Low detection rate in Nigerian study offers hope, but experts warn resistance spreads faster than expected.

The discovery seems modest at first glance. Out of 30 bacterial samples tested at hospitals in Onitsha, Nigeria, only one carried a gene that makes bacteria resistant to our strongest antibiotics. A 3.33% prevalence rate might sound reassuring, perhaps even negligible.

Yet infectious disease specialists viewing the new research, published in Global Multidisciplinary Journal, see something quite different: a warning signal that one of the world’s most dangerous resistance mechanisms has gained a foothold in West Africa, a region where healthcare systems are already stretched thin and surveillance capacity remains limited.

The gene in question, NDM-1, has been spreading globally since its identification in 2008. Its presence in Nigeria, now confirmed through systematic molecular testing, raises urgent questions about how to prevent what remains a manageable problem from becoming a full-blown crisis.

When Antibiotics Stop Working

To understand why a single positive test result matters, you need to understand what NDM-1 does. The gene codes for an enzyme that destroys carbapenem antibiotics, drugs that doctors turn to when standard treatments fail.

Carbapenems work differently than older antibiotics. They’re more stable, harder for bacteria to break down, and effective against organisms resistant to multiple other drugs. In hospital intensive care units worldwide, carbapenems save lives daily, treating severe pneumonias, bloodstream infections, and post-surgical complications that would otherwise prove fatal.

When bacteria acquire NDM-1, they produce an enzyme that cleaves carbapenem molecules, rendering them ineffective. The bacteria survive. The patient’s infection persists. And clinicians face an increasingly desperate search for alternatives that might work.

“We’re talking about infections that were treatable becoming untreatable,” explains Dr Chinaza Maria Ozuluoha from Nnamdi Azikiwe University, who led the research team. “A patient comes in with a urinary tract infection, normally a straightforward condition. But if the bacteria carry NDM-1, suddenly you’re looking at an infection that resists nearly everything we have. That changes the entire clinical picture.”

The enzyme is indiscriminate. It breaks down virtually all beta-lactam antibiotics, a class that includes penicillins, cephalosporins, and carbapenems. Bacteria with NDM-1 are typically resistant to many non-beta-lactam drugs as well, leaving doctors with a handful of toxic older antibiotics or, in some cases, nothing at all.

The Onitsha Investigation

The research focused on a specific question: how prevalent is NDM-1 among bacteria causing urinary tract infections in this Nigerian city?

Urinary tract infections are extraordinarily common. Millions occur annually worldwide, affecting people of all ages. Most resolve with standard antibiotics. However, when caused by resistant bacteria, they can lead to serious complications including kidney infections, bloodstream spread, and sepsis.

The scientists collected 30 bacterial isolates from patients diagnosed with urinary tract infections at Onitsha healthcare facilities. These weren’t random samples but bacteria already causing clinical disease, making their resistance patterns directly relevant to treatment decisions.

Laboratory analysis involved extracting genetic material from each isolate and testing specifically for NDM-1 using polymerase chain reaction, a technique that amplifies and detects specific DNA sequences. The process is precise, revealing presence or absence of the gene with high accuracy.

Results showed one positive sample among the 30 tested. The prevalence of 3.33% sits well below figures from regions where NDM-1 has become endemic. Some hospitals in India, Pakistan, and parts of the Middle East report prevalence exceeding 20% or even 30% among carbapenem-resistant bacteria.

However, comparisons require caution. Different sampling strategies, populations, and testing methods produce different results. The Nigerian study examined all urinary tract infection isolates, not just those already showing carbapenem resistance, which tends to yield lower prevalence estimates.

Why Early Detection Changes Everything

Public health responses to antimicrobial resistance follow a predictable pattern. Detection occurs. Concern is expressed. Reports are written. Time passes. Then, often abruptly, prevalence increases to levels requiring urgent action that proves far more difficult and expensive than earlier intervention would have been.

Countries that responded early to emerging resistance sometimes succeeded in limiting spread. The Netherlands, for instance, implemented aggressive screening and isolation protocols when MRSA (methicillin-resistant Staphylococcus aureus) first appeared, maintaining prevalence well below rates seen elsewhere in Europe.

Conversely, delays in response typically result in resistance becoming entrenched. Once genes like NDM-1 establish themselves in hospital bacterial populations, elimination becomes nearly impossible. The focus shifts from prevention to damage control.

“We have a brief opportunity here,” suggests Dr Kennedy Oberhiri Obohwemu, Senior Researcher and Project Coordinator from PENKUP Research Institute, who co-authored the research paper. “Low prevalence means interventions can still work. Strengthen infection control, improve antibiotic stewardship, enhance surveillance. These measures are effective when resistance is emerging. They’re far less effective when it’s already widespread.”

The study’s timing matters. Nigeria, like much of sub-Saharan Africa, faces multiple competing health priorities. Infectious diseases including malaria, HIV, and tuberculosis demand resources and attention. Non-communicable diseases are rising. Healthcare infrastructure requires investment. Antimicrobial resistance can seem abstract compared to immediate crises.

Yet resistance undermines treatment for every condition. Surgery becomes riskier when post-operative infections can’t be treated. Cancer chemotherapy, which suppresses immune function, becomes more dangerous when resistant bacteria cause opportunistic infections. Even routine procedures like catheter insertion carry greater risks.

The Mechanics of Spread

Understanding how NDM-1 spreads helps explain why early intervention matters. The gene doesn’t pass only from parent bacteria to offspring, as chromosomal genes do. Instead, it resides on plasmids, mobile genetic elements that bacteria can transfer horizontally to unrelated organisms.

This horizontal gene transfer occurs through several mechanisms. Conjugation involves direct cell-to-cell contact, with one bacterium transferring plasmid DNA to another through a physical bridge. Transformation allows bacteria to take up DNA from their environment, incorporating it into their own genetic material. Transduction involves viruses that infect bacteria, inadvertently carrying resistance genes between hosts.

These processes mean a single bacterium carrying NDM-1 can spread the gene to many others, potentially across species boundaries. Klebsiella can share resistance genes with Escherichia coli. E. coli can pass them to other Enterobacteriaceae. The result is that resistance spreads through bacterial communities far faster than reproduction alone would allow.

Environmental reservoirs complicate control. Bacteria carrying NDM-1 have been detected in water systems, soil, and food animals. Healthcare settings aren’t the only places where resistance genes circulate, though they’re certainly important amplification points given concentrated antibiotic use and vulnerable patient populations.

“You can’t think of this as isolated cases,” notes Dr Kenneth Oshiokhayamhe Iyevhobu from Edo State University, a team member. “Bacteria don’t respect institutional boundaries. They move between patients, between facilities, between hospitals and communities. A gene detected in one place today could be widespread in a year or two without proper controls.”

Healthcare System Vulnerabilities

Nigeria’s healthcare system faces structural challenges that create favourable conditions for resistance emergence and spread.

Antibiotics remain widely available without prescription despite regulatory efforts to restrict access. Patients often purchase drugs from pharmacies or informal vendors without medical consultation, leading to inappropriate selection, dosing, and duration of therapy.

Diagnostic infrastructure varies dramatically. Major teaching hospitals have microbiology laboratories capable of identifying bacteria and testing antibiotic susceptibility. However, most smaller facilities lack even basic culture capacity. Clinicians prescribe antibiotics blindly, making educated guesses about what organism might be present and what drugs might work.

This empiric prescribing tends toward broad-spectrum agents. When you don’t know what you’re treating, you choose antibiotics that cover multiple possibilities. The practice drives overuse of powerful drugs including carbapenems, creating exactly the selective pressure that favours resistant bacteria.

Infection prevention practices are inconsistent. Water supply interruptions compromise hand hygiene. Overcrowding places patients in close proximity. Inadequate staffing ratios limit time available for proper cleaning and disinfection. Personal protective equipment may be scarce or used incorrectly.

Surveillance for antimicrobial resistance remains fragmented. A few institutions conduct systematic monitoring, but national coordination is limited. Data collection, analysis, and dissemination all face challenges. The result is that resistance patterns are poorly characterised, making evidence-based responses difficult.

Recent policy reviews have called for strengthening Nigeria’s antimicrobial resistance response, emphasising surveillance, stewardship, infection control, and public awareness. However, implementation requires sustained political commitment and resource allocation that compete with numerous other priorities.

Regional and Global Implications

The Nigerian finding matters beyond national borders. West Africa has been relatively understudied regarding carbapenemase genes like NDM-1. This research provides important baseline data for a region where surveillance has been sparse.

NDM-1 has shown consistent ability to spread geographically. Identified first in South Asia, it reached the Middle East, North Africa, Europe, and the Americas within several years. Sub-Saharan Africa has seen increasing detections, though systematic surveillance remains limited in most countries.

Regional spread occurs through multiple pathways. Patient movement for medical care, including medical tourism, can introduce resistance to new areas. Trade in food and agricultural products may carry resistant bacteria. Environmental contamination can seed resistance genes in new locations.

Climate and ecological factors influence bacterial survival and transmission in ways that remain incompletely understood. Temperature, humidity, sanitation infrastructure, and population density all affect how resistance genes circulate. These factors vary substantially across African regions, potentially creating different epidemiological patterns than observed elsewhere.

“We need to think regionally, not just nationally,” argues Dr Abba Sadiq Usman from Action Against Hunger, a co-author. “Bacteria don’t stop at borders. Effective surveillance and control require coordination across countries, sharing data, learning from each other’s experiences, and implementing compatible approaches.”

Treatment Realities

When clinicians encounter NDM-1-positive infections, options narrow dramatically. Standard treatments fail. Guidelines recommend combinations of drugs, but evidence supporting specific regimens remains limited.

Colistin, an antibiotic largely abandoned in the 1970s because of kidney toxicity, has returned to use by necessity. It works against many carbapenem-resistant bacteria but carries significant risks. Patients require careful monitoring for renal damage, and resistance to colistin itself is emerging.

Tigecycline shows activity against some resistant organisms but has limitations. It doesn’t achieve adequate concentrations in urine or bloodstream, restricting its use for certain infection types. Side effects including nausea can be problematic.

Newer agents like ceftazidime-avibactam combine a beta-lactam antibiotic with a beta-lactamase inhibitor, offering activity against some carbapenemase-producing bacteria. However, they’re expensive, often unavailable in resource-limited settings, and resistance is already being reported.

The pharmaceutical pipeline offers little immediate hope. Antibiotic development has slowed dramatically over recent decades. Economic incentives favour drugs for chronic conditions over antibiotics that cure infections in days. Regulatory pathways for antibiotics are complex. The result is very few new drugs in development.

“We’re running out of options,” says Dr Christabel Ovesuor from Federal Medical Center Asaba, a team member. “For some infections, we’re already there. We have patients with resistant bacteria where nothing works reliably. That was unthinkable a generation ago. It’s becoming routine now.”

The Prevention Imperative

Given limited treatment options, prevention becomes paramount. The study’s authors emphasise several interventions.

Antimicrobial stewardship programmes promote appropriate prescribing through education, guidelines, audit and feedback, and formulary restrictions. Evidence shows these reduce unnecessary antibiotic use without harming patient outcomes. However, implementation requires resources, expertise, and institutional commitment.

Infection prevention and control measures reduce transmission within healthcare facilities. Hand hygiene compliance, environmental cleaning, appropriate isolation of patients with resistant infections, and proper medical waste disposal all matter. Yet maintaining high standards requires adequate staffing, reliable infrastructure, and ongoing training.

Diagnostic capacity needs expansion. Clinicians need access to rapid, accurate testing that identifies causative organisms and their resistance profiles. This enables targeted therapy rather than broad-spectrum empiric treatment, reducing selective pressure favouring resistance.

Regulatory enforcement around antibiotic sales could limit inappropriate access. Requiring prescriptions, enforcing dispensing rules, and addressing informal drug markets would reduce self-medication and incomplete treatment courses.

Public education campaigns might shift behaviours. Many people hold misconceptions about antibiotics, believing they treat viral infections, that stopping treatment early is acceptable when symptoms improve, or that stronger drugs are always better. Targeted communication could address these beliefs.

Looking Ahead

The research team calls for expanded surveillance as an immediate priority. This study examined 30 isolates from one city. Nigeria needs systematic, ongoing monitoring across multiple sites, infection types, and patient populations.

Such surveillance requires investment in laboratory capacity, training, and coordination systems. It needs sustainable funding rather than short-term project support. And it requires mechanisms for translating findings into action, not just collecting data.

Larger studies would enable more detailed epidemiological investigation. What risk factors predict NDM-1 carriage? Do certain patient populations show higher prevalence? Are specific healthcare facilities hotspots? Do geographic patterns exist? Answering these questions requires sample sizes in hundreds or thousands rather than dozens.

Genetic characterisation beyond simple presence or absence would illuminate transmission dynamics. Whole-genome sequencing could reveal whether cases represent multiple independent introductions or local spread from a single source. Comparison with global databases would show how Nigerian isolates relate to those from other regions.

Longitudinal monitoring would track temporal trends. Is prevalence stable, increasing, or decreasing? Are interventions working? Where should efforts intensify? These questions require repeated surveillance over years.

“This study is a beginning, not an end,” concludes Dr Oladipo Vincent Akinmade from University of Warwick, a team member. “We’ve confirmed NDM-1 is present. Now the real work starts: understanding its distribution, preventing its spread, and protecting the antibiotics we still have. The stakes couldn’t be higher.”

About the Study

The research, “Low Prevalence of Carbapenemase Gene NDM-1 in Uropathogenic Klebsiella pneumoniae and Escherichia coli: A Molecular Surveillance Study,” appears in Global Multidisciplinary Journal, Volume 5, Issue 1. The study was conducted by researchers from Nnamdi Azikiwe University and other Nigerian institutions, with support from PENKUP Research Institute in Birmingham, UK.