Australia’s diphtheria outbreak shows why boosters, antibiotics, and better housing all matter

By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Jun 15 2026

A 131-case outbreak reveals how a vaccine-preventable disease regained a foothold in the Northern Territory, exposing the urgent need for booster vaccination, rapid treatment, genomic surveillance, and better housing.

Study: Diphtheria outbreak, Northern Territory of Australia, 2025 to 2026. Image Credit: Chatchouliya / Shutterstock

In a recent study published in the journal Eurosurveillance, a group of researchers investigated the epidemiology, laboratory characteristics, genomic features, and public health response associated with the 2025-2026 diphtheria outbreak in Australia’s Northern Territory.

Background

Although diphtheria vaccination coverage among 5-year-old children in the Northern Territory is high, outbreaks continue to emerge worldwide, reminding public health authorities that vaccine-preventable diseases can return under the right conditions.

Diphtheria is caused by toxigenic corynebacteria, usually Corynebacterium diphtheriae and less commonly Corynebacterium ulcerans. It can lead to severe respiratory illness, heart damage, and death. It spreads through respiratory droplets or contact with wound exudate, and crowded living conditions, limited healthcare access, and socioeconomic disadvantage can facilitate transmission even in highly vaccinated populations.

Understanding how environmental and social factors influence disease spread remains essential. Effective control requires vaccination, early antibiotic treatment, contact tracing, laboratory surveillance, and action on the social conditions that enable transmission.

About the study

Researchers investigated all notified diphtheria cases reported in the Northern Territory of Australia between January 2025 and April 2026. A confirmed case required isolation of toxigenic Corynebacterium diphtheriae or Corynebacterium ulcerans from a clinically relevant respiratory or skin specimen together with compatible symptoms.

Researchers collected and analyzed epidemiological data, including vaccination history and clinical information, and cross-referenced these variables against the geographic distribution of diphtheria using routine health department data.

Laboratory analyses were performed by Territory Pathology. Wound and throat specimens were cultured on selective media, and bacterial colonies suspected to be Corynebacterium species were identified using mass spectrometry. DNA was isolated from each isolate, and quantitative polymerase chain reaction (qPCR) was used to detect the diphtheria toxin gene. The gradient diffusion strip method (GDS) was used to test antimicrobial susceptibility to a range of commonly used antibiotics.

Whole-genome sequencing of 19 toxin-positive cutaneous isolates was conducted to examine the genomic characteristics of circulating strains. Sequence quality was examined prior to further analysis. Investigators used multilocus sequence typing, screening for antimicrobial resistance, identification of virulence genes, and single-nucleotide polymorphisms (SNPs) to confirm the genetic characteristics of the toxin-positive isolates.

Phylogenetic methods were used to compare Northern Territory isolates with publicly available genomes from Queensland, Papua New Guinea, and the Solomon Islands. Time-calibrated evolutionary analyses were performed to estimate evolutionary relationships among the outbreak strains.

Study results

Between January 2025 and April 2026, 131 diphtheria cases were identified in the Northern Territory. These included 97 cutaneous cases involving skin lesions and 34 respiratory cases. This was the first documented recurrence of locally acquired diphtheria in the Northern Territory in over 20 years, with cutaneous cases emerging in May 2025 and respiratory cases in March 2026.

The majority of reported cases were among Aboriginal Australians, who accounted for 125 of 131 notifications (approximately 95%). Respiratory infections were more common in Central Australia, whereas cutaneous infections predominated in the Top End region. The outbreak was ongoing as of 30 April 2026.

The majority of infections were relatively mild, likely due to high vaccination rates, but some severe infections were observed. There were 12 respiratory patients requiring hospitalization, 2 requiring admission to intensive care, and 1 adult died, most likely from myocarditis linked to the diphtheria toxin. The deceased adult had completed a childhood vaccination series but had not received a booster dose in the last 10 years. The majority of patients with severe respiratory infections either had no prior vaccination or had gone more than 10 years since receiving their last diphtheria-containing vaccine.

Respiratory symptoms commonly included sore throat, tonsillitis, fever, cough, pharyngitis, pharyngeal exudate, and swollen cervical lymph nodes. Only a small number of patients developed the classic pseudomembrane associated with severe diphtheria. These findings suggest that modern outbreaks may present differently from historical descriptions, making clinical recognition more challenging.

During the outbreak, there was also a substantial increase in the detection of toxin-positive Corynebacterium diphtheriae in cutaneous samples. Most positive skin samples originated from lesions on the lower limbs. Most tested cutaneous samples were polymicrobial, with co-isolated organisms including Staphylococcus aureus, Group A streptococcus, Arcanobacterium haemolyticum, and other bacterial species. This demonstrates the continued complexity of health-related challenges faced by the affected communities, although the researchers noted that the exact pathogenic role of toxigenic C. diphtheriae in polymicrobial skin lesions remains uncertain.

Testing on 76 isolates revealed that all were susceptible to erythromycin and susceptible to penicillin with increased exposure. The lack of detectable clinically relevant antimicrobial resistance supports the use of standard treatment regimens, and no major antimicrobial resistance genes were identified.

Based on genomic characterization, the dominant strain in the outbreak belonged to sequence type 381, and the Northern Territory isolates were genetically closely related but distinct from the Queensland strains isolated during previous outbreaks. The median genetic difference among local isolates was only three SNPs, indicating recent transmission. Time-scaled phylogenetic analysis suggested that the outbreak strain shared a common ancestor dating back to approximately 2017.

No significant resistance genes were found, and all 19 sequenced isolates carried the tox gene allele type 20. Five isolates were confirmed to produce toxin using the Elek immunoprecipitation assay at an overseas public health laboratory. National surveillance data further supported the finding that sequence type 381 was the dominant strain across multiple jurisdictions in Australia.

Conclusion

The findings show that diphtheria can re-emerge even in populations with high vaccination coverage when social and environmental conditions support transmission. Although vaccination appeared to reduce disease severity, it did not completely prevent infection or spread.

Aboriginal communities with overcrowded housing, poor skin health, and continued health inequities were disproportionately affected by the outbreak of diphtheria, while a dominant ST381 strain was responsible for most cases, and the strain was susceptible to the standard antibiotics used for treatment.

The researchers concluded that future outbreaks could be controlled and reduced through booster vaccination, early antibiotic treatment, contact tracing, judicious use of diphtheria antitoxin, genomic surveillance, collaboration with Aboriginal Community Controlled Health Organizations, and sustained improvements to housing, healthcare access, and education.

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