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Temporal dynamics & determinants of antibiotic resistance gene profiles in the infant gut during the first year of life
For correspondence: Dr Mamatha Ballal, Enteric Diseases Division, Department of Microbiology, Kasturba Medical College, Manipal Academy of Higher Education, Manipal 576 104, Karnataka, Indiae-mail: mamatha.ballal@manipal.edu
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Received: ,
Accepted: ,
Abstract
Background & objectives
To evaluate the progressive changes in the antibiotic resistance gene (ARG) profile by investigating their presence at different time points in the gut of infants during early life.
Methods
Stool samples of 54 full-term healthy infants at birth at 6, 14, and 36 wk were processed to examine the presence of 20 antibiotic-resistance genes. McNemar’s test was used to check the statistical significance of the change in prevalence of genes across various time points. Chi-square test and logical regression were performed to evaluate the influence of clinical and demographic factors on the carriage of ARGs during early life.
Results
Infants predominantly carried genes that conferred resistance to beta-lactams (80.6%), macrolides (MSLB) (70%), and the sulphonamide (61%) class of antibiotics. ARG carriage peaked at 6 wk and 14 wk with a significant increase in the proportion of genes like blaTEM, catB, oqxA, sul1, ermB, tet, blaSHV (P: <0.05) from birth to 6 wk. Caesarean-section [P = 0.001; odds ratio (OR): 6.93; confidence interval (CI): 2.06-23.26] and maternal exposure to cephalosporins postpartum (P value = 0.013; OR: 4.16; CI: 1.31-13.17) had a significant influence on the increased carriage of the blaCTX-M gene at 6 wk of life.
Interpretation & conclusions
Our findings demonstrate that infants carry a diverse range of ARGs, with peak prevalence observed at 6 and 14 wk. Delivery mode and maternal antibiotic exposure significantly impact ARG carriage, emphasising the need for targeted interventions to reduce antibiotic resistance in early life.
Keywords
Antibiotic resistance genes
blaCTX-M
gut microbiota
infant
resistome
The escalating threat of antimicrobial resistance (AMR) has emerged as a critical global health crisis, responsible for millions of deaths annually and requiring urgent, coordinated strategies to mitigate its impact1. A key contributor to this crisis is the human gut, which serves as a major reservoir for antibiotic resistance genes (ARGs), facilitating their transmission across bacterial species and shaping the broader AMR landscape2. Understanding its dynamics is crucial, particularly from a One Health perspective, as it links human, animal, and environmental health systems.
The gut resistome consists of two main components: the resident resistome, comprising ARGs in commensal bacteria, and the transitory resistome, carried by transient species capable of horizontal gene transfer3. Studies have shown that the gut resistome establishes as early as the first week of life, even without direct antibiotic exposure4-6. ARGs for beta-lactamase (e.g., TEM, CTX-M, SHV, CMY, KPC, VIM, OXA) and other resistance mechanisms are frequently identified during this period, highlighting the dynamic nature of the gut resistome7-10. However, most of these findings are from non-Indian cohorts, leaving significant gaps in our understanding of the establishment and progression of the gut resistome in Indian infants.
In India, sociocultural, clinical, and environmental factors uniquely shape the infant gut resistome. Practices related to complementary feeding11 and family structure12 shape early microbial exposure. Factors such as healthcare access, over-the-counter medication use, and traditional medicine can further modulate gut microbial composition13. High population density and community-level transmission can contribute to the acquisition of ARGs14. Despite the growing interest in AMR research, the temporal evolution and diversity of the infant gut resistome in Indian infants remain poorly understood. Existing studies have focused narrowly on ARGs in specific bacterial families, such as Enterobacteriaceae, without exploring the broader resistome or its longitudinal development14,15. Moreover, there is limited information on the impact of clinical and sociodemographic factors on resistome development in this population.
This study aimed to address these critical knowledge gaps by investigating the longitudinal changes in the diversity and prevalence of ARGs in Indian infants. Stool samples were collected and analysed using molecular methods to explore the temporal dynamics of the gut resistome during early life. Furthermore, the study assessed the influence of clinical and sociodemographic factors on ARG diversity and prevalence. This research offers novel insights into AMR gut reservoirs within an understudied population.
Materials & Methods
This study was undertaken by the Enteric Diseases Division, Department of Microbiology, Kasturba Medical College, Manipal. The newborns were recruited at Dr. TMA Pai Rotary Hospital, Karkala and Kasturba Hospital, Manipal, between October 2020 and December 2022. The laboratory work was carried out at the Enteric Diseases Division, Department of Microbiology, Kasturba Medical College, Manipal, Karnataka. This study was approved by the Institutional Ethics Committee of Kasturba Medical College and Hospital, Manipal. Written informed consent was obtained from the mothers after providing detailed oral and written information about the study. Stool samples were collected prospectively at four time points, viz., meconium (birth), 6, 14, and 36 wk along with clinical and demographic information. Data confidentiality and participant anonymity were ensured by using unique infant identifiers.
Participant recruitment and sample collection
Healthy full-term neonates were recruited into the study. Newborns with neonatal infections, complications or congenital anomalies were excluded from the study. The sample size for this study was determined based on prior data from our pilot study on the prevalence of antibiotic-resistant bacteria in the infant gut. Using the formula for estimation of proportion, with an accepted margin of error (d) at 5 per cent and anticipated proportion prevalence (p) of 8/76, and accounting for a 20 per cent dropout rate, the sample size for the study was calculated as 182 infants. However, due to multiple constraints, including COVID-related disruptions during the study period, we were able to collect samples at all four time points only from a total of 54 infants.
Stool DNA extraction
Microbial DNA was extracted from stool samples using the QIAGEN PowerFecal Pro DNA Kit (QIAGEN, Germany) following the manufacturer’s instructions. DNA concentration (ng/μL) and purity were checked using a BioSpectrometer (Eppendorf, Germany) by measuring the 260/280 and 260/230 absorbance values. Extracted DNA was stored at -20°C until further processed.
Primer designing and antimicrobial resistance gene detection using conventional PCR
Genes conferring resistance to various antibiotic classes were selected from The Comprehensive Antibiotic Resistance Database (CARD)16 based on their high prevalence, widespread dissemination across bacterial genomes, frequent reporting in infant gut resistome studies, and high corresponding antibiotic usage. Given the study’s focus on Gram-negative bacteria, gene selection was limited to resistance determinants commonly associated with these organisms. Sequences of multiple gene variants for an ARG were selected to ensure broad coverage. Multiple gene sequences were aligned using ClustalW to identify suitable regions for primer design. Primers were designed to cover over 108 variants of 20 ARGs associated with eight antibiotic classes. The primers were grouped into five sets of four genes based on their annealing temperatures, and multiplex PCR assays were standardised. Positive control strains were sourced from Translational Health Science and Technology Institute (THSTI), Faridabad, and Christian Medical College (CMC), Vellore. Details of the genes, primers and groups are listed in supplementary table. The PCR reaction mixture (25 μL) consisted of 12.5 μL of 2X Master mix, standardised quantities of primers, nuclease-free water and template DNA for each group. PCR conditions included initial denaturation at 95°C for 120s, followed by 30 cycles of denaturation at 96°C for 30s, group-specific amplification temperatures (Supplementary Table), and extension at 72°C for 60s, with a final extension at 72°C for 300s. PCR amplicons were analysed by agarose gel electrophoresis (2% gel incorporated with ethidium bromide) for 30-45 mins at 100V in a 1X TAE buffer, and the bands were visualised using a UV Transilluminator.
Statistical analysis
ARGs were analysed as categorical variables (present/absent). McNemar’s test was used to assess changes in ARG presence/absence between any two time points (paired categorical data). Chi-square or Fisher’s exact test was used to check the association of demographic/clinical characteristics and ARG carriage in the infant gut. A P value of <0.05 was considered statistically significant. Binomial logistic regression was performed with clinical/demographic data (independent variable) and ARGs (dependent variable), reporting P<0.05, odds ratios, and 95% confidence intervals. Statistical analysis was performed using DATAtab17 and IBM SPSS Statistics (version 25)18.
Results
Sample collection and population characteristics
The study enrolled 68 healthy, full-term newborns, of which 54 infants completed the study protocol by providing samples at all four timepoints, viz., at birth, 6, 14 and 36 wk. In total, 216 samples were collected and analysed. Infants who failed to provide one or more samples were excluded from further analysis. Demographic and clinical characteristics of the infants are described in table I. Notably, the cohort included a nearly equal distribution of infants born by caesarean section (48%) and vaginal delivery (52%), with 44 per cent of the mothers receiving cephalosporin antibiotics postpartum.
| Characteristics | n (%) | |
|---|---|---|
| Family type | Nuclear | 31 (57) |
| Joint | 23 (43) | |
| Siblings | Yes | 25 (46) |
| No | 29 (54) | |
| Gender | Male | 28 (52) |
| Female | 26 (48) | |
| Mode of Birth | Vaginal | 28 (52) |
| Caesarean-section | 26 (48) | |
| Class of antibiotics prescribed to mothers postpartum | Beta-Lactams | 26 (48) |
| Cephalosporins | 24 (44) | |
| Mixed | 3 (6) | |
| Quinolones | 1 (2) | |
| Infants administered antibiotics at | Birth | 3 (6) |
| 6-wk | 8 (15) | |
| 14-wk | 5 (9) | |
| 36-wk | 7 (13) | |
| Feeding Pattern | ||
| At Birth | Exclusive breast feeding | 23 (43) |
| Mixed | 31 (57) | |
| 6 wk | Exclusive breast feeding | 46 (85) |
| Mixed | 8 (15) | |
| 14 wk | Exclusive breast feeding | 43 (80) |
| Mixed | 6 (20) |
The overall prevalence of antimicrobial resistance genes
Molecular analysis of stool samples revealed a widespread prevalence of ARGs in the infant gut microbiota during the first nine months of life. Overall, the most frequently detected ARGs were ermB (64.8%; CI: 0.58-0.71), sul1 (56%; CI: 0.49-0.63), blaTEM (53.2%; CI: 0.46-0.60), blaCTX-M (40.3%; CI: 0.34-0.47), blaSHV (38.4%; CI: 0.32-0.45) and oqxA (38.4%; CI: 0.32-0.45). Individual infants carried between 3 and 14 unique ARGs throughout the study period, with 80 per cent harbouring genes conferring resistance to beta-lactam antibiotics, followed by MLSB (70%) and Sulphonamides (61%). One infant carried ARGs from all eight analysed antibiotic classes at various timepoints, highlighting the diversity of the resistome in early life (Supplementary Fig. 1).
Distribution of antimicrobial resistance genes across time points
ARG prevalence changed dynamically over time. At birth, 88per cent (44/54) of infants carried at least one ARG, with ermB (24/54, 44.4%) being the most prevalent. At 6 wk and 14 wk, all infants (100%) carried ARGs, with a notable increase in the prevalence of ermB (37/54, 68.5%) at 6 wk and sul1 at 14 wk (43/54, 79.6%). By 36 wk, 88 per cent of infants carried ARGs, with the prevalence tapering or remaining stable compared to 14 wk. The frequency and proportion of infants carrying the genes at various time points have been described in table II. Temporal analysis revealed a significant increase in specific genes between birth and later time points. The tet gene increased 7-fold from birth to 6 wk (P= 0.039), while oqxA and blaSHV exhibited 3.3-fold (P< 0.001) and 1.5-fold (P= 0.001) increase, respectively. Conversely, sul1 showed a continuous and marked increase through 14 wk but decreased significantly by 36 wk (P= 0.004).
| Gene | Class | Time points | |||
|---|---|---|---|---|---|
| Birth, n (%) | 6-wk, n (%) | 14-wk, n (%) | 36-wk, n (%) | ||
| blaNDM | Beta lactams | 6 (11.1) | 6 (11.1) | 0 (0) | 2 (3.7) |
| blaCTX-M | 16 (29.6) | 23 (42.6) | 27 (50) | 21 (38.9) | |
| blaKPC | 0 (0) | 0 (0) | 0 (0) | 0 (0) | |
| blaTEM | 17 (31.5) | 33 (61.1) | 33 (61.1) | 32 (59.3) | |
| blaOXA | 13 (24.1) | 15 (27.8) | 17 (31.5) | 8 (14.8) | |
| blaIMP | 3 (5.6) | 2 (3.7) | 1 (1.9) | 0 (0) | |
| blaSHV | 12 (22.2) | 30 (55.6) | 20 (37) | 21 (38.9) | |
| blaVIM | 0 (0) | 0 (0) | 1 (1.9) | 0 (0) | |
| blaOXA-48 | 0 (0) | 3 (5.6) | 3 (5.6) | 2 (3.7) | |
| aac(6’) | Aminoglycosides | 8 (14.8) | 17 (31.5) | 12 (22.2) | 10 (18.5) |
| aadA | 6 (11.1) | 5 (9.3) | 4 (7.4) | 7 (13) | |
| tet | Tetracycline | 1 (1.9) | 8 (14.8) | 9 (16.7) | 5 (9.3) |
| catB | Chloramphenicol | 9 (16.7) | 18 (33.3) | 15 (27.8) | 7 (13) |
| sul1 | Sulphonamides | 16 (29.6) | 34 (63) | 43 (79.6) | 28 (51.9) |
| sul2 | 6 (11.1) | 13 (24.1) | 14 (25.9) | 10 (18.5) | |
| dfrA | Trimethoprim | 5 (9.3) | 6 (11.1) | 7 (13) | 8 (14.8) |
| oqxA | Fluoroquinolones and Quinolones | 8 (14.8) | 34 (63) | 25 (46.3) | 16 (29.6) |
| qnrS | 11 (20.4) | 16 (29.6) | 20 (37) | 18 (33.3) | |
| ermB | Macrolides, Lincosamides and Streptogramin-B (MLSB) | 24 (44.4) | 37 (68.5) | 42 (77.7) | 37 (68.5) |
| mphA | 5 (9.3) | 12 (22.2) | 17 (31.5) | 17 (31.5) | |
Class-wise distribution ofantimicrobial resistance genes
Analysis of ARGs by antibiotic class revealed that genes belonging to the beta-lactam class of antibiotics were the most commonly detected at all time points. At birth, 59 per cent (32/54) of infants harboured beta-lactam ARGs that increased to 94 per cent (51/54) at both 6 wk and 14 wk and decreased to 74 per cent (40/54) at 36 wk (Supplementary Fig. 2). Interestingly, 92.5 per cent (50/54) of infants carried ARGs spanning three or more antibiotic classes at 6 wk, compared to 37 per cent (20/54) at birth, 81.5 per cent (44/54) at 14 wk, and 70 per cent (38/54) at 36 wk. One infant harboured ARGs from all eight classes at 36 wk. A heatmap depicting the ARG distribution of various classes at each time point highlights the variability in ARG profiles (Supplementary Fig. 1). Notable, 74 per cent (40/54) of the infants harboured ARGs spanning multiple classes at both 6 and 14 wk. Nine infants carried ARGs from multiple classes at all four time points (Supplementary Fig. 1).
Temporal dynamics of ARG acquisition and loss
Individual-level analysis revealed the dynamic nature of ARG carriage. Some infants maintained consistent ARG profiles from birth through 36 wk, while others acquired new ARGs or lost previously present genes. Among the cohort, seven infants exhibited peak ARG carriage at birth, with 5 to 10 distinct ARGs. Most of the infants reached their highest ARG load at 6 wk (19/54, carrying 4-13 ARGs) or 14 wk (15/54, carrying 5-11 ARGs), and by 36 wk, only 13/54 infants carried their highest number of ARGs compared to the other time points (Supplementary Fig. 1). The highest ARG count detected in a single infant was at 6 weeks, where one infant harboured 13 of the 20 analysed ARGs (Supplementary Fig. 1).
Association between clinical and demographic factors and ARG carriage
The influence of clinical and demographic factors on ARG carriage was analysed using chi-square tests and logistic regression models. A marked increase in the prevalence of the blaCTX-M gene was seen in infants delivered via caesarean section (P=0.001), born to mothers who were administered cephalosporin antibiotics for 3-5 days postpartum (P=0.013). These findings suggest that delivery mode and maternal antibiotic use may influence the infant gut resistome during early life. Binomial logistic regression confirmed caesarean delivery (P=0.001; OR = 6.93; CI: 2.06-23.26) and maternal postpartum cephalosporin exposure (P=0.013; OR = 4.16; CI: 1.31-13.17) as independent predictors of blaCTX-M carriage in infants at six week. Among infants who were exclusively breastfed and those who received formula feed in addition to breast milk at birth, the latter group was the predominant carrier of ARGs. While this did not reach statistical significance, we observed a marked increase in the number of infants carrying ARGs at birth. Other clinical or demographic factors, including feeding practices at later time points, family structure, gender, or direct antibiotic exposure, did not show significant associations with ARG prevalence at any time point examined.
Discussion
Antibiotic resistance genes (ARGs) in the infant gut microbiome remain underexplored in the Indian context. While a few studies have focused on ARGs in drug-resistant Enterobacteriaceae from infant stool samples14,15, this study provides a comprehensive profile of ARGs at four critical time points: at birth, 6 wk, 14 wk, and 36 wk. Our aim was to investigate the influence of demographic and clinical factors – such as delivery mode, antibiotic exposure, and feeding patterns – on ARG prevalence and diversity. The key findings demonstrate that ARGs are present from birth and persist through 36 wk, with the highest prevalence and diversity observed at 6 and 14 wk. These results offer valuable insights into the temporal dynamics of antimicrobial resistance (AMR) in Indian infants, addressing a significant gap in our understanding of AMR in this population.
Infants in our study cohort predominantly carried genes conferring resistance to beta-lactams and MLSB antibiotics, with antibiotic resistance genes detectable from birth. The prevalence of resistance genes peaked at 6 wk and 14 wk before declining at 36 wk. This finding aligns with previous studies that reported high levels of AMR in infants during early life, a period when the gut microbiota is rapidly establishing itself8,19,20 . Notably, the diversity and prevalence were highest at 6 wk, supporting previous reports by Lebeaux et al20, who also observed a peak in ARG abundance at 6 wk compared to one year.
Our cohort most frequently harboured genes from the MLSB (ermB), beta-lactam (blaTEM, blaCTX-M, blaSHV), sulphonamide (sul1), and quinolone (oqxA) classes. These findings are consistent with previous studies showing a high prevalence of beta-lactams and MLSB genes in the infant gut microbiome8,19,21,22 . Reyman et al23 noted that ermB and blaTEM were enriched in infants who received antibiotic treatments. Interestingly, in our study, ermB was detected across all time points, irrespective of direct antibiotic exposure. There was no statistically significant association between direct antibiotic exposure and the prevalence of ARGs. This could be attributed to the skewed distribution of data since only a small number of infants in our cohort were exposed to antibiotics during the study period (Table II). We observed an overall higher prevalence of the sul1 gene, in contrast to studies that commonly report a higher prevalence of sul25,8,22. The presence of sul1, often associated with Class 1 integrons located on plasmids24-26, suggests that further metagenomic sequencing of our samples could shed light on the presence of mobile genetic elements in the gut of infants in our study sample.
We found a strong association between caesarean-section delivery, maternal postpartum exposure to cephalosporins, and the prevalence of the blaCTX-M gene in infants. This observation aligns with findings by Nogacka et al27, who documented higher levels of blaTEM and blaCTX-M in infants whose mothers were administered intrapartum antibiotic prophylaxis. In our study group, mothers undergoing caesarean-section deliveries were frequently administered cephalosporins postpartum, suggesting a potential link between maternal antibiotic exposure and selection of the blaCTX-M gene in infants. A related study demonstrated a positive correlation between the antibiotic resistance gene load in infant gut microbiomes and the concentration of cephalosporin in cord blood28, further supporting our findings. According to our findings, although not statistically significant, a higher number of infants in the formula-fed group carried ARGs compared to those exclusively breastfed. While the distribution of exclusively breastfed and mixed-fed infants was nearly equal at birth, the number of formula-fed infants declined markedly at later time points (8/54 at 6 wk and 6/54 at 14 wk), limiting statistical significance.
Despite the valuable insights provided by this study, there were several limitations. Our study primarily focused on key factors known to influence ARG prevalence in the infant gut, such as delivery mode, antibiotic exposure (mother/ infant), and feeding patterns. Although data on environmental factors like family type (nuclear/ joint), duration of hospital stay (mother/ infant), and room type (private/ ward) were collected, they were excluded from the final analysis due to skewed distribution and lack of statistical significance. Another key limitation of this study the lack of data on gene abundance and the absence of shotgun metagenomic sequencing. Information on the relative abundance of genes would have helped track the antibiotic resistance gene load dynamics in response to various factors (e.g., antibiotic exposure, diet). Furthermore, shotgun metagenome sequencing of the samples could have revealed further ARG variants and their microbial hosts. Together, these approaches would offer a more comprehensive understanding of resistance burden, potential ARG enrichment under selective pressure, and its impact on gut microbiome composition. This study was based on a single cohort, which limits its generalisability given the cultural, geographical, and dietary diversity across India that may influence the infant gut resistome. Multicentre studies across diverse populations are therefore required to validate these findings. Further exploration of the functional roles of ARGs and their association with mobile genetic elements would enhance understanding of AMR transmission and persistence. Despite these limitations, this first study from the region provides valuable exploratory insights into the infant gut resistome and establishes a foundation for future large-scale, multicentre cohort studies.
In conclusion, this study highlights that infants carry a diverse and persistent repertoire of ARGs during early life, shaped by postnatal ecological factors. The strong association of caesarean delivery with maternal antibiotic use on the increased prevalence of blaCTX-M underscores the importance of targeted interventions, such as administering probiotics to antibiotic-exposed mothers and infants, to restore microbial balance and reduce ARG carriage. Promoting exclusive breastfeeding practices will enrich beneficial microbes and bioactive compounds crucial for healthy microbiome development. It is crucial for clinicians to be informed about the increased likelihood of AMR carriage in infants during critical time points in early life, such as the ARG peak observed at 6 wk in our study, to guide evidence-based antibiotic prescribing to minimise selection pressure. Future research should be guided towards large multi-centre cohort studies to explore the mechanisms driving ARG persistence, assess the influence of various factors shaping the resistome, and evaluate the impact of healthcare interventions on AMR patterns in infants across different regions in the country. Integrating gut microbiome and resistome data provide valuable clinical insights, which will be essential to developing effective strategies to mitigate AMR in early life and beyond.
Acknowledgment
Authors acknowledge Drs Bhabatosh Das (Translational Health Science and Technology Institute, Faridabad) and Balaji Veeraraghavan (Christian Medical College, Vellore) for providing the bacterial strains used as positive controls to standardise and perform PCR in this study. Authors also acknowledge Dr Arun Kumar (Consultant Biostatistician), for his valuable contributions to the statistical analysis of the data.
Financial support & sponsorship
Dr. T.M.A. Pai PhD Scholarship program was awarded by (MAHE) to first author (SM).
Conflicts of Interest
None.
Use of Artificial Intelligence (AI)-Assisted Technology for manuscript preparation
The authors confirm that there was no use of AI-assisted technology for assisting in the writing of the manuscript and no images were manipulated using AI.
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