Haemophilus ducreyi drives a prolonged childhood ulcer outbreak in Sierra Leone
A cutaneous ulcer outbreak that began in Kayassie, Safroko Limba Chiefdom, in late October 2025 has been traced to Haemophilus ducreyi, a bacterium better known for chancroid but increasingly recognized as a cause of nonvenereal skin ulcers in tropical regions. The outbreak primarily affected schoolchildren in Bombali District and expanded over several months, reaching 403 cases by February 10, 2026. Lesions were concentrated on the lower limbs and often appeared as irregular ulcers with dry, crusted bases rather than purulent drainage. Some children also had localized edema. The clinical picture was severe enough to prompt an early suspicion of Bacillus anthracis, a concern that shaped the first phase of the field response.
What emerged instead was a much more familiar pathogen for yaws-endemic settings, but one that still sits outside many clinicians’ first differential diagnosis. In a region where lower-extremity ulcers often trigger a yaws workup, this outbreak makes plain that H. ducreyi can move through school populations with little warning and present as a sustained cluster of apparently similar skin lesions.
Laboratory testing shifted the differential away from anthrax and yaws
The first seven skin swabs were tested by quantitative PCR targeting B. anthracis markers, including rpoB, pagA (pXO1), and capC (pXO2). All seven were negative for anthrax. Metagenomic sequencing on MinION then found H. ducreyi sequences in four of those seven samples, and no other relevant pathogen stood out. Real-time PCR confirmed H. ducreyi in all first seven swabs. Those initial results established a consistent microbiologic signal before the outbreak had even peaked.
The larger testing set strengthened that conclusion. Among 156 total swabs collected during the event, 96, or 61.5%, were positive for H. ducreyi. None showed DNA evidence of Treponema pallidum subsp. pertenue, subsp. pallidum, or subsp. endemicum by quantitative PCR. In practical terms, the outbreak behaved like a yaws-like ulcer cluster clinically, but molecular testing pointed elsewhere.
Genome sequencing tied the outbreak strains together
A subset of 22 swabs, including 12 H. ducreyi-positive and 10 negative specimens, underwent DNBSEQ-G99 sequencing. Metagenomic analysis again found no evidence of T. pallidum subsp. pertenue, and no other etiologic pathogen was linked to the ulcers. Across those specimens, the most abundant bacterial species were Staphylococcus aureus and Klebsiella pneumoniae, organisms that likely reflected colonization or secondary bacterial presence rather than the primary cause of disease.
The investigators also attempted culture. Sixty-one swabs were inoculated in the field onto Columbia blood agar base enriched with yeast extract, vancomycin, and rabbit blood, then incubated under microaerophilic conditions at 33°C for 96 hours. Only nine samples yielded H. ducreyi, a reminder of how fragile culture confirmation can be when transport temperature and carbon dioxide conditions are not ideal. Still, the isolates were enough to support full genome sequencing of nine strains. Phylogenetic analysis placed the Sierra Leone isolates in a cluster with strains from Ghana, where they separated into two clades.
The genetics matter because they reinforce a regional transmission pattern rather than a random assortment of unrelated skin infections. A shared cluster across countries in West Africa fits with prior work showing that H. ducreyi is a recurring cause of cutaneous ulcers in tropical, yaws-endemic settings.
The outbreak behaved like a low-fatality skin infection, not a systemic emergency
Despite the prolonged case count, the outbreak caused no fatalities and gradually resolved under enhanced surveillance and case management. Recovery was documented after treatment, with lesions improving over time rather than progressing to deeper invasive disease. This clinical course is important. H. ducreyi cutaneous infection can create substantial morbidity, school disruption, and diagnostic confusion without producing the kind of dramatic systemic toxicity that usually pushes an outbreak into the highest emergency tier.
The bedside challenge is still substantial. Lower-limb ulcers in children from endemic regions can point clinicians toward yaws, anthrax, traumatized insect bites, or mixed bacterial skin infection. A dry crust, irregular border, and localized edema do not reliably distinguish these entities. Molecular confirmation becomes decisive when syndromic appearance alone is misleading.
The source of infection remains unresolved
Investigators searched for a reservoir or environmental source by testing 60 saline-soaked fly samples, eight pond water samples, and tissue from two goats that died during the outbreak. None were positive for H. ducreyi. No clear source was identified, leaving the transmission pathway open. That uncertainty leaves public health teams with an operational problem: the outbreak agent is known, but the route sustaining child-to-child spread in the community is not.
The unresolved source is not a minor gap. Without it, control efforts rest mainly on surveillance, diagnosis, and treatment rather than on a precise interruption strategy. The field response did reduce transmission, but the reservoir question remains unanswered.
Sierra Leone’s history as a yaws-endemic country adds another layer to the interpretation. National eradication campaigns have been conducted in past decades, yet the region still appears vulnerable to nonvenereal ulcer syndromes that resemble yaws at first glance. In that setting, clinicians need to keep H. ducreyi in mind when a cluster of childhood leg ulcers emerges, even when the first assumption points elsewhere.
Clinical recognition now matters as much as outbreak response
This investigation shows how easily a cutaneous ulcer outbreak can be misclassified at the start, especially in a pediatric cluster with lower-limb lesions and limited local laboratory capacity. The combination of PCR, metagenomics, and culture provided a layered diagnostic approach, and the final answer was consistent across platforms: H. ducreyi was the causative agent in the Bombali District outbreak.
For clinicians working in yaws-endemic regions, the practical message is direct. A child with a chronic or clustered lower-extremity ulcer is not automatically a yaws case, and anthrax is not the only feared diagnosis when lesions spread through a school community. Molecular testing can separate these entities early, avoid misdirected control measures, and clarify when a nonvenereal skin pathogen is driving the outbreak.