
  183. Schwartz, I.S.; McLoud, J.D.; Berman, D.; Botha, A.; Lerm, B.; Colebunders, R.; Levetin, E.; Kenyon, C. Molecular detection of airborne Emergomyces africanus, a thermally dimorphic fungal pathogen, in Cape Town, South Africa. PLoS Negl. Trop. Dis. 2018, 12, e0006174. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  184. Schwartz, I.S.; Lerm, B.; Hoving, J.C.; Kenyon, C.; Horsnell, W.G.; Basson, W.J.; Otieno-Odhiambo, P.; Govender, N.P.; Colebunders, R.; Botha, A. Emergomyces africanus in Soil, South Africa. Emerg. Infect. Dis. 2018, 24, 377–380. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  185. Kenyon, C.; Bonorchis, K.; Corcoran, C.; Meintjes, G.; Locketz, M.; Lehloenya, R.; Vismer, H.F.; Naicker, P.; Prozesky, H.; van Wyk, M.; et al. A dimorphic fungus causing disseminated infection in South Africa. New Engl. J. Med. 2013, 369, 1416–1424. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  186. Moodley, A.; Mosam, A.; Govender, N.P.; Mahabeer, Y.; Chateau, A.V. Emergomyces africanus: The Mimicking Fungus. Dermatopathology 2019, 6, 157–162. [Google Scholar] [CrossRef] [PubMed]
  187. Schwartz, I.S.; Kenyon, C.; Lehloenya, R.; Claasens, S.; Spengane, Z.; Prozesky, H.; Burton, R.; Parker, A.; Wasserman, S.; Meintjes, G.; et al. AIDS-Related Endemic Mycoses in Western Cape, South Africa, and Clinical Mimics: A Cross-Sectional Study of Adults with Advanced HIV and Recent-Onset, Widespread Skin Lesions. Open Forum Infect. Dis. 2017, 4, ofx186. [Google Scholar] [CrossRef] [Green Version]
  188. Rooms, I.; Mugisha, P.; Gambichler, T.; Hadaschik, E.; Esser, S.; Rath, P.-M.; Haase, G.; Wilmes, D.; McCormick-Smith, I.; Rickerts, V. Disseminated Emergomycosis in a Person with HIV Infection, Uganda. Emerg. Infect. Dis. 2019, 25, 1750–1751. [Google Scholar] [CrossRef]
  189. Lochan, H.; Naicker, P.; Maphanga, T.; Ryan, A.; Pillay, K.; Govender, N.P.; Eley, B. A case of emmonsiosis in an HIV-infected child. S. Afr. J. HIV Med. 2015, 16, 352. [Google Scholar] [CrossRef]
  190. Van Hougenhouck-Tulleken, W.G.; Papavarnavas, N.S.; Nel, J.S.; Blackburn, L.Y.; Govender, N.P.; Spencer, D.C.; Lippincott, C.K. HIV-associated disseminated emmonsiosis, Johannesburg, South Africa. Emerg. Infect. Dis. 2014, 20, 2164–2166. [Google Scholar] [CrossRef]
  191. Bonifaz, A.; Vázquez-González, D.; Perusquía-Ortiz, A.M. Endemic systemic mycoses: Coccidioidomycosis, histoplasmosis, paracoccidioidomycosis and blastomycosis. J. Ger. Soc. Dermatol. JDDG 2011, 9, 705–714. [Google Scholar] [CrossRef]
  192. Schwartz, I.S.; Kauffman, C.A. Blastomycosis. Semin. Respir. Crit. Care Med. 2020, 41, 31–41. [Google Scholar] [CrossRef]
  193. Salzer, H.J.; Burchard, G.; Cornely, O.A.; Lange, C.; Rolling, T.; Schmiedel, S.; Libman, M.; Capone, D.; Le, T.; Dalcolmo, M.P.; et al. Diagnosis and Management of Systemic Endemic Mycoses Causing Pulmonary Disease. Respiration 2018, 96, 283–301. [Google Scholar] [CrossRef]
  194. Abdallah, F.C.B.; Bachouch, I.; Belloumi, N.; Kacem, M.; Mlika, M.; El Mezni, F.; Fenniche, S. Pulmonary blastomycosis. Pan Afr. Med. J. 2020, 36, 220. [Google Scholar] [CrossRef]
  195. Bongomin, F.; Fayemiwo, S.A. Epidemiology of fungal diseases in Africa: A review of diagnostic drivers. Curr. Med. Mycol. 2021, 7, 63–70. [Google Scholar] [CrossRef]
  196. Schwartz, I.S.; Kenyon, C.; Thompson, G.R., 3rd. Endemic Mycoses: What’s New About Old Diseases? Curr. Clin. Microbiol. Rep. 2016, 3, 71–80. [Google Scholar] [CrossRef]
  197. Chapman, S.W.; Dismukes, W.E.; Proia, L.A.; Bradsher, R.W.; Pappas, P.G.; Threlkeld, M.G.; Kauffman, C.A. Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2008, 46, 1801–1812. [Google Scholar] [CrossRef]
  198. Maphanga, T.G.; Birkhead, M.; Muñoz, J.F.; Allam, M.; Zulu, T.G.; Cuomo, C.A.; Schwartz, I.S.; Ismail, A.; Naicker, S.D.; Mpembe, R.S.; et al. Human Blastomycosis in South Africa Caused by Blastomyces percursus and Blastomyces emzantsi sp. nov., 1967 to 2014. J. Clin. Microbiol. 2020, 58, e01661-19. [Google Scholar] [CrossRef]
  199. El Euch, D.; Cherif, F.; Aoun, K.; Mokni, M.; Bouratbine, A.; Haouet, S. Cutaneous blastomycosis: Description of two cases in Tunisia. Med. Trop. 2004, 64, 183–186. [Google Scholar]
  200. Motswaledi, H.M.; Monyemangene, F.M.; Maloba, B.R.; Nemutavhanani, D.L. Blastomycosis: A case report and review of the literature. Int. J. Dermatol. 2012, 51, 1090–1093. [Google Scholar] [CrossRef]
  201. Salem, M.B.; Hamouda, M.; Mohamed, M.; Aloui, S.; Letaief, A.; Moussa, A.; Skhiri, H.; Zakahama, A.; Dhia, N.B. Blastomyces dermatitidis in a Renal Transplant Recipient: A Case Report. Transpl. Proc. 2017, 49, 1583–1586. [Google Scholar] [CrossRef]
  202. Ferchichi, L.; Mekni, A.; Bellil, K.; Haouet, S.; Zeddini, A.; Bellil, S.; Kchir, N.; Cherif, F.; Ben Osman, A.; Zitouna, M. Three cases of cutaneous blastomycosis. Med. Mal. Infect. 2006, 36, 285–287. [Google Scholar] [CrossRef]
  203. Harket, A.; Oukabli, M.; Al Bouzidi, A.; Zoubeir, Y.; Quamous, O.; Baba, N.; Doghmi, K.; Mikdame, M.; Rimani, M.; Sedrati, O.; et al. Cutaneous blastomycosis revealing intravascular B-cell lymphoma: A case in Morocco. Med. Trop. 2007, 67, 278–280. [Google Scholar]
  204. Rais, H.; Jghaimi, F.; Baalal, H.; Naji, Y.; Essaadouni, L.; Essadki, O.; Oussehal, A.; Mejjati, M.; Aitbenali, S.; Elyazidi, A.A.; et al. Blastomycosis in Morocco: Imported mycosis. Rev. Pneumol. Clin. 2012, 68, 45–49. [Google Scholar] [CrossRef] [PubMed]
  205. Rouhou, S.C.; Racil, H.; Ismail, O.; Trabelsi, S.; Zarrouk, M.; Chaouch, N.; Hantous, S.; Khaled, S.; El Mezni, F.; Chabbou, A. Pulmonary Blastomycosis: A Case from Africa. Sci. World J. 2008, 8, 1098–1103. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  206. Alvarez, G.G.; Burns, B.F.; Desjardins, M.; Salahudeen, S.R.; Al Rashidi, F.; Cameron, D.W. Blastomycosis in a young African man presenting with a pleural effusion. Can Respir. J. 2006, 13, 441–444. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  207. Ibrahim, T.M.; Edinol, S.T. Pleural effusion from blastomycetes in an adult Nigerian: A case report. Niger. Postgrad. Med. J. 2001, 8, 148–149. [Google Scholar]
  208. Fisher, M.C.; Koenig, G.L.; White, T.J.; Taylor, J.W. Molecular and phenotypic description of Coccidioides posadasii sp. nov., previously recognized as the non-California population of Coccidioides immitis. Mycologia 2002, 94, 73–84. [Google Scholar] [CrossRef] [Green Version]
  209. Colombo, A.L.; Tobón, A.; Restrepo, A.; Queiroz-Telles, F.; Nucci, M. Epidemiology of endemic systemic fungal infections in Latin America. Med. Mycol. 2011, 49, 785–798. [Google Scholar] [CrossRef] [Green Version]
  210. Benedict, K.; Thompson, G.R., 3rd; Deresinski, S.; Chiller, T. Mycotic Infections Acquired outside Areas of Known Endemicity, United States. Emerg. Infect. Dis. 2015, 2, 2935–2941. [Google Scholar] [CrossRef]
  211. Indhirajanti, S.; Maartense, E.; Posthuma, E.F.M.; Pannekoek, B.J.M.; Vreede, R.W. Pulmonary coccidioidomycosis: Import illness and the importance of travel history. Neth. J. Med. 2009, 67, 353–355. [Google Scholar]
  212. Yoo, S.D.; Lusiba, J.K.; Lukande, R.; Shin, K. Disseminated Coccidioidomycosis in Africa. Eur. J. Case Rep. Intern. Med. 2020, 7, 1659. [Google Scholar]
  213. Connor, D.H. Pathology of Infectious Diseases; Appletion & Lange: Norwalk, CT, USA, 1997; pp. 947–950. [Google Scholar]
  214. Van Dyke, M.C.C.; Thompson, G.R.; Galgiani, J.N.; Barker, B.M. The Rise of Coccidioides: Forces Against the Dust Devil Unleashed. Front. Immunol. 2019, 10, 2188. [Google Scholar] [CrossRef]
  215. McHardy, I.H.; Dinh, B.-T.N.; Waldman, S.; Stewart, E.; Bays, D.; Pappagianis, D.; Thompson, G.R. Coccidioidomycosis Complement Fixation Titer Trends in the Age of Antifungals. J. Clin. Microbiol. 2018, 56, e01318-18. [Google Scholar] [CrossRef] [Green Version]
  216. Ampel, N.M.; Giblin, A.; Mourani, J.P.; Galgiani, J.N. Factors and outcomes associated with the decision to treat primary pulmonary coccidioidomycosis. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2009, 48, 172–178. [Google Scholar] [CrossRef]
  217. Blair, J.E.; Chang, Y.-H.H.; Cheng, M.-R.; Vaszar, L.T.; Vikram, H.R.; Orenstein, R.; Kusne, S.; Ho, S.; Seville, M.T.; Parish, J.M. Characteristics of Patients with Mild to Moderate Primary Pulmonary Coccidioidomycosis. Emerg. Infect. Dis. 2014, 20, 983–990. [Google Scholar] [CrossRef] [Green Version]
  218. Wagner, G.; Moertl, D.; Eckhardt, A.; Sagel, U.; Wrba, F.; Dam, K.; Willinger, B. Chronic Paracoccidioidomycosis with adrenal involvement mimicking tuberculosis—A case report from Austria. Med. Mycol. Case Rep. 2016, 14, 12–16. [Google Scholar] [CrossRef]
  219. Sylvestre, T.F.; Silva, L.R.F.; Cavalcante, R.D.S.; Moris, D.V.; Venturini, J.; Vicentini, A.P.; de Carvalho, L.R.; Mendes, R.P. Prevalence and Serological Diagnosis of Relapse in Paracoccidioidomycosis Patients. PLOS Negl. Trop. Dis. 2014, 8, e2834. [Google Scholar] [CrossRef] [Green Version]
  220. Yoshimura, Y.; Tachikawa, N.; Oosawa, T.; Kosuge, Y.; Kamei, K. A case of paracoccidioidomycosis with severe adrenal insufficiency. Kansenshogaku Zasshi J. Jpn. Assoc. Infect. Dis. 2012, 86, 291–294. [Google Scholar] [CrossRef] [Green Version]
  221. Shikanai-Yasuda, M.A.; Telles Filho, F.; Mendes, R.P.; Colombo, A.L.; Moretti, M.L. Guidelines in paracoccidioidomycosis. Rev. Soc. Bras. Med. Trop. 2006, 39, 297–310. [Google Scholar] [CrossRef] [Green Version]
  222. De Camargo, Z.P. Serology of paracoccidioidomycosis. Mycopathologia 2008, 165, 289–302. [Google Scholar] [CrossRef] [Green Version]
  223. Queiroz-Telles, F.; Goldani, L.Z.; Schlamm, H.T.; Goodrich, J.M.; Espinel-Ingroff, A.; Shikanai-Yasuda, M.A. An open-label comparative pilot study of oral voriconazole and itraconazole for long-term treatment of paracoccidioidomycosis. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 2007, 45, 1462–1469. [Google Scholar] [CrossRef] [Green Version]
  224. De Cavalcante, R.S.; Sylvestre, T.F.; Levorato, A.D.; de Carvalho, L.R.; Mendes, R.P. Comparison between itraconazole and cotrimoxazole in the treatment of paracoccidiodomycosis. PLoS Negl. Trop. Dis. 2014, 8, e2793. [Google Scholar] [CrossRef] [PubMed]
  225. Lawande, R.V.; Sturrock, R.D.; Jacyk, W.K.; Subbuswamy, S.G. A case of paracoccidioidal granuloma in norther Nigeria. J. Trop. Med. Hyg. 1979, 82, 173–176. [Google Scholar] [PubMed]
  226. Rasamoelina, T.; Rakotozandrindrainy, N.; Raberahona, M.; Rabenja, F.R.; Andrianarivelo, M.R.; Andrianarison, M.; Ranaivo, I.; Ramarozatovo, L.; Cornet, M. Chromoblastomycosis and sporotrichosis in Madagascar: Epidemiology, molecular diagnostic and perspectives. J. Mycol. Med. 2016, 26, e15. [Google Scholar] [CrossRef]
  227. Rasamoelina, T.; Maubon, D.; Andrianarison, M.; Ranaivo, I.; Sendrasoa, F.; Rakotozandrindrainy, N.; Rakotomalala, F.A.; Bailly, S.; Rakotonirina, B.; Andriantsimahavandy, A.; et al. Endemic Chromoblastomycosis Caused Predominantly by Fonsecaea nubica, Madagascar(1). Emerg. Infect. Dis. 2020, 26, 1201–1211. [Google Scholar] [CrossRef] [PubMed]
  228. Rasamoelina, T.; Raharolahy, O.; Rakotozandrindrainy, N.; Ranaivo, I.; Andrianarison, M.; Rakotonirina, B.; Maubon, D.; Rakotomalala, F.; Andrianarivelo, M.R.; Andriantsimahavandy, A.; et al. Chromoblastomycosis and sporotrichosis, two endemic but neglected fungal infections in Madagascar. J. Mycol. Med. 2017, 27, 312–324. [Google Scholar] [CrossRef]
  229. Santos, D.W.C.L.; Azevedo, C.D.M.P.E.S.D.; Vicente, V.A.; Queiroz-Telles, F.; Rodrigues, A.M.; de Hoog, G.S.; Denning, D.W.; Colombo, A.L. The global burden of chromoblastomycosis. PLOS Negl. Trop. Dis. 2021, 15, e0009611. [Google Scholar] [CrossRef]
  230. Abate, D.A.; Ayele, M.H.; Mohammed, A.B. Subcutaneous mycoses in Ethiopia: A retrospective study in a single dermatology center. Trans. R. Soc. Trop. Med. Hyg. 2021, 115, 1468–1470. [Google Scholar] [CrossRef]
  231. Orofino-Costa, R.; de Macedo, P.M.; Rodrigues, A.M.; Bernardes-Engemann, A.R. Sporotrichosis: An update on epidemiology, etiopathogenesis, laboratory and clinical therapeutics. Bras Dermatol. 2017, 92, 606–620. [Google Scholar] [CrossRef] [Green Version]
  232. Chakrabarti, A.; Bonifaz, A.; Gutierrez-Galhardo, M.C.; Mochizuki, T.; Li, S. Global epidemiology of sporotrichosis. Med. Mycol. 2015, 53, 3–14. [Google Scholar] [CrossRef] [Green Version]
  233. Quintal, D. Sporotrichosis infection on mines of the Witwatersrand. J. Cutan. Med. Surg. 2000, 4, 51–54. [Google Scholar] [CrossRef]
  234. Govender, N.; Maphanga, T.G.; Zulu, T.G.; Patel, J.; Walaza, S.; Jacobs, C.; Ebonwu, J.I.; Ntuli, S.; Naicker, S.D.; Thomas, J. An Outbreak of Lymphocutaneous Sporotrichosis among Mine-Workers in South Africa. PLOS Negl. Trop. Dis. 2015, 9, e0004096. [Google Scholar] [CrossRef]
  235. Rasamoelina, T.; Maubon, D.; Raharolahy, O.; Razanakoto, H.; Rakotozandrindrainy, N.; Rakotomalala, F.A.; Bailly, S.; Sendrasoa, F.; Ranaivo, I.; Andrianarison, M.; et al. Sporotrichosis in the Highlands of Madagascar, 2013-20171. Emerg. Infect. Dis. 2019, 25, 1893–1902. [Google Scholar] [CrossRef]
  236. Lurie, H.I. Five unusual cases of sporotrichosis from South Africa showing lesions in muscles, bones, and viscera. Br. J. Surg. 1963, 50, 585–591. [Google Scholar] [CrossRef]
  237. Gadre, A.; Enbiale, W.; Andersen, L.K.; Coates, S.J. The effects of climate change on fungal diseases with cutaneous manifestations: A report from the International Society of Dermatology Climate Change Committee. J. Clim. Change Health 2022, 6, 100156. [Google Scholar] [CrossRef]
  238. Pijper, A.; Pullinger, B.D. An Outbreak of Sporotrichosis among South African Native Miners. Lancet 1927, 210, 914–915. [Google Scholar] [CrossRef]
  239. El-Mofty, A.M.; Nada, M. Sporotrichosis in Egypt. Brit. J. Derm. 1965, 77, 357–364. [Google Scholar] [CrossRef]
  240. Brandt, F.A.; Van Niekerk, V. A case of disseminating sporotrichosis from South Africa. Sabouraudia 1969, 7, 46–50. [Google Scholar] [CrossRef]
  241. Berson, S.D.; Brandt, F.A. Primary pulmonary sporotrichosis with unusual fungal morphology. Thorax 1977, 32, 505–508. [Google Scholar] [CrossRef] [Green Version]
  242. Gumaa, S.A. Sporotrichosis in Sudan. Trans R. Soc. Trop. Med. Hyg. 1978, 72, 637–640. [Google Scholar] [CrossRef]
  243. Ross, M.D.; Gelfand, M. Deep fungal infections in Rhodesia—A 10-year survey of histological material. Part, I. Cent. Afr. J. Med. 1978, 24, 208–212. [Google Scholar]
  244. Hull, P.R.; Vismer, H.F. Treatment of cutaneous sporotrichosis with terbinafine. Br. J. Dermatol. 1992, 126, 51–55. [Google Scholar] [CrossRef]
  245. Pönnighaus, M.; Grosser, S.; Baum, H.P.; Mischke, D.; Kowalzick, L. Sporotrichosis as the cause of a leg ulcer. Hautarzt 2002, 54, 64–66. [Google Scholar] [PubMed]
  246. Benchekroun, L.; Kabbaj, L.; El Kadi, M.A.; Ghfir, B.; Moustachi, A.; Senoussi, K.; Lyagoubi, M. Sporotrichose à Sporothrix schenckii: À propos d’une observation. J. Mycol. Med. 2008, 18, 43–45. [Google Scholar] [CrossRef]
  247. Patel, A.; Mudenda, V.; Lakhi, S.; Ngalamika, O. A 27-Year-Old Severely Immunosuppressed Female with Misleading Clinical Features of Disseminated Cutaneous Sporotrichosis. Case Rep. Derm. Med. 2016, 2016, 9403690. [Google Scholar] [CrossRef] [PubMed]
  248. Jacyk, W.K.; Lawande, R.V.; Tulpule, S.S. Deep mycoses in West Africa: A report of 13 cases and review of the Nigerian literature. J. Natl. Med. Assoc. 1981, 73, 251–256. [Google Scholar]
  249. Tshisevhe, V.; Skosana, L.; Motse, K.; Maphosa, T.; Mitton, B. Disseminated sporotrichosis in a person with human immunodeficiency virus disease. Access Microbiol. 2021, 3, 000262. [Google Scholar] [CrossRef]
Table 2. Prevalence of cryptococcal disease across Africa.
Table 2. Prevalence of cryptococcal disease across Africa.
Country Pub YearStudy DesignStudy
Study PopSample
CD4 Mean/
ART StatusCrAg
Prevalence (N°)
Prevalence (N°)
Togo 2017Retrospective
and descriptive
2006–2016 Hospitalized HIV
infected patients
802565 ± 2283% on ARTNA1.5 (102/8025)Wateba et al.,
Botswana 2019Cross sectional2000–2015Hospitalized patients with
2156091 (37–216)47% on ARTNA89(4432/5004)Tenforde et al.
Ghana 2011Retrospective 2008–2009Advanced HIV out-
9228 (8–54)Naïve 2 (2/92)NAMamoojee et
al. [78]
Ghana2022Cross sectional2020–2021Adult HIV-infected
1501049.1 (258.4–1480.6)52% on ART2.7% (4/150)100(3/3)Ocansey et al.
Ghana 2012Retrospective 2008–2010Patients suspected of
163NANANA11.7 (19)Owusu et al.
Sierra Leone2020Cohort 2018Adults HIV patients17045 (23–63)44% on ART4.7 (8/170)62.5 (5/8)Lakoh et al.
Senegal 2013Retrospective and
2004–2011Hospitalized patients
with meningitis
134227 (1–375)35.8% on ART
NA7.8 (106/1342)Sow et al.
Senegal 2016Cross sectional2009–2013Hospitalized adults
HIV patients
541102 ± 16533.5 on ART
9.2(50/541)34 (17/50)Manga et al.
Uganda 2013Cohort 2009–2010HIV positive patients56351 (16–171)18.4% on ART
5.7(32/563)NAAndama et al.
Uganda 2012Cross sectional2009–2010HIV infected adults36723 (9–51)NA19(69/367)6.5 (24/367)Oyella et al.
Mali2008Prospective 2001–2002Hospitalized patients
with meningitis
204NANANA8.3 (17/204)Oumar et al.
Mali 2011Prospective 2003–2004Hospitalized patients with
569NANANA2.5 (14/569)Minta et al. [13]
Kenya 2010Prospective and
2008–2009HIV suspected CM patient34041 (2–720)29.7% on ARTNA33 (111/340)Mdodo et al.
Mozambique 2020Retrospective 2018–2019Hospitalized HIV patients179579 (31–193)53.7% on ART7.5 (134/1795)71.6 (96/134)Deiss et al. [62]
Tanzania 2011Cohort 2009–2010HIV outpatients333209 (87–278)49.3% on ART5.1 (17/333)4.4 (15/333)Wajanga et al.
DRC2021Retrospective 2015–2017Hospitalized HIV patients4283168.7 ± 137.135.2 on ARTNA2.8 (108/4283)Katabwa et al.
DRC2020Descriptive 2011–2014Hospitalized HIV patients
with meningitis
26179 (66–105)NANA8.8 (23/261)Zono et al. [72]
DRC2021Retrospective and
2018Hospitalized HIV patients1877NANANA21.8 (409/1877)Ngoy et al. [75]
South Africa2015Retrospective 2009–2010HIV infected patients1494NANA2.1 (30/1460)NAGovender et al.
Ethiopia 2017Cross sectional2016–2017HIV infected patients267NA52% on ART3.4 (9/267)NAHailu et al.
Ethiopia 2019Cross sectional2017HIV infected patients183434.4 ± 286.3All on ART7.7 (14/183)NAGeda et al. [58]
Ethiopia 2021Cross sectional2019Hospitalized HIV patients140NA50% on ART11.43 (16/140)NAJemal et al. [57]
Ethiopia 2020Cross sectional2018–2019HIV infected outpatients20054 (2–97)73.5% on ART4 (8/200)NANegash et al.
Burkina Faso2012Retrospective 2002–2010Hospitalized patients with
512956 (13–387)NANA1.8(61/5129)Bamba et al.
Nigeria2016Cross sectional
and prospective
2012–2014HIV infected patients43274 (6–1264)Naïve 1.6 (7/432)NABologun et al.
Nigeria 2021Case controlNAHIV positive and HIV
Negative outpatients
342NANA8.5 (29/342)NAOdegbeni et
al. [51]
Nigeria 2021Cross sectional2017–2018Hospitalized patients
with meningitis
18432.5 (8–109)NANA16.8 (31/184)Okolo et al.
Nigeria 2016Retrospective, cross-
2004–2016HIV infected outpatients2752NANaïve 2.3 (63/2752)NAEzeanolue et al.
Nigeria2016Cross sectional2014–2015Adult HIV-infected
214160 (90–210)95.3% on ART8.9 (19/214)NAOladele et al.
Nigeria 2017Cross sectional2016HIV infected patients215NANaïve 16.7 (37/215)NAGoni et al.
Nigeria2020Cross sectional2014–2017HIV infected patients300NA NA19.67 (59/300)25.4(15/59)Ezenabike et al.
Nigeria 2017Cross sectional2016–2017HIV positive patients326NA81.3% on ART11 (36/326)NAMohammed et
al. [23]
Nigeria 2012Cross sectional2011HIV infected outpatients150NANaïve 12.7 (19/150)NAOsazuwa et al.
Nigeria 2019Cross sectional2018HIV infected patients290NANA1.4 (4/290)NAChukwuanukwu
et al. [38]
Nigeria 2010Cross sectionalNAHIV infected patients10089 ± 60NANA36 (36/100)Gomorep et al.
Cameroon 2018Cross sectional2015–2017HIV infected outpatients18644 (27–75)Naïve 23.1 (43/186)21.7 (5/23)Temfack et al. [55]
Cameroon 2013Cross sectional2004–2009Hospitalized HIV infected
67223 (10–61)NANA11.2 (75/672)Luma et al.
Cameroon2021Cross sectional2018HIV infected children147NA96.60 on ART6.12 (9/147)NAKalla et al. [67]
Cameroon 2015Cross sectional2009–2011HIV infected patients with
Signs of meningitis
146NANANA28.08 (41/146)Ngouana et al.
Cameroon 2020Retrospective and
2010–2018Hospitalized children with
33129 (10–100)NANA3.6 (12/331)Nguefack et al.
Cameroon 2012Cross sectional2010HIV positive patients105NANANA9.86 (29)Dzoyem et al.
NA: not available/not applicable.
Table 3. Observational studies and case series on histoplasmosis from Africa.
Table 3. Observational studies and case series on histoplasmosis from Africa.
CountryAuthorsStudy DesignNumber of Males/FemalesStudy Size/
AgeAffected SiteNumber of Cases (%)Diagnostic ToolIncidence
NigeriaOladele et al., 2022 [82]Cross-sectional377 males, 611 females988Median age-39-year-oldLungs, skin76 (7.7%)Histoplasma urinary antigen assay-
NigeriaEkeng et al., 2022 [80]Descriptive cross-sectional 114 males, 119 females213Mean age-39-year-oldLungs27 (12.7)Histoplasma urinary antigen test and/or PCR-
NigeriaLucas 1970 [91]Case seriesNS-10 months–65 yearsSkin, bones, subcutaneous-Histopathology-
GhanaOcansey et al., 2022 [12]Prospective cross-sectional 41 males, 109 females150Age range: 18–62NS5 (4.7)Histoplasma urinary antigen test, histopathology-
TanzaniaLofgren et al., 2012 [92]Retrospective323 males, 647 females970Median age: 31NS9 (0.9)Histoplasma antigen assay in serum and urine-
CameroonKuate et al., 2021 [81]Descriptive cross-sectional 37 males, 101 females138Mean age: 43.7Lungs, skin36 (26)Histoplasma urinary antigen test-
CameroonMandengue et al., 2015 [93]Cross-sectional studyNS56NSLungs, bronchus, skin7 (13)Histopathology-
Republic of CongoAmona et al., 2021 [94]Retrospective (Case series)30 males, 14 females, unclear in the remainder-Mean age-24 years, Median age 22 yearsSkin, lymph nodes, bones57Histopathology, Histoplasma antigen assay, Direct examination1–3 cases each year
TogoDarre et al., 2017 [95]Retrospective and descriptive11 males, 6 females-Mean age-27.2Skin, mucosa, bones, ganglion17Histopathology, Culture, Microscopy1.1
DRCPakasa et al., 2018 [96]Case series13 males, 23 females-Median age-20.5 yearsSkin, lymph nodes, bones36Histopathology, Immunohistochemistry, RT-PCR (n = 3)-
South AfricaKthali et al., 2021 [97]Retrospective and descriptive14 males, 10 females-Mean age-34.5, Median age-36.5 yearsSkin24Histopathology,
Culture, PCR
UgandaKwizera et al. [98]Retrospective- -Skin64 (9.2)Histopathology-
NS: Not stated.
Table 4. Cases of IA that have been reported from Africa.
Table 4. Cases of IA that have been reported from Africa.
AuthorsCountryStudy TypeSex/Age/
Number of Cases
Clinical PresentationComorbidityDiagnostic ToolAetiology Clinical TypesTreatmentOutcomes
Northern Africa
Bakhti et al. 2015 [107]AlgeriaCase reportF/7Subcutaneous abscess on the chest and right arm, seizure, intracranial hypertensionChronic granulomatous diseaseSerology, Histopathology, CT scanA. nidulansInvasive disseminated aspergillosis with intracranial localizationVRZ D
Trabelsi et al. 2013 [108]TunisiaCase seriesM/48Fever, repeated pneumopathyRenal transplant recipients, CMV, DM, broad spectrum antibiotics, renal failureSerum galactomannan assay, CT scan, A. terreusIPAVRZFv
M/41Fever, cough, dyspnoeaRenal transplant recipient, CMV, broad spectrum antibiotics, renal failureSerum galactomannan assay, CT scan, CXRA. flavusAMB, VRZD
El Hakkouni et al. 2018 [109]MoroccoCase reportM/44Cough, bloody diarrhoeaHIVCT scanA. fumigatusIPANSD
El-Sayed et al. 2012 [110]EgyptProspective N = 30.
F (n = 9), M (n = 21)
3 mths to 14 years
Fever (n = 27), bronchopneumonia (n = 3)SCID (n = 2), neutropenia (n = 4), broad spectrum antibioticsPCR-IPA (n = 6)NSNS
Gheith 2014 et al. [111]Tunisia Prospective N = 175
1–65 years
Cough, chest pain, haemoptysisNeutropenia secondary to haematological malignanciesCulture (n = 23), CT scan (n = 11), Serum galactomannan assay (n = 23), PCRA. niger, A. tubingensis, A. flavus, A. westerdijkiae, A. fumigatus, A. nidulans(n = 23)
IPA, Invasive ethmoiditis
with periorbital
AMB, VRC or bothD (n = 14)
Hadrich et al. 2020 [112]Tunisia Prospectiven = 105
F (n = 13), M (n = 16)
NSAML (n = 45), ALL (n = 35), medullar aplasia (n = 15), other diseases (n = 10)Culture, CT scan (n = 18), Serum galactomannan assay (n = 29)A. flavus, A. fumigatus, A. niger, A. ochraceus, Aspergillus speciesIPA (n = 29)NSD (n = 20), Fv (n = 9)
Eastern Africa
Ahmed et al. 2018 [113]SudanCase seriesF/9Proptosis, nasal obstruction, headacheNSSerology, Histopathology, CT scan and MRIA. flavusInvasive rhinosinusitis with orbital extension Surgery, ITC, and nasal sprayNS
F/10NSHistopathology. MRI, CT scanA. flavusInvasive rhinosinusitis with orbital extensionITC, nasal spray, SurgeryNS
M/8NSHistopathology, CT scan and MRI A. flavusInvasive rhinosinusitis with orbital extensionITC, surgeryNS
M/9NSHistopathology, CT scan, MRI, Serology A. flavusInvasive rhinosinusitis with orbital extensionSurgery, ITC, nasal sprayNS
Kwizera et al. 2020 [98]Uganda RetrospectiveN = 23NSBronchiectasis (n = 2), HIV (n = 2), anti-koch’s (n = 1)Histopathology *NSIPA (n = 8) NSNS
West Africa
Onyekonwu et al. 2005 [114]NigeriaCase report
F/60Nasal blockage, discharge, proptosis, seizure-CT scanAspergillus speciesSino-orbital aspergillosis with CNS complicationSurgery, ketoD
Aleksenko et al. 2006 [115]Ghana Case report M/20Fever, generalized body pain, ascending stiffness, headache, chest pain, cough, vomiting, diarrhoea, difficulty in breathingAntibioticsHistopathology *Aspergillus speciesDisseminated IANTD
Southern Africa
Wong et al. 2012 [116]South AfricaProspective(n = 39) F = 19, M = 20. Age-range 32–40 yearsWeakness, fever, LAD, pancytopeniaHodgkin lymphoma, HIVHistopathology *ND IPA (n = 1) NT D
F, Female; M, Male; Fv, Favourable; D, Death; NS, not specified/not stated; *, post-mortem; IPA, invasive pulmonary aspergillosis; CT, computed tomography; MRI, magnetic resonance imaging; ITC, itraconazole; AMB, amphotericin B; Keto, ketoconazole; VRZ, voriconazole; NT, not treated; ND, not done; mths, months; AML, acute myeloid leukaemia; ALL, acute lymphoblastic leukaemia; HIV, Human immunodeficiency virus; CMV, cytomegalovirus; CR, case report; LAD, lymphadenopathy; SCID, severe combined immunodeficiency; DM, diabetic mellitus.
Table 5. Published cases of candidaemia in Africa.
Table 5. Published cases of candidaemia in Africa.
CountryYearNumber of CasesAetiologyDiagnostic ToolTreatmentOutcomesAuthors
South Africa20171C. aurisBlood cultureamphotericin B (n = 1)Death (n = 1)Lockhart et al.[132]
South Africa2020108C. albicans (n = 51), C. glabrata (n = 32), C. parapsilosis (n = 11), C. tropicalis (n = 5), Others (n = 9)Blood cultureNone (n = 31)
Fluconazole resistance
C. glabrata (n = 35)
C. krusei (n = 3)
Death (n = 59)Hussain et al.
South Africa201848C. kruseiBlood cultureAntifungal therapy (n = 37)
Fluconazole and amphotericin B (n = 3)
Fluconazole only (n = 1)
amphotericin B (n = 2)
Death (n = 7)Van Schalkwyk et al.
South Africa20162172C. albicans (n = 517), C.parapsilosis (n = 488), C. glabrata (n = 100), C. tropicalis (n = 54) and C.krusei (n = 22)Blood culture--Naicker et al.
South Africa20212996C. parapsilosis (42%),
C. albicans (36%)
Blood cultureFluconazole alone (32%)
amphotericin B alone (35%)
amphotericin B and Fluconazole (30%)
-Shuping et al.[138]
Algeria202066C. tropicalis (n = 19)
C. parapsilosis (n = 18)
C. albicans (n = 18)
C. glabarata (n = 6)
C. dubliniensis (n = 1)
Blood cultureFluconazole (n = 12)
Caspofungin (n = 7)
amphotericin B (n = 3)
None (n = 21)
Dead (n = 21)Megri et al
Kenya2019224C. auris (n = 77)
C. albicans (n = 50)
Other (n = 74)
Blood culture-Death (n = 28)Adam et al.
South Africa2013268C. albicans (n = 123),C. parapsilosis (n = 67), C. glabrata (n = 58), C. krusei (n = 9), C. tropicalis (n = 9), C. guilliermondii (n = 1) C. lustitaniae (n = 1).Blood culture-Death (n = 122)Kreusch et al.
Egypt201336C. albicans (n = 3)
Non-albicans Candida (n = 2), others were not specified
Blood culture, Seminested PCR-Death (n = 17)
Ramy et al.
South Africa20196669C. parapsilosis (n = 2600) C. albicans (n = 1353), C. auris (n = 794), C. glabarata (n = 598), C. tropicalis (n = 140)
C. krusei (n = 98)
Mixed cases (C.auris and a non-auris species) (n = 29)
Blood culture--Van Schalkwyk et al. [145]
Nigeria201727C. albicans (n = 21), C.krusei (n = 2)
Others (n = 4)
Blood cultureFluconazole (n = 27)Death (n = 5)Ezenwa et al. [142]
South Africa202245C. auris (n = 45)Blood cultureamphotericin B
Death (n = 19)Parak et al. [135]
Egypt201488C. albicans (40%)
C. parapsilosis (25%), C. tropicalis (17%), C. glabarata (8%)
Blood culture-Death (16.7%)Hegazi et al. [139]
Tunisia2011130C. tropicalis (37.7%), C. albicans (22.3%), C. glabrata (19.2%), C. parapsilosis (12.2%).Blood culture--Sellami et al. [146]
South Africa2022618C. albicans (n = 193), C. parapsilosis (n = 82), C. auris (n = 72), C. glabarata (n = 21), C. krusei (n = 54)Blood culture--Chibabhai et al. [137]
Tunisia20124C. albicans (n = 3)
C. parapsilosis (n = 1)
C. krusei (n = 1)
C. tropicalis (n = 1)
Blood culture, PCRFluconazole
and amphotericin B (n = 2)
Fluconazole and Voriconazole (n = 1)
Death (n = 2)Saghrouni et al. [147]
Table 6. Published cases of Mucormycosis in Africa.
Table 6. Published cases of Mucormycosis in Africa.
AuthorsCountryNumber of Males/FemalesNumber of CasesMean AgeClinical Type Diagnostic ToolOutcomes
Elmahallawy et al. 2005 [157]Egypt4 males
1 female
57.1Rhinocerebral and pulmonary mucormycosisHistopathology,
3 Death
1 Survival
Bodenstein et al. 1993 [158]South Africa3 males
4 females
7NSRhinocerebral mucormycosisHistopathology4 Death
3 Survivals
Hauman et al. [151]South Africa2 females27.4Orofacial mucormycosisMicroscopy1 Death
1 NS
Zaki et al. 1989 [152]Egypt8 males
2 females
1 Death
9 survivals
Alfishaway et al. 2021 [159]Egypt14 males
7 females
2153.8Rhinocerebral and pulmonary mucomycosisMicroscopy,
7 Death
14 survivals
Alloush et al. 2022 [160]Egypt9 males
5 females
Microscopy3 Death
11 survivals
Anane et al. 2009 [161]Tunisia8 males
9 females
17NSRhinocerebral mucormycosisMicroscopy11 Death
6 Survival
Thomson et al. 1991 [162]South AfricaNS20NSGastointestinal mucormycosisHistopathology7 Death
13 Survival
Kahn et al. 1963 [163]South Africa6 males
10 females
1622Gastric and abdominal mucormycosisHistopathologyNS
Feki et al. 2018 [164[Tunisia3 males366Pulmonary mucormycosisHistopathology,
3 survivals
Madeney et al. 2017 [165]EgyptNS458Rhinocerebral and gastrointestinal mucormycosisHistopathology,
15 Death
30 survivals
NS: Not stated.
Table 9. Studies published on Blastomycosis in Africa.
Table 9. Studies published on Blastomycosis in Africa.
CountryClinical TypeNumber of CasesAffected siteAetiologyDiagnostic ToolTreatmentOutcomesYearAuthors
South Africa
Cutaneous (n = 4), Subcutaneous (n = 1), Pulmonary (n = 3), Vertebral (n = 1), Multisystem (n = 6)20
-B. persursus, B. emzantsiHistopathology,
Culture, Microscopy,
Voriconazole, posaconazole, itraconazole, amphotericin B and micafunginDeath (n = 5), Favourable (n = 5),
Unknown (n = 10)
2020Maphanga et al. [198]
TunisiaPulmonary, Subcutaneous disease1Right and left Lungs,
Left paravertebral swelling around T10
B. dermatitidisCulture,
ItraconazoleFavourable2020Abdallah et al. [194]
South AfricaCutaneous disease1Scalp, Face, NeckB. dermatitidisHistopathology,
ItraconazoleFavourable2012Motswaledi et al. [200]
MoroccoPulmonary, Vertebral disease1Left lung, VertebraB. dermatitidisRadiology,
KetoconazoleFavourable2012Rais et al. [204]
TunisiaCutaneous disease 2Right leg (patient 1),
Left knee and Left shoulder (patient 2)
B. dermatitidisHistopathology,
--2004El Euch et al. [199]
TunisiaCutaneous disease1Right legB. dematitisHistopathology,
Enzyme linked immunosorbent assay
ItraconazoleFavourable2017Ben Salem et al. [201]
TunisiaCutaneous disease 3Right cheek (patient 1),
Left cheek (Patient 2),
Right iliac fossa
-Histopathology, Culture
KetoconazoleFavourable2006Ferchichi et al. [202]
TunisiaPulmonary, Vertebral disease1Right lower limb,
Right lung
B. dermatitidisHistopathology,
ItraconazoleFavourable2008Cheikh Rouhou et al. [205]
TanzaniaPulmonary, Cutaneous disease1Lung, Nose, Right hand and right forearm, Left buttock, Left upper armB. dermatitidisHistopathologyItraconazoleFavourable2006Alvarez et al. [206]
NigeriaPulmonary1Right LungB. dermatitidis-KetoconazoleFavourable2001Ibrahim et al. [207]
MoroccoCutaneous disease1ForearmB. dermatitidisHistopathology
-Death2007Harket et al. [203]
UgandaPulmonary, Cutaneous disease11Lower limbs (n = 7),
Upper limbs (n = 1),
Abdominal wall (n = 1)
B. dermatitidisHistopathology--2020Kwizera at al [98]
Table 10. Case studies on Coccidioidomycosis published in Africa.
Table 10. Case studies on Coccidioidomycosis published in Africa.
AuthorsYear CountryStudy TypeNumber of CasesSexAgeSymptomsDiagnosisTreatment
Yoo SD et al., 2020 [212]2020UgandaCase report1Male23haemoptysis and difficulty breathing, weight
loss and drenching sweats localized swellings on the extremities
HistopathologyIntravenous amphotericin B deoxycholate 0.7 mg/kg was given for 10 days daily and followed by oral itraconazole 200 mg/day
Kwizera et al. [98]2021UgandaRetrospective 4NSNSNSHistopathologyNS
NS: Not stated.
Table 11. Published cases of chromoblastomycosis in Africa.
Table 11. Published cases of chromoblastomycosis in Africa.
YearCountryClinical ManifestationsNo. of CasesAetiologyDiagnostic ToolTreatmentOutcomesAuthors
2021AfricaCutaneous lesions1875Fonsecaea spp.,
Cladophialophora spp.,
Phialophora spp.
Microscopy, Histopathology, Culture, PCR Surgical excision, Itraconazole, Fluconazole, Terbinafine, Ketoconazole, -Santos et al. [229]
2020MadagascarCutaneous lesions50Fonsecaea spp., Cladophialophora spp.Microscopy, Histopathology, PCR, MALDI-TOF ItraconazoleFavourableRasamoelina et al. [227]
2021EthiopiaCutaneous lesions12-Microscopy, Histopathology --Abate et al. [226]
2020Uganda-34-Histopathology--Kwizera et al. [98]
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Bongomin, F.; Ekeng, B.E.; Kibone, W.; Nsenga, L.; Olum, R.; Itam-Eyo, A.; Kuate, M.P.N.; Pebolo, F.P.; Davies, A.A.; Manga, M.; et al. Invasive Fungal Diseases in Africa: A Critical Literature Review. J. Fungi 2022, 8, 1236.

AMA Style

Bongomin F, Ekeng BE, Kibone W, Nsenga L, Olum R, Itam-Eyo A, Kuate MPN, Pebolo FP, Davies AA, Manga M, et al. Invasive Fungal Diseases in Africa: A Critical Literature Review. Journal of Fungi. 2022; 8(12):1236.

Chicago/Turabian Style

Bongomin, Felix, Bassey E. Ekeng, Winnie Kibone, Lauryn Nsenga, Ronald Olum, Asa Itam-Eyo, Marius Paulin Ngouanom Kuate, Francis Pebalo Pebolo, Adeyinka A. Davies, Musa Manga, and et al. 2022. "Invasive Fungal Diseases in Africa: A Critical Literature Review" Journal of Fungi 8, no. 12: 1236.

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop