Yes, it matters who is spreading monkeypox.

Schneider and Eichner posed an important question when discussing the increased transmissibility of the monkeypox outbreak—“Does it matter who is spreading monkeypox?”. The authors argue that such knowledge is largely irrelevant, stating, “Whether this change [in transmissibility] was due to mutations in the virus or due to a different type and frequency of contacts is interesting, but not necessarily relevant when contemplating how to stop the outbreak.”

Understanding the mechanisms behind such increased transmissibility is a basic principle in infectious disease epidemiology and remains crucial to inform an optimal outbreak response. The authors point out the need for improved contemporary estimates of the basic reproductive number (R 0), particularly given historical estimates have been informed by populations partially protected by smallpox vaccinations. However, for many infectious diseases, R 0 poorly characterises the distribution of secondary infections caused by an infectious host, which is often heavily skewed.2, 3, 4 Quantifying such individual-level transmission heterogeneity, classically quantified as the parameter k, is crucial in understanding the epidemiology and trajectory of an outbreak. A smaller k value suggests increased heterogeneity, resulting in rare but explosive outbreaks; as k increases, transmission becomes more uniform.

The authors' argument that underlying mechanisms driving increased transmissibility can be ignored is demonstrably flawed. For a given R 0, the proportion of infectious cases driving secondary transmission and can vary widely depending on the degree of individual heterogeneity (k; figure ). These relationships hold when varying the value of R 0 (appendix). Moreover, substantial individual-level heterogeneity might result in a large number of transmission events occurring despite a declining epidemic (R 0<1). Such emergent heterogeneity has been observed in other infectious diseases and suggests an effective response to the current monkeypox outbreak is not as simple as reducing the effective reproductive number to lower than 1·0, as the authors state.

Figure

Examining the influence of individual-level transmission heterogeneity

A) Expected proportion of tuberculosis transmission attributed to a given proportion of infectious cases. B) Probability of observing an outbreak of size Y. Value of R0=3 chosen from Schneider and Eichner; values for k were arbitrarily chosen.

Substantial morbidity can be avoided with targeted, informed interventions accurately incorporating the transmission dynamics of the current outbreak. These interventions require an understanding of where, and among whom, monkeypox is spreading. Knowing if the observed increase in transmissibility is attributed to a factor that increases transmissibility uniformly across the population (ie, a mutation) or to an increased number of transmission events in a high-risk subset is essential public health information. In addition to the authors' call for improved estimates of R 0, quantifying and understanding the source of potential individual-level heterogeneity is essential to monitoring and characterising the risk of this emerging outbreak.

I declare no competing interests.