How Antibiotic-Resistant Germs Spread in Newborn Units, and What Helps Stop Them

What three 2026 studies — on Klebsiella infections in Africa and South Asia (Odih and colleagues), resistant gut bacteria in European newborn units (Cook and colleagues) and programmes to reduce resistance in lower-income countries (Him and colleagues) — mean for babies and families

Some of the germs that cause serious infections in newborn babies no longer respond to common antibiotics. Three studies published in 2026 suggest that, in many hospitals, these resistant germs pass from baby to baby within the newborn unit, and that the approaches most strongly linked with saving lives combine cleaner, safer units, well-trained staff and careful antibiotic use.

Why resistant infections in newborns matter

Newborn babies, especially those born early or small, have immune systems that are still learning to fight germs. When bacteria get into a baby's bloodstream, the result is called sepsis, a medical emergency that is usually treated with antibiotics. Antibiotics are medicines that kill bacteria. Over time, however, some bacteria have developed ways to survive them; this is called antimicrobial resistance, or AMR. One common way is by making enzymes, a kind of chemical tool, called extended-spectrum beta-lactamases (ESBLs), which break down many widely used antibiotics.

Resistance is not a small or distant problem. Him and colleagues report an estimate that about 214,000 newborns die every year from sepsis caused by resistant germs [1]. A large international analysis found that, across all ages, bacterial resistance directly caused about 1.14 million deaths in 2021, and highlighted preventing infection as one of the most important responses [2]. Experts have also long pointed out a difficult balance: making sure every sick baby can get effective antibiotics, while avoiding unnecessary use that breeds resistance [3].

How doctors came to suspect the hospital itself

For many years, doctors have worried that some infections in newborns are picked up in hospital rather than at birth. In 2005, a major review found that babies born in hospitals in poorer countries had infection rates 3 to 20 times higher than babies born in hospitals in wealthier countries, and that about 70% of the bacteria found in their blood would not be killed by the two standard first-choice antibiotics [4]. A germ called Klebsiella pneumoniae (often just "Klebsiella") kept appearing near the top of the list. Across sub-Saharan Africa it was found in about 21% of newborn blood infections [5]. A large research network called the Burden of Antibiotic Resistance in Neonates from Developing Societies (BARNARDS) study, which followed 36,285 newborns in seven lower-income countries in Africa and South Asia, found that Klebsiella was the main cause of sepsis and that every germ it found resisted several types of antibiotic [6]. Another study, NeoOBS (a global study following sick newborns at 19 hospitals in 11 countries, mainly in Asia and Africa), found that about one in three Klebsiella samples resisted even a powerful reserve group of antibiotics called carbapenems [7].

Two clues hinted that the hospital itself was playing a role. A hospital in Malawi that studied the genetic "fingerprints" of its Klebsiella germs over many years saw waves of near-identical germs, often confined to particular wards, which suggested spread inside the building [8]. And in Zambia, a simple package of measures — staff training, text-message reminders, alcohol hand rub, better cleaning and weekly antiseptic baths for babies weighing at least 1.5 kg — was followed by fewer hospital-related deaths: 18.0% of babies compared with 23.6% before [9]. At the same time, doctors realised that antibiotics were used very widely: a one-day survey called the No-More-Antibiotics and Resistance (NO-MAS-R) study, covering 84 newborn intensive care units in 29 countries, found that about one in four babies was receiving them [10]. What was missing was a clear picture of how often resistant infections spread between babies, and which hospital programmes actually help.

Three studies, three pieces of the puzzle

The first study, by Odih and colleagues, looked at 1,523 Klebsiella samples from sick newborns in 27 newborn units across 13 countries in Africa and South Asia, collected between 2013 and 2023 [11]. The researchers read each germ's full genetic code. When germs from two babies in the same unit were almost identical and were collected within four weeks of each other, they counted this as a likely chain of spread. About two in every three infections (1,035 of 1,523, or 68.0%) belonged to such chains, and at least 879 of all 1,523 infections (57.7%) had probably been caught from another baby's infection. The amount of spread varied a great deal from unit to unit. Nine in every ten germs (90.9%) carried genes that let them resist widely used antibiotics, including the cephalosporins recommended for treating newborn sepsis, and germs with these resistance genes were more likely to spread.

The second study, by Cook and colleagues, took place in 24 specialist newborn units in eight European countries between 2022 and 2024 [12]. On four occasions over about four weeks, stool samples were collected from every baby on the unit at the time, and the laboratory looked for genes that make bacteria resistant. This tells us about "carriage" (also called colonisation): germs living quietly in a baby's gut without making the baby ill. Of 533 babies who were born in the hospital and stayed there, 90 picked up resistant gut bacteria during the study. The key finding was about "colonisation pressure", meaning how many babies on the unit already carried resistant bacteria. For every extra 10 babies in 100 who were carriers, the chance (strictly, the odds) that another baby would pick them up was roughly 1.7 to 1.9 times higher. This happened in babies born both early and closer to term.

The third study, by Him and colleagues, brought together 31 earlier studies from hospitals in lower- and middle-income countries that had tried to reduce resistance in newborns [1]. The researchers sorted these efforts into three types: hospital-wide rules and infection-control systems such as hand hygiene and checking practice ("regulation"), staff training ("education"), and careful antibiotic prescribing ("optimisation"). Only programmes that combined all three were linked to fewer newborn deaths — about 25 fewer deaths for every 1,000 babies, although the true effect could be anywhere from 6 to 39 fewer — and to fewer infections or carriage with germs resistant to many antibiotics. Careful prescribing on its own reduced antibiotic use but did not change the number of deaths. In practice, the combined programmes included things like written unit rules for managing suspected infection, regular checks of practice with feedback to staff, a reliable supply of alcohol hand rub, training sessions and reminder posters, and agreed "stop points" — for example, reviewing antibiotics at 48 hours and stopping them when early infection has not been confirmed. Fewer babies in these units received antibiotics, and fewer received long courses.

Reading the results with care

These studies fit together well, but they do not prove cause and effect. None of them was a randomised trial, the kind of study in which babies or hospitals are assigned by chance to one approach or another. Most of the programmes in the third study were judged by comparing results before and after a change, and the researchers rated their confidence in the effect on deaths as very low. A group of skin germs called coagulase-negative staphylococci was found more often in blood samples after the combined programmes, which is something researchers will keep watching. The European study looked for resistance genes rather than identifying the germs themselves, and when its researchers repeated the analysis in a smaller group of units, the results pointed the same way but were less certain. The first study did not have information on whether each infection began at birth or later in hospital.

What this means for your baby and family

If your baby is in a newborn unit, it can be unsettling to hear about resistant germs. It may help to know that carrying a germ in the gut is common and is not the same as being ill; a review of earlier studies found that 7.9% of babies carrying certain gut germs went on to develop a blood infection, compared with 2.4% of babies who did not carry them [13]. One of the most important protections is something everyone can share: careful hand cleaning by staff, parents and visitors every time they touch a baby or the cot. Families can feel comfortable asking about hand rub, cleaning routines and how the unit tracks infections. If your baby's doctors stop antibiotics after tests show no infection, that is usually a deliberate step to protect your baby and other babies, not a sign that care is being withheld. You may also find it helpful to read In[Neo]Sight's article on early antibiotics and the preterm gut.

What researchers are working on next

Researchers now want to test infection-control programmes more rigorously, by comparing groups of hospitals in a planned way, and to link germ fingerprints with information about each baby so they can tell exactly where infections begin. A study that modelled infection risk across many lower-income countries estimated that better infection prevention in health facilities could prevent at least 337,000 deaths linked to resistance each year, across all ages [14]. Experts also stress that very few such prevention studies have so far been done in newborn units with limited resources [15].

Bringing it together

Taken together, these three studies suggest that many resistant infections in newborns are passed on within the unit [11], that the risk to each baby rises as more babies on the unit carry resistant germs [12], and that the programmes most strongly linked with saving lives combine safer units, trained staff and careful antibiotic use [1]. That is a hopeful message: much of this spread can, in principle, be prevented by things hospitals and families can do together.

References

  1. Him RL, Sihota D, Harrison L, et al. Strategies to reduce antimicrobial resistance in newborns in low-income and middle-income countries: a systematic review and meta-analysis. Lancet Glob Health. 2026;14(4):e524-e538. doi:10.1016/S2214-109X(25)00533-900533-9) ↩
  2. GBD 2021 Antimicrobial Resistance Collaborators. Global burden of bacterial antimicrobial resistance 1990-2021: a systematic analysis with forecasts to 2050. Lancet. 2024;404(10459):1199-1226. doi:10.1016/S0140-6736(24)01867-101867-1) ↩
  3. Laxminarayan R, Matsoso P, Pant S, et al. Access to effective antimicrobials: a worldwide challenge. Lancet. 2016;387(10014):168-175. doi:10.1016/S0140-6736(15)00474-200474-2) ↩
  4. Zaidi AK, Huskins WC, Thaver D, Bhutta ZA, Abbas Z, Goldmann DA. Hospital-acquired neonatal infections in developing countries. Lancet. 2005;365(9465):1175-1188. doi:10.1016/S0140-6736(05)71881-X71881-X) ↩
  5. Okomo U, Akpalu ENK, Le Doare K, et al. Aetiology of invasive bacterial infection and antimicrobial resistance in neonates in sub-Saharan Africa: a systematic review and meta-analysis in line with the STROBE-NI reporting guidelines. Lancet Infect Dis. 2019;19(11):1219-1234. doi:10.1016/S1473-3099(19)30414-130414-1) ↩
  6. Sands K, Carvalho MJ, Portal E, et al. Characterization of antimicrobial-resistant Gram-negative bacteria that cause neonatal sepsis in seven low- and middle-income countries. Nat Microbiol. 2021;6(4):512-523. doi:10.1038/s41564-021-00870-7 ↩
  7. Russell NJ, Stöhr W, Plakkal N, et al. Patterns of antibiotic use, pathogens, and prediction of mortality in hospitalized neonates and young infants with sepsis: A global neonatal sepsis observational cohort study (NeoOBS). PLoS Med. 2023;20(6):e1004179. doi:10.1371/journal.pmed.1004179 ↩
  8. Heinz E, Pearse O, Zuza A, et al. Longitudinal analysis within one hospital in sub-Saharan Africa over 20 years reveals repeated replacements of dominant clones of Klebsiella pneumoniae and stresses the importance to include temporal patterns for vaccine design considerations. Genome Med. 2024;16(1):67. doi:10.1186/s13073-024-01342-3 ↩
  9. Mwananyanda L, Pierre C, Mwansa J, et al. Preventing Bloodstream Infections and Death in Zambian Neonates: Impact of a Low-cost Infection Control Bundle. Clin Infect Dis. 2019;69(8):1360-1367. doi:10.1093/cid/ciy1114 ↩
  10. Prusakov P, Goff DA, Wozniak PS, et al. A global point prevalence survey of antimicrobial use in neonatal intensive care units: The no-more-antibiotics and resistance (NO-MAS-R) study. EClinicalMedicine. 2021;32:100727. doi:10.1016/j.eclinm.2021.100727 ↩
  11. Odih EE, Abdulahi JA, Amulele AV, et al. Contribution of nosocomial transmission to Klebsiella pneumoniae neonatal sepsis in Africa and South Asia: An observational study of infection clusters inferred from pathogen genomics and temporal data. PLoS Med. 2026;23(5):e1005077. doi:10.1371/journal.pmed.1005077 ↩
  12. Cook A, Berkell M, van Werkhoven CH, et al. Neonatal Unit Colonization Pressure and Acquisition of Extended-Spectrum β-Lactamase Gut Colonization. JAMA Netw Open. 2026;9(9):e2632644. doi:10.1001/jamanetworkopen.2026.32644 ↩
  13. Folgori L, Tersigni C, Hsia Y, et al. The relationship between Gram-negative colonization and bloodstream infections in neonates: a systematic review and meta-analysis. Clin Microbiol Infect. 2018;24(3):251-257. doi:10.1016/j.cmi.2017.08.008 ↩
  14. Lewnard JA, Charani E, Gleason A, et al. Burden of bacterial antimicrobial resistance in low-income and middle-income countries avertible by existing interventions: an evidence review and modelling analysis. Lancet. 2024;403(10442):2439-2454. doi:10.1016/S0140-6736(24)00862-600862-6) ↩
  15. Dramowski A, Aucamp M, Beales E, et al. Healthcare-Associated Infection Prevention Interventions for Neonates in Resource-Limited Settings. Front Pediatr. 2022;10:919403. doi:10.3389/fped.2022.919403 ↩