Author response:
The following is the authors’ response to the current reviews.
We again thank the editor and reviewers for their detailed attention to our work. In our previous revisions we endeavored to address the principal concerns raised by reviewers that we were capable of addressing. We recognize that asymptomatic pertussis transmission represents a particularly thorny area of epidemiology and public health, where multiple (and sometimes overlapping) mechanisms have been proffered even as empirical evidence remains thin, particularly in low-resource settings such as sub-Saharan Africa. A key finding of our work is that prospective surveillance in such a low-resource setting revealed abundant evidence of otherwise unobserved asymptomatic incidence. Moreover, as we note in our prior revisions, this finding is supported by recent work in South Africa and elsewhere (Kayina et al., 2015; Moosa et al., 2019, 2025). As such, we believe that further prospective surveillance in similar settings would be highly informative, a point that we have sought to emphasize in our present manuscript (and associated commentary).
While we broadly agree with many of the concerns raised by the reviewers, we believe that we are unable to significantly strengthen the present work through further revisions. We do, however, wish to respond to several points raised in these reviews. Of note, a reviewer raises the possibility of a "breakthrough strain" without reference to existing literature. We agree that we cannot test this hypothesis, and though it is not incompatible with our own findings, it is, however, not consistent with recent molecular surveillance in South Africa (Moosa et al., 2023). The reviewer also raises the potential of low adult vaccination coupled with recent reintroduction. This hypothesis relies on our investigation looking "at the right place and the right time", and further does not explain how immunologically naive adults would have escaped morbidity. We have adopted what we believe is a more parsimonious interpretation of our results (i.e., that asymptomatic infection represents evidence of previous immune exposure), though we agree that a more thorough exploration of this particular issue is warranted, particularly in light of our persistently colonized mothers. In addition, we have noted similar studies in sub-Saharan Africa that also found widespread evidence of asymptomatic pertussis, which we believe is inconsistent with a “right time, right place” interpretation.
A reviewer also pointed to the work of Warfel et al. (2014) and Althouse and Scarpino (2015). We are familiar with both of these studies and agree with their broad relevance to the field (our apologies for omitting Warfel et al.). The reviewer states that, "If the mechanism underlying the results in Zambia is that either WP or natural infection does not block transmission (in the absence of a breakthrough strain), that would upend many of the assumptions in pertussis research." Critically, we believe that our prospective field study of human patients in a real-world public health system complements previous research, including animal trials and simulation studies. Simply put, given that our study was unable to establish the prior vaccination or exposure status of participants, we do not claim to have shown evidence for transmission despite wP vaccination or prior infection.
Regarding Althouse & Scarpino (2015), we believe that, for the majority of readers, the most compelling analysis in their paper was the examination of genome sequences that pointed to substantial asymptomatic transmission in the US. This conclusion emerged from their population model, which required that “births” (representing transmission events) exceeded “deaths” (representing recovery of infectious individuals) in order to be consistent with the sequence data. Unfortunately, this paper does not provide a detailed explanation of their methods and data sources, nor is this work directly reproducible through, for example, an open-access code/data repository. We have explored the availability of US genome sequences over the time period of their study and were able to find only 36 sequences: 2 from the pre-vaccine era, 8 from the wP vaccine era, and 26 from the aP vaccine era. Given this notable imbalance in the number of sequences (and thus sequence diversity) that was biased in favour of the most recent time period, is it then surprising that the “birth rate” in their model had to exceed the “death rate” in order to match the genetic diversity in the data? Based on a careful inspection of this work, we do not consider its conclusions to represent a gold standard against which all subsequent studies should be judged. We also note that genomic surveillance and analysis of pertussis remains sparse relative to other fields, though recent works have added dramatically to the corpus of available sequences (Bridel et al., 2022).
Finally, we note that our previous revisions addressed several concerns raised in the present reviews. For example, we previously sought to address reviewers' about our presentation of the strength of our evidence. In this regard, we broadly agree with the reviewers, and we now state that our results "suggest that pertussis transmission occurs between minimally symptomatic mothers and their newborn infants." We believe this largely addresses a present reviewer's concern that 'the mother-to-infant transmission pathway should be framed as "highly suggestive" rather than "confirmed"'. We also note that our results examine three different threshold Ct values (survival analysis, Fig 4), a point that we believe partially addresses a reviewer's suggestion to "including a sensitivity analysis using a stricter cut-off" and concerns about "the decision to use a Ct<45 threshold, as this is higher than standard clinical cut-offs". Indeed, we discuss the issue of clinical cut-offs (and their appropriateness) at some length in the section, "Test reliability, disease surveillance, and public health where we state, "We recognize that such weak and potentially ambiguous signals may not be appropriate for clinical diagnosis. However, our results demonstrate that they nonetheless contain valuable information about pathogen presence and infection intensity that can (and should) be leveraged for disease surveillance." We have also included in the present work a detailed discussion of qPCR sensitivity and efficiency that we believe should interest others working in pertussis surveillance.
We do not view our own research as the "last word" in this rather controversial subject. In this spirit, we have attempted to present our work transparently, state our claims carefully, and underscore future activities that we believe would benefit the pertussis research community going forward. For example, we agree that further attention to shared exposure and functional immune data among low-resource communities could provide valuable insights into epidemiology and ecology of pertussis. However, we also believe the trade-offs of including one set of activities over another should be clearly acknowledged by researchers, clinicians, and public health officials. To simply state that we must measure more fails to account for the very real resource constraints that we all face.
Althouse, B. M., & Scarpino, S. V. (2015). Asymptomatic transmission and the resurgence of Bordetella pertussis. BMC Medicine, 1–12. https://doi.org/10.1186/s12916-015-0382-8
Bridel, S., Bouchez, V., Brancotte, B., Hauck, S., Armatys, N., Landier, A., Mühle, E., Guillot, S., Toubiana, J., Maiden, M. C. J., Jolley, K. A., & Brisse, S. (2022). A comprehensive resource for Bordetella genomic epidemiology and biodiversity studies. Nature Communications, 13(1), 3807. https://doi.org/10.1038/s41467-022-31517-8
Kayina, V., Kyobe, S., Katabazi, F. A., Kigozi, E., Okee, M., Odongkara, B., Babikako, H. M., Whalen, C. C., Joloba, M. L., Musoke, P. M., & others. (2015). Pertussis prevalence and its determinants among children with persistent cough in urban Uganda. PLoS One, 10(4), e0123240.
Moosa, F., du Plessis, M., Weigand, M. R., Peng, Y., Mogale, D., de Gouveia, L., Nunes, M. C., Madhi, S. A., Zar, H. J., Reubenson, G., & others. (2023). Genomic characterization of Bordetella pertussis in South Africa, 2015–2019. Microbial Genomics, 9(12), 001162.
Moosa, F., du Plessis, M., Wolter, N., Carrim, M., Cohen, C., von Mollendorf, C., Walaza, S., Tempia, S., Dawood, H., Variava, E., & others. (2019). Challenges and clinical relevance of molecular detection of Bordetella pertussis in South Africa. BMC Infectious Diseases, 19, 1–11.
Moosa, F., Kleynhans, J., Makhathini, L., du Plessis, M., Tempia, S., McMorrow, M. L., Moyes, J., Buys, A., Maake, L., Smit, S., & others. (2025). Bordetella pertussis infection and antibody dynamics in household cohorts in two South African communities, 2016–2018: Findings from the PHIRST study. Journal of Infection, 106550.
Warfel, J. M., Zimmerman, L. I., & Merkel, T. J. (2014). Acellular pertussis vaccines protect against disease but fail to prevent infection and transmission in a nonhuman primate model. Proceedings of the National Academy of Sciences, 111(2), 787–792. https://doi.org/10.1073/pnas.1314688110
The following is the authors’ response to the original reviews.
Public Reviews:
Reviewer #1 (Public review):
Summary:
The study investigates the role of asymptomatic pertussis carriage in transmission between mothers and their infants, in particular. The authors used a longitudinal cohort study that involved 1,315 mother-infant dyads in Lusaka, Zambia, and they utilized qPCR-based detection of IS481 to track Bordetella pertussis transmission over time. Insights from the study suggest that minimally symptomatic or asymptomatic mothers may act as a reservoir for B. pertussis transmission in the infants, thus challenging the traditional surveillance methods that focus on symptomatic cases. Additionally, the study also identified a subgroup of persistently colonized individuals where mothers were majorly asymptomatic despite sustained bacterial presence.
The authors aimed to improve comprehension of pertussis transmission dynamics in high-burden low-resource settings, and they advocated for enhanced molecular surveillance strategies to capture full pertussis infection, including those that might have gone undetected.
Strengths:
The strengths are the use of innovative study design, especially the longitudinal approach and routine sampling, rather than symptom-driven testing that minimizes bias in the study. The methodology was also rigorous and transparent by evaluating the IS481 signal strength to classify pertussis detection and conducting retesting to assess qPCR reliability. There were also important epidemiological insights, and the findings challenge the traditional wisdom by suggesting that pertussis transmission may frequently occur outside of symptomatic cases. The findings also showed its relevance to global health and policy by arguing for the incorporation of molecular tools like qPCR for surveillance of pertussis in low-resource settings.
Weaknesses:
These include reliability on qPCR-based detection without additional validation measures like confirmatory culture or serology. There are also potential alternate explanations for transmission patterns observed in the study such as shared environmental exposure or household transmission. Additionally, there is limited generalizability as the study was done in a single urban site in Zambia. There is also a lack of functional immune data.
Reviewer #2 (Public review):
Summary:
In this paper, the authors describe the results of a longitudinal study of pertussis infection in mother/infant dyads in Lusaka, Zambia. Unlike many past studies, the authors assessed the infection status of individuals independently of whether they were symptomatic for a respiratory infection. As a result, this work represents one of the first studies specifically designed to assess asymptomatic transmission of pertussis. Using qPCR, the authors find strong evidence for the role of asymptomatic transmission from mothers to infants and also evidence for long-term bacterial carriage. This work represents an important contribution to our understanding of the global burden of pertussis. Also, it highlights the still under-appreciated role of asymptomatic transmission across many infectious diseases (including vaccine-preventable ones).
Strengths:
Unlike many past studies, the authors assessed the infection status of individuals independently of whether they were symptomatic for a respiratory infection. As a result, this work represents one of the first studies specifically designed to assess asymptomatic transmission of pertussis. Using qPCR, the authors find strong evidence for the role of asymptomatic transmission from mothers to infants and also evidence for long-term bacterial carriage.
Weaknesses:
While I am quite enthusiastic about the work, I am concerned that a number of likely relevant confounders were not discussed and that the broader implications of their findings were not well grounded in the existing literature. For example, I could not find information on the vaccination status of the mothers in the study. Given the conclusions about asymptomatic transmission and the durability of immunity, it is important to know the vaccination status of the mothers. Moreover, did the authors have other metadata on the mother/infant dyads, e.g., household size, vaccination status of household members, etc.? Given the potential implications of more widespread asymptomatic transmission associated with pertussis infection, I believe the authors should better couch their results in the context of the broader debate around asymptomatic transmission.
We appreciate the reviewers' detailed feedback. We provide an overview of our responses here and we address specific recommendations below. In light of reviewers’ comments, we have revised our manuscript in order to improve the clarity of our presentation and to better situate our results within the context of the existing literature. Unfortunately, as the field study has been concluded, many of the reviewers’ recommendations are not possible. These include additional testing (i.e., culture or serology) or sequencing. We have updated the manuscript to more clearly indicate our knowledge regarding maternal vaccine status and immunological immunity of study participants. We have also provided a more comprehensive overview of existing pertussis studies, including genomic surveillance and details regarding sub-Saharan Africa and Zambia in particular. Finally, we have revised the formatting of Figure 4 (survival analysis) to more clearly highlight differences between mothers and infants and to better align with the text, and note that the underlying results are unchanged.
A particular concern raised in the reviews that we wish to address is the recommendation of culture- or serology-based tests as "confirmatory". We have revised the manuscript in light of this feedback to better reflect our own position on this matter. We believe these recommendations do not adequately account for important trade-offs between testing sensitivity and specificity that are widely recognized in both clinical practice and epidemiology (Enøe et al., 2000; Florkowski, 2008; Swift et al., 2020). When the results of different testing methodology disagree, rarely is one method, a priori, correct. Rather, the disagreement may point to specific test limitations or important biological questions about the study system.
In the case of pertussis detection, cell culture is recognized for its very low sensitivity, while serological detection is complicated by debate around appropriate threshold levels and time horizons for seroconversion and subsequent decay (Lee et al., 2018; van der Zee et al., 2015). Furthermore, while anti-PT antibodies are a common target of serological detection, these are not reliable correlates of protection (Mills, 2001; Wilk et al., 2019), nor are they reliably generated in response to colonization (de Cellès & Rohani, 2024; Graaf et al., 2020). Overall, the detailed relationship between exposure, carriage, transmissible infection, and the dynamics of anti-PT serology remains poorly characterized (Craig et al., 2020; de Cellès et al., 2025).
While we agree that these are important questions in epidemiology and public health, we nonetheless wish to highlight that there is no “free lunch": each additional test and protocol comes with additional cost and complexity that should be evaluated based on the specific goals of the intended surveillance. In our case, the repeated sampling of longitudinal surveillance serves as a low-cost "confirmatory" testing regime. We disagree that cell culture would have added value to the present study and would not recommend its addition to future studies (primarily due to low sensitivity). While we agree that before-and-after serology of mothers would have added important context to the present study, we nonetheless expect that significant ambiguity would have surrounded any such results (e.g., Moosa et al. (2025)).
One area that we strongly agree warrants further attention is the household dynamics in pertussis transmission, particularly in low-resource settings where crowding is common. In our study we were not able to rule out environmental and/or shared transmission events, though our survival analysis did demonstrate a greater impact of mothers on infants than vice versa, results which suggest a causal mechanistic role. In previous studies we detailed the demographics of household size, number of children, and mothers' age (Gill et al., 2021; Gunning et al., 2020), though we have not conducted formal analyses of these important covariates here. We also note that the code and data are freely available, allowing for others to build on our work.
We believe that future prospective studies are an invaluable tool for directly tracking pertussis disease transmission, including both community and household studies. We have argued here for the value of qPCR-based community surveillance, which could integrate into existing public health activities. Regarding household studies, we note that a key challenge in implementing these studies is selecting an appropriate sampling interval and duration to best capture epidemiological linkages. Our results suggest that qPCR-based real-time population-level surveillance could be used to initiate such a prospective household study during a pertussis outbreak so that a higher sampling frequency (e.g., weekly swabs) could be gainfully employed over a shorter time period.
Recommendations for the authors:
Reviewer #1 (Recommendations for the authors):
(1) Enhance Validation of qPCR Findings:
We address these comments above at greater length. We also note that the term “false positive” is rather ambiguous here, as we lack a clear distinction between carriage and transmissible infection. We note that our manuscript includes a considerable discussion of qPCR validation, including negative controls and sample retesting. We agree that test sensitivity and specificity remains an important question, and have endeavored to clearly indicate these concerns throughout the manuscript.
(2) Clarify Transmission Dynamics:
While we agree that this is an important question, we lack the relevant sequence data to test it. Notably, we suspect that any such phylodynamic linkage would require genomic sequencing due to the relatively low genetic diversity observed in pertussis (see, e.g., population-level estimates of time to most common ancestor in Lefranc et al., (2022). However, sequencing pertussis genomes remains resource-intensive, and we expect that the deployment of such sequencing at scale would be cost-prohibitive in low-resource settings.
We have revised our manuscript to underscore uncertainties around shared/household exposure. We also direct the reviewer’s attention to our survival analysis, where a notable asymmetry exists between mothers and infants. Here, mothers’ prior qPCR signals exhibit a larger impact on their infants than infants on their mothers (Fig 4). If shared exposure was the principal cause of the observed increase in hazard in ego from alter, then we would expect no such asymmetry between mothers and infants.
(3) Expand Discussion on Public Health Implications:
As noted above, we have revised our introduction and expanded our discussion to better account for the existing literature. And, while we are hesitant to put forward specific recommendations based on our study, we feel confident in stating that active pertussis surveillance in low-resource settings is A) almost entirely absent B) possible to achieve, and C) necessary to resolve long-standing questions about pertussis epidemiology at regional and national levels. We have endeavored to clarify these points, particularly within the discussion.
(4) Address the Role of Immunity More Directly:
While we lack such immune data, we have pointed to recent work from the notable PHIRST study in South Africa, as well as highlighted ambiguities surrounding these data.
Reviewer #1 (Recommendations for the authors):
(1) Do we know the vaccination status of the mothers in the study? … If these data are not available, I think that the paper must be re-framed to acknowledge that all the conclusions are statistical in nature, based on publicly available vaccine coverage data from Zambia.
We do not have information on the immunization status of mothers, though we cite national rates for Zambia across the relevant time period. We have clarified this point in the revised manuscript. We have endeavored to clearly acknowledge that many of our conclusions are statistical in nature and to clearly quantify the strength of evidence.
We strongly disagree that anomalously low vaccination rates amongst mothers (i.e., relative to national averages) would materially alter the interpretation of our findings.
Overall, our findings strongly suggest ongoing pertussis transmission in this population. Based on this, we expect that mothers in our study who were not vaccinated would likely have some degree of infection-derived immunity. Indeed, some have argued that the preponderance of mild/asymptomatic infections in mothers is, of itself, evidence of prior immunological exposure (Fine & Clarkson, 1982).
(2) Do we know anything about rates of pertussis in Zambia, especially in the study site?
We address this important question in the discussion. In particular, we state that: “As a populous, middle-income and primarily urban country, Zambia offers an evocative example of pertussis surveillance, where no cases have appeared in official WHO reports since 2009”.
(3) I couldn't find information in the paper related to the severity of infection in the infants. It's mentioned in the section describing results in Figure 5, but I only saw analyses with symptoms (as opposed to severe symptoms). Do you have outcome data from infants testing positive?
This question was addressed in more detail in our previous work (Gill et al., 2021), which we briefly summarize in the Introduction. We also show the frequency of severe symptoms in Fig 5 (bottom panel), and detail mild versus serious symptoms in our subgroup analysis (Fig 7D).
(4) Do we know anything about vaccine-resistant strains of pertussis in Zambia?
We are not aware of any such work. As we noted above (and now address in our Discussion), widespread genomic surveillance and microbiological characterization of pertussis are sorely lacking across Africa.
(5) While I believe sequencing is beyond the scope of the current study, the authors should comment on the potential utility of sequencing elements of the pertussis genome and use that to demonstrate causality and direction of transmission more strongly.
We believe that existing literature has addressed the potential of sequence data and phylodynamics to infer transmission, particularly for pathogens with high mutation rates such as RNA viruses. To date, research into the phylodynamics of pertussis has focused exclusively on population-level dynamics (Lefrancq et al., 2022), where estimates of time to most recent common ancestor (TMRCA) are long, indicating low genomic variability at the scale of countries and years. To our knowledge, no work on pertussis has directly inferred transmission chains from sequence data. Given the existing evidence, we expect that any such work would require genome-level sequencing, which would likely be cost-prohibitive in low-resource settings.
(6) … However, it would be helpful to understand more about how your results fit into the broader story around pertussis resurgence. … if the infant cases were all mild, they might never have been captured in surveillance data sets.
We believe that a key result of our study is the remarkable mismatch between country-level symptoms-based surveillance and prospective surveillance, which demonstrates that such mild cases have almost certainly not been captured. These findings are mirrored by recent work in South Africa (now addressed in our Discussion, see Moosa et al. (2025)). We believe that prospective surveillance, particularly in under-surveilled regions, is critical to understanding pertussis transmission writ large, which we have attempted to communicate throughout our discussion.
(7) Relatedly, if there are still high rates of asymptomatic mother-to-infant transmission with whole cell vaccination, then why is there an observed drop in infant pertussis following whole vaccination in most countries?
In previous work, we demonstrated that some infants in this cohort exhibited asymptomatic infection (Gill et al., 2021). We note that a drop in pertussis incidence amongst infants after the roll-out of the whole-cell vaccine is not contradictory with our findings. We want to clarify that our results, and evidence that mother-to-infant transmission can occur, does not imply that the whole-cell vaccine fails to protect against transmission.
We have previously used epidemiological evidence to infer the population-level impacts following the roll-out of whole-cell pertussis infant immunization. For example, we observed an increase in the inter-epidemic period that, together with the drop in infant cases, are consistent with a reduction in transmissible infections (Broutin et al., 2010; Rohani et al., 2000).
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