Early Release – Detection of Mycobacterium ulcerans DNA in African Fruit Bats, Cameroon, 2024 – Volume 32, Number 12—December 2026 – Emerging Infectious Diseases journal

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Figure. Number of annual human BU cases in study of Mycobacterium ulceransDNA in African fruit bats, Cameroon, 2024. Graph indicates the temporal evolution of Buruli ulcer incidence in Africa…

Buruli ulcer, caused by Mycobacterium ulcerans, remains endemic in West and Central Africa, although case numbers have declined markedly (1). In Akonolinga, Cameroon, the number of Buruli ulcer cases fell by ≈80% after 2011 (Figure), and M. ulcerans DNA, detected in aquatic invertebrates from the Nyong River in 2008 and 2012, was undetectable at the same sites in 2024 (2,3). In Australia, possums are established mammal reservoirs of M. ulcerans (4). Experimentally infected fruit bats can also recover from M. ulcerans lesions (5). Moreover, several fruit bat lineages have altered or lost G protein–coupled receptor 84 (GPR84), which was recently linked to reduced disease severity (6,7). Those observations prompted us to investigate M. ulcerans in fruit bats in Akonolinga, Cameroon.

In June 2024, we sampled fruit bats and aquatic macroinvertebrates at sites along the Nyong River previously investigated for M. ulcerans (2) (Appendix Figure 1). We captured fruit bats with mist nets, identified them morphologically, and collected oral and rectal swab samples before release (Appendix Figure 2). We collected aquatic macroinvertebrates, as previously described (2), and pooled them according to taxonomic groups.

We extracted DNA and performed quantitative PCR, as previously described (2). We screened samples for insertion sequence (IS)2404 and the ketoreductase (KR) B domain of mycolactone polyketide synthase. We considered samples to be positive when we detected both IS2404 and KR with PCR quantification cycle (Cq) values of Appendix).

We captured 46 fruit bats comprising 5 taxa: Eidolon helvum (n = 24), Epomops franqueti (n = 10), Micropteropus sp. (n = 5), Hypsignathus monstrosus (n = 4), and Nanonycteris sp. (n = 3) (Table; Appendix Table 1, Figure 2). None of the bats had cutaneous lesions compatible with Buruli ulcer. Two (4.2%) bat samples tested positive for M. ulcerans DNA: 1 rectal swab sample from an adult female Micropteropus sp. bat (IS2404 Cq = 28.8; KR Cq = 33.3) and 1 oral swab sample from a juvenile male E. helvum bat (IS2404 Cq = 33.85; KR Cq = 35.76) (Table; Appendix Table 1).

We collected 413 aquatic macroinvertebrates from previously investigated sites (2,3) and grouped them into 111 taxonomically homogeneous pools as follows: 50 Heteroptera pools (179 specimens), 42 Coleoptera pools (180 specimens), 11 Araneae pools (35 specimens), and 8 Odonata pools (19 specimens) (Table; Appendix Table 2, Figure 3). All pools tested negative for M. ulcerans DNA (Table; Appendix Table 2), whereas previous surveys at those sites detected M. ulcerans DNA in ≈5%–10% of aquatic invertebrate samples (2,3). All negative controls remained negative, positive controls amplified as expected, and we did not detect PCR inhibition.

Together, M. ulcerans DNA detection in 2 clinically healthy fruit bats and the absence of detectable DNA in aquatic macroinvertebrates from previously positive sites (2,3) suggest a change in the ecologic context of residual Buruli ulcer transmission in Akonolinga. Our findings do not establish bats as reservoir hosts or demonstrate bacterial viability or transmission. Detection of M. ulcerans in oral and rectal samples could reflect transient exposure through food or water, digestive passage, or more persistent carriage. Because both M. ulcerans–positive bats belonged to frugivorous taxa, the ingestion of contaminated fruits or other plant material cannot be excluded. That possibility is biologically plausible, because plant-derived carbohydrates, particularly glucose polymers, can stimulate M. ulcerans growth in vitro (8). Longitudinal fecal sampling, together with investigation of dietary and environmental sources, could help distinguish exposure from carriage.

M. ulcerans DNA has been detected in lesions from terrestrial mammals in West Africa (9). The absence of visible lesions in fruit bats from Akonolinga is compatible with experimental observations showing that fruit bats can recover from M. ulcerans lesions (5). The absence of lesions is also consistent with our recent findings showing that GPR84 influences disease outcome and is consistent with reports that several fruit bat lineages have altered or lost that receptor (6,7). Those observations provide a biologic rationale for investigating fruit bats as potential permissive hosts, although a role for GPR84 in natural carriage has not been demonstrated.

If fruit bats contribute to M. ulcerans carriage, their high mobility could promote bacterial dissemination among distant environments. That possibility is consistent with a molecular epidemiologic study that reported identical or closely related M. ulcerans genotypes across geographically separated disease endemic regions (10).

An epidemiologic and ecologic shift similar to our findings was recently observed in Benin; ≈80% decline in Buruli ulcer incidence and aging of the affected population coincided with the disappearance of M. ulcerans DNA from previously positive aquatic environments (1). The changing profile resembles that observed in Australia, where Buruli ulcer predominantly affects adults, and mammals are clearly implicated in M. ulcerans ecology. The contributions of aquatic and nonaquatic ecologic compartments to M. ulcerans persistence in Akonolinga appear to change over time. Therefore, broader longitudinal surveillance of M. ulcerans circulation in Cameroon and Africa will be needed.

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