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A global chromoblastomycosis strategy and development of the global chromoblastomycosis working group [1]

['Dallas J. Smith', 'Mycotic Diseases Branch', 'Centers For Disease Control', 'Prevention', 'Atlanta', 'Georgia', 'United States Of America', 'Flávio Queiroz-Telles', 'Department Of Public Health', 'Federal University Of Paraná']

Date: 2024-12

These findings led to the formation of a Global Chromoblastomycosis Working Group to advance the scientific and programmatic work on chromoblastomycosis globally. Initial virtual meetings were held in February, April, and May 2024 with over 20 combined individuals from 12 countries on 6 continents. Members include those from government, academia, and international organizations including WHO.

The working group developed a global strategy proposal to meet the 2030 targets set forth by the WHO roadmap. This proposed strategy provides an in-depth discussion and steps needed to achieve the actions in the WHO roadmap and added additional actions to help in the global control of chromoblastomycosis. The strategy follows the 11 specific dimensions laid out in the WHO roadmap (Table 1).

Technical progress

Scientific understanding. Chromoblastomycosis is an implantation mycosis and is known to be acquired when fungi enter the skin after a traumatic transcutaneous injury. Melanized, filamentous fungi cause chromoblastomycosis and produce melanin in both reproductive and vegetative cells. Melanin may play a role in the virulence of chromoblastomycosis-causing fungi with potential mechanisms such as protection against proteolytic enzymes, protection against oxygen or nitrogen derivatives, or reduction of phagocytosis [9]. Melanin was shown to protect the transformation of hyphae and conidia into pigmented muriform bodies (sclerotic) with an increase in the thickness of the cell wall that provides a potentially resistance mechanism to host immune responses and antifungal drugs. Interestingly, melanin is extremely resistant to several physiochemical agents, including ultraviolet rays [11]. This phenomenon may help the chromoblastomycosis agents survive under the sun light in the environment. Chitin also plays a role in fungal structure and differentiation and may contribute to virulence and cell signaling [12]. Chromoblastomycosis can affect immunocompetent and immunosuppressed individuals, and better understanding the role of melanin, muriform cells, and chitin in fungal virulence can lead to novel therapeutic targets and clinical interventions. Certain genetic predisposing factors (e.g., HLA-A29, Card9) may interplay with melanin, muriform cells, and chitin for increased host-susceptibility and virulence and could be explored further to determine if infections may become more common in immunocompromised populations [13,14]. Most chromoblastomycosis-causing fungi have strong evidence to be climate-sensitive organisms [15]. Two of the most commonly reported genera have climate-niches, a finding supported by epidemiological data from Venezuela, Madagascar, and India; F. pedrosoi and F. nubica are commonly acquired in tropical regions while C. carrionii infections occur in more semiarid regions [4,16]. The impact of climate change could potentially restrict certain causative fungi while expanding niches for other fungi; further understanding of the impact of climate change is warranted. Increased severe weather events (e.g., hurricanes, flooding) from climate change can impact rates of chromoblastomycosis, and this association should be further studied for potential public health interventions [17,18]. In addition to climate change’s impact on chromoblastomycosis-causing fungi, further understanding of the natural history and reservoirs of these fungi can inform prevention and awareness raising efforts. Previous chromoblastomycosis infections or causative fungi have been associated with certain plants (e.g., thorns of Mimosa pudica, several species of the Palmacea family including Madagascar palm house plant, Jurubeba, Murta tree, Tucum tree, Vassourinha tree, Bacuri tree, and babassu coconut, and hydrocarbon-polluted environments such as wood treated with phenolic preservatives, toxic mine waste, oil-polluted soils) [19–24]. Even some injuries caused by animals like birds, insects’ stings, and snakes have been associated as the port of entry in some patients [9,19]. Some molecular environmental tests and metagenomics of soils and plants could be used to overcome culture drawbacks (e.g., difficult to isolate from environment) to elucidate differences in reservoirs of various chromoblastomycosis-causing fungi. Whole genome sequencing, if cultures are obtained, can help establish links between environmental isolates, ecological niches, and human infections [25,26]. Chromoblastomycosis can lead to tissue fibrosis, lymphedema, secondary bacterial infections, squamous cell carcinoma, ankylosis, ectropium, and other serious and debilitating complications. [9] Some of these complications seem to be associated with illness duration, severity of traumatic injury, and vegetating lesions; however, risk factors for and the overall magnitude of chromoblastomycosis complications are relatively unknown despite their severity [27,28].

Diagnostics. Diagnosis of chromoblastomycosis depends heavily on clinical expertise and access to direct mycological examination (e.g., potassium hydroxide preparation) or histopathology. Identification of muriform bodies provides a confirmed diagnosis, but it is dependent on obtaining a sample from a correct location on the lesion and having materials and technical expertise in microscopy [29]. With proper training, even in resource-limited settings, direct microscopy can elucidate a diagnosis with high sensitivity and can be a high-yield, low-cost public health intervention [7]. Dermoscopy may be able to improve identification of the most suitable locations (i.e., black dots within the verrucous plaques) on lesions to sample, but equipment is expensive, and its use has not been validated thoroughly [30]. A practical and low-cost method for collecting samples in the field could be the use of vinyl adhesive tape; this tape could be subsequently used for direct microscopy [31]. Development of a universally available, affordable method for easy visualization of muriform bodies could improve early identification of chromoblastomycosis and allow primary health care to diagnose and treat infections. Late diagnostic strategies, when muriform bodies or culture cannot be obtained, to detect refractory or relapsing infection after months of therapy are critical to develop to prevent further complications and quality of life problems. Previous research has been completed on the potential of serologic diagnosis and could be explored further to help establish a diagnosis of chromoblastomycosis and inform prevalence studies [32,33]. Antifungal resistance continues to emerge globally in a variety of fungi. Antifungal susceptibility testing (AFST) on chromoblastomycosis-causing fungi is rarely performed as the technology is often unavailable in areas where chromoblastomycosis occurs; however, the development of epidemiolocal cutoff values for common causative fungi can help monitor for rising minimum inhibitory concentrations (MICs) and potential treatment failure. One study demonstrated that MICs of sequential isolates of F. pedrosoi increased over time during treatment and may have contributed to microbiological resistance to itraconazole with some isolates resulting in a lack of clinical response [34]. Increased AFST can provide clues into reasons for treatment failure and inform change of therapy. Cultures may be difficult to obtain routinely from the slow growth of fungi and inaccessibility to culture supplies; programs to routinely perform surveillance on DNA to identify resistant genetic markers for causative fungi would improve clinical care and inform public health interventions.

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[1] Url: https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0012562

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