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Okey-kalu E U, Okoli I, Nwankwo E O. Detection of the mecA gene and methicillin-resistant Staphylococcus aureus isolated from inanimate surfaces and healthcare workers in tertiary hospitals in Abia state, Nigeria. mljgoums 2026; 20 (2) :11-15
URL: http://mlj.goums.ac.ir/article-1-1930-en.html
URL: http://mlj.goums.ac.ir/article-1-1930-en.html
1- Department of Applied Microbiology and Brewing, Faculty of Biosciences, Nnamdi Azikiwe University, Awka, Anambra state, Nigeria , ulomamgbeokwere@yahoo.com
2- Department of Applied Microbiology and Brewing, Faculty of Biosciences, Nnamdi Azikiwe University, Awka, Anambra state, Nigeria
3- Department of Microbiology, College of Natural sciences, Michael Okpara University of Agriculture, Umudike, Abia state, Nigeria
2- Department of Applied Microbiology and Brewing, Faculty of Biosciences, Nnamdi Azikiwe University, Awka, Anambra state, Nigeria
3- Department of Microbiology, College of Natural sciences, Michael Okpara University of Agriculture, Umudike, Abia state, Nigeria
Keywords: Staphylococcus aureus, Methicillin-Resistant Staphylococcus Aureus, Healthcare Workers, Inanimate Surfaces
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| Abstract (HTML) (6942 Views)
When the prevalence of S. aureus on inanimate surfaces and among healthcare workers was compared, healthcare workers had a higher percentage (68.85%) than inanimate surfaces (45.69%).
The antibiotic susceptibility profile of S. aureus isolates is provided in Table 3. The isolates were more susceptible to meropenem, augmentin, tetracycline, ceftazidime, cefuroxime, and cephalexin. Of the 206 S. aureus isolates tested for MRSA using cefoxitin disk diffusion, 43.69% (n = 90) were methicillin-resistant (Table 4).
Discussion
S. aureus (45.69%) was the prevalent bacterium isolated from inanimate surfaces/fomites in this study. These results are comparable to those of the Brazilian study, which found that S. aureus was the primary organism isolated from fomites 53.3 percent of the time (25). The findings of Munveshyaka et al. (26) on inanimate surfaces and equipment are also consistent with these findings. S. aureus can form biofilms on inanimate surfaces/fomites, and these biofilms can be more resistant to disinfectants and cleaning efforts, making them a more persistent source of infection.
S. aureus was observed more frequently in the nostrils than on the palms of the hands in this study, which corresponds to the findings of Pant and Sharma (27) and Junu et al. (28). This result is consistent with the notion that S. aureus most frequently colonizes the nostrils. Compared with nasal carriers, there are fewer reports of hand carriers. Compared with Mukhiya et al. (29) and Pant and Sharma (27), the prevalence of palm-of-hand carriers was lower, which may suggest that the healthcare workers who took part in this study practiced better hand hygiene. In this investigation, every hand carrier was also a nasal carrier, and the isolates from both locations shared similar antibiograms, indicating that they were phenotypically identical. The notion that hands are the primary vector for spreading S. aureus from surfaces to the nostrils and from the nostrils to surfaces is further supported by the possibility that these carriers tend to pick their noses.
The bacterial isolates were resistant to frequently used antibiotics. Erythromycin (29.13%), cotrimoxazole (29.13%), gentamicin (33.98%), ampicillin (33.98%), and ciprofloxacin (36.41%) had low susceptibility rates against S. aureus. S. aureus was more resistant to these drugs. This could be due to their availability, cost, and misuse. This is in line with the findings of Sanusi et al. (30). Adam et al. (31), on the other hand, found that the highest rate of S. aureus resistance was to trimethoprim-sulfamethoxazole. This could be due to the development of resistance mechanisms such as reduced antibiotic accumulation within the bacteria and bypassing the antibiotic's inhibitory effects.
Of the 390 bacterial isolates obtained from the two tertiary hospitals in Abia State, 206 (52.82%) were positive for S. aureus. Mukhiya et al. (32) and Firesbhat et al. (33) reported the presence of S. aureus on hospital surfaces in Nepal and Ethiopia, respectively, despite the scarcity of data regarding the prevalence of MRSA in Nigeria. These results contradict those of this investigation. The findings of this study are in line with those of Anyadoh et al. (34) and Sanusi et al. (30), who found that more than 50% of hospital surfaces were contaminated with S. aureus.
The rise of MRSA, which is resistant to cephalosporins, a class of antibiotics commonly used to treat Staphylococcus infections, as well as monobactams and all beta-lactam drugs, has worsened the emergence of S. aureus infections (35). Identifying MRSA accurately requires prompt and early diagnosis because MRSA infections lead to treatment issues and spread (36).
In this study, 90 (43.69%) S. aureus isolates were found to be resistant by the cefoxitin disk diffusion test for MRSA. This is comparable to the study by Khairullah et al. (37), which revealed that 47.62% of the isolates tested positive for MRSA. In comparison, Adam et al. (31) and Oguzkaya-Artan et al. (38) reported 2.1% of MRSA positivity, while Sanusi et al. (30) reported 5.4%. According to this study, a number of variables, such as improper hand hygiene and failure to clean surfaces, might contribute to the development of MRSA contamination on fomites/inanimate surfaces and healthcare personnel. MRSA contamination raises the possibility of the spread of hard-to-treat Staphylococci, posing a major public health danger.
According to Miragaia (39), mecA genotyping by PCR remains the primary recommendation despite its inability to be carried out on a regular basis, and phenotypic detection of MRSA via disk diffusion has not yet yielded fully reliable results. Nevertheless, because of its speed and affordability, disk diffusion identification of MRSA is still often utilized (40).
Oxacillin and cefoxitin diffusion disks exhibit the same 100% sensitivity and 74.07% and 92.59% specificities, respectively (41). However, because there is still a high percentage of false positives with the oxacillin disk diffusion approach, a number of earlier investigations found that cefoxitin disk diffusion had a higher sensitivity level than oxacillin for identifying MRSA (42). According to Vyas et al. (41), beta-lactamase hyperproduction may contribute to false positives by causing oxacillin resistance to manifest phenotypically without a genotypic resistance mechanism.
A total of 20 suspected methicillin-resistant S. aureus isolates were tested for the mecA gene, and only 4 isolates (20% of all isolates tested by PCR) were mecA gene-positive. This might be due to false positives in the phenotypic analysis. Suspected MRSA isolates were found to have the mecA gene, as shown by the PCR results. This is similar to Khirullah et al. (37), where 30% of the MRSA isolates tested were mecA gene-positive. However, this contrasts with Sanusi et al. (30), who reported that 83.33% of MRSA isolates were positive for the mecA gene. These findings are in line with the study by Ramandinianto et al. (43). Because it can increase the expression of PBP2a, which the mecA gene encodes, cefoxitin is an effective inducer of mecA gene expression (44). This also agrees with Reichmann and Pinho (45).
Conclusion
This study was conducted to detect the mecA gene and MRSA from S. aureus isolated from inanimate surfaces, palms of the hands, and nostrils of healthcare workers in selected hospital wards in the two tertiary hospitals in Abia State. This study found an MRSA prevalence of 43.69% and mecA gene positivity of only 20%.
The hospital wards evaluated in this study showed the presence of bacterial pathogens on inanimate surfaces and in the nostrils of healthcare workers, with S. aureus being the prevalent bacterial isolate in this study. Nasal carriage was higher than hand carriage in this study.
The presence of MRSA in the two tertiary hospitals poses a risk to healthcare and community environments by contaminating healthcare workers, patients, visitors, and surrounding surfaces. This could ultimately lead to community exposure to resistant bacteria. Therefore, prevention and control measures are required to stop the spread of S. aureus infections on fomites/inanimate surfaces and among healthcare personnel at tertiary hospitals in Abia State.
However, the unavailability of molecular laboratories in close proximity to run the mecA gene analysis immediately limited this study.
Acknowledgement
We thank the management of the Federal Medical Centre, Umuahia, and the Abia State University Teaching Hospital, Aba, Abia State, for granting ethical approval. We are grateful to the healthcare workers who participated in this study for their informed consent. We also acknowledge Sir and Lady O. Mgbeokwere for their financial support.
Funding Sources
Not applicable.
Ethical Statement
The ethics committees of the Federal Medical Centre, Umuahia (Code: FMC/QEH/G.596/Vol.10/746), and Abia State University Teaching Hospital (Code: ABSUTH/MAC/117/VOL1/60) approved the study.
Conflicts of Interest
The authors have no competing interests.
Author Contributions
EUO: Conceptualization; Methodology; Data curation; Formal analysis; Funding acquisition; Investigation; Resources; Visualization; Writing-Original draft; Writing-Review and Editing. IO: Supervision; Methodology. EON: Methodology; Investigation; Interpretation.
Data Availability Statement
All data are available upon request from the corresponding author.
Use of Artificial Intelligence
The authors declare that no artificial intelligence tools were used in this work.
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Introduction
Infections acquired in hospitals or other healthcare facilities are a significant public health issue (1). In developed nations, the prevalence of healthcare-associated infections (HAIs) is already high, affecting between 5% and 15% of patients admitted to standard wards and up to 50% of critically ill patients in intensive care units (ICUs) (2,3).
It is obvious that monitoring the hospital environment is crucial for preventing nosocomial infections. Although hand-to-hand contact is likely the greatest risk, surface contamination may also serve as a potential source of infection. Multidrug-resistant (MDR) microorganisms may contaminate high-contact communal items, such as telephones and medical charts, as well as the surfaces of frequently used medical equipment, necessitating laborious, expensive, and complicated operations to improve patient safety (4,5). The problem of environmental contamination presents an even greater challenge in the intensive care unit (ICU), where critically ill patients have multiple risk factors for nosocomial infections (6).
This issue becomes especially significant when multiresistant bacteria, such as non-fermenting rods, methicillin-resistant Staphylococcus, and vancomycin-resistant enterococci, arise in hospital settings (7-9).
MRSA, methicillin-resistant S. aureus, is among the most prevalent bacterial strains causing hard-to-control infections in hospital settings (10).
Coagulase-positive staphylococci (Such as S. aureus) and coagulase-negative staphylococci (S. epidermidis and S. saprophyticus) are germs that readily contaminate the hospital environment. People with venous catheters, individuals with diabetes, and healthcare workers are more susceptible to S. aureus. However, methicillin-resistant S. aureus (MRSA) poses the greatest threat because it causes nosocomial infections with exceptionally high rates of morbidity and mortality (11). S. aureus was one of the frequently isolated pathogens between 2006 and 2007 linked to nosocomial infections reported to the National Healthcare Safety Network. Of hospital supplies and equipment contaminated with S. aureus, 56% involved MRSA. Colonized or infected individuals are the most significant source of MRSA in hospitals because they can readily contaminate nearby electronic and medical equipment. MRSA can persist on dry surfaces for several months (12,13). Although the contaminated hands of healthcare workers are the main route by which MRSA is spread to patients, evidence indicates that patient infections can also result from exposure to MRSA-contaminated surfaces (14,15).
According to evidence from the literature review, S. aureus can survive on dry surfaces for anywhere from one week to three years (16). Although there is evidence that S. aureus may survive in both home and clinical environments, the dissemination of these organisms, especially MRSA, across the population has received less attention (17). According to certain studies, S. aureus may survive on a wide range of inanimate surfaces, including polyethylene for 90 days, sterile packaging for 266 days, screw-cap bottles for 318 days, and polypropylene for more than 1097 days (18). However, these results appear to be based on optimization of the experimental setup. These studies employed an inoculum of 107-109 CFU and staphylococcal strains that were highly resistant to desiccation. Although these findings were clear and consistent in the laboratory, they may not truly represent S. aureus survival in the general population. Because of their limited survival on dry surfaces for longer than 24 hours, dangerous and pathogenic S. aureus strains, such as MRSA, which cause hospital-associated infections, are rarely isolated from environmental fomites (19).
The epidemiology of MRSA, particularly on inanimate surfaces, has remained understudied in Abia State, Nigeria, and this may have contributed to its increase in hospital-acquired infections. The main aim of this study was to detect MRSA among S. aureus isolates and to detect the presence of the mecA gene among selected MRSA isolates.
This study was necessary because the majority of isolates recovered from inanimate surfaces, nostrils, and palms of the hands of healthcare workers in tertiary hospitals in Abia State were S. aureus.
Methods
This cross-sectional study was carried out in selected hospital wards in Federal Medical Centre, Umuahia, and Abia State University Teaching Hospital, Aba. Ethical approval was obtained from the healthcare facilities before sampling and analysis. Informed consent was obtained from the participating healthcare workers with utmost confidentiality.
The present study focused on 206 S. aureus isolates collected from inanimate surfaces, palms of the hands, and nostrils of healthcare workers after laboratory analysis. One hundred and twenty-two S. aureus isolates were collected from inanimate surfaces, while 84 S. aureus isolates were collected from the palms of the hands and nostrils of healthcare workers. A total of 14 S. aureus isolates were collected from the palms of the hands, while 70 S. aureus isolates were collected from nostrils. Sterile swab sticks dampened with sterile water were used to swab the surfaces of mattresses, tables, footwear, clinical coats, bed sheets, and pillows. These inanimate surfaces were selected based on their frequent use and direct contact with patients, healthcare workers, and visitors. Sterile swab sticks dampened with sterile water were used to swab the palms of the hands of healthcare workers, and sterile swab sticks were used to swab the nostrils of healthcare workers. To ensure that each surface area was well covered, the swab sticks were rotated.
Gram-stained isolates were identified using standard biochemical tests after the swab sticks were inoculated onto appropriate media (Blood agar and mannitol salt agar) and incubated for 24 to 48 hours at 37°C. Pigment production, acid production, coagulase, and catalase tests were the biochemical tests used to confirm S. aureus isolates from mannitol salt agar (20).
The disk diffusion method was used to test antibiotic susceptibility, and the results were interpreted in accordance with Clinical Laboratory Standards Institute guidelines (21). Sterile cotton wool swabs were dipped into a suspension of the organism's overnight growth prepared to the density of a 0.5 McFarland opacity standard to inoculate Mueller-Hinton culture plates. Any excess liquid from the swab was then expressed using the spread plate procedure before inoculation.
The antibiotic disks (Biomark, India) used had the following concentrations: tetracycline, 30 µg; ampicillin, 10 µg; meropenem, 10 µg; gentamicin, 10 µg; erythromycin, 5 µg; ciprofloxacin, 5 µg; cotrimoxazole, 25 µg; cefuroxime, 10 µg; augmentin, 30 µg; cefalexin, 10 µg; vancomycin, 30 µg; ceftazidime, 10 µg; chloramphenicol, 10 µg; ceftriaxone, 30 µg; cefotaxime, 30 µg; and amikacin, 30 µg.
To ensure that the growth was confluent or near confluent, the control and test plates were examined after overnight incubation. The diameter of each zone of inhibition was measured in mm using a ruler on the underside of the plate. Growth began at the endpoint of inhibition (22).
The Clinical and Laboratory Standards Institute criteria (23) were followed when conducting the test. Each isolate was suspended to a turbidity of 0.5 McFarland standard before being plated onto a Mueller-Hinton agar plate (Hardy Diagnostics, USA). On each plate, a 30 µg cefoxitin disk (Oxoid) was placed. Zone sizes were assessed after a 24-hour incubation period at 35°C. Resistance was defined as an inhibitory zone size of less than or equal to 19 mm. ATCC 33591 (MRSA) and ATCC 29213 (MSSA) were used as control strains.
To provide a detailed explanation, each isolate was cultured in 1 mL of sterile water in different 1.5 mL microcentrifuge tubes. For one minute, the samples were centrifuged at 10,000 rpm, and the supernatants were discarded.
After adding 200 µL of lysis buffer to each tube containing the pelleted samples, a vortex mixer was used to mix it thoroughly for a few seconds. The samples were incubated in a heating block machine (Biobase) at 55°C for 10 minutes. The samples were allowed to cool after incubation and were then centrifuged at 10,000 rpm for 30 seconds.
After this step, 200 µL of absolute ethanol was added to each sample, and the supernatants were carefully transferred into well-labeled spin columns fitted into collection tubes without dislodging the pellets.
The spin columns were centrifuged at 10,000 rpm for 1 minute, and the flow collected in the collection tubes was discarded.
Using 500 µL of wash buffer 1 and 2, respectively, the DNA trapped on the silica membrane in the spin columns was washed.
At each washing stage, the spin columns were centrifuged at 10,000 rpm for 30 seconds to allow the wash buffer to pass into the collection tubes.
To remove any traces of ethanol, the spin columns were spin-dried at 14,000 rpm. DNA samples were eluted into well-labeled, nuclease-free 1.5 mL microcentrifuge tubes with 50 µL of elution buffer. After elution, the DNA samples were stored at -20°C until further analysis (24).
The mecA gene was amplified by polymerase chain reaction (PCR) using specific primer pairs (mecA-F: 5'-AAAATCGATGGTAAAGGTTGGC-3'; mecA-R: 5'-AGTTCTGCAGTA CCGGATTTGC-3') (24).
For each isolate's DNA samples, a total reaction volume of 25 µL was prepared using 5X HOT FIREPol Blend Master Mix with 7.5 mM MgCl2 (Solis Biodyne). This was diluted to 1X concentration using 1X Blend Master Mix buffer (Solis Biodyne), 1.5 mM MgCl2, 200 µM of each deoxynucleoside triphosphate (dNTP) (Solis Biodyne), 25 pMol of each forward and reverse primer (BIOMERS, Germany), 2 units of Hot FIREPol DNA polymerase (Solis Biodyne), proofreading enzyme, 5 µL of extracted DNA, and sterile distilled water.
After five minutes of initial denaturation at 95°C, 30 amplification cycles of 30 seconds at 95°C, 30 seconds at 58°C, and 45 seconds at 72°C were carried out using a PTC 200 gradient thermal cycler Eppendorf. A final extension phase of 10 minutes at 72°C followed. Electrophoresis was performed at 80 V for 60 minutes after the resultant amplicons were separated on a 1.5% agarose gel. After electrophoresis, ethidium bromide staining and a UV transilluminator were used to view the DNA bands. A 100 bp DNA ladder was used as the DNA molecular weight marker (24).
Statistical analysis
SPSS statistical software version 20.0 was used for data analysis. Categorical variables, such as the frequency of the bacterial isolates, were summarized using proportions expressed as percentages.
Results
The prevalence of S. aureus on inanimate surfaces is provided in Table 1. Of the 122 S. aureus isolates collected from inanimate surfaces, footwear harbored the highest proportion (39.34%, n = 48), followed by mattresses (38.52%, n = 47), while clinical coats had the lowest proportion (0.82%, n = 1). At a 95% confidence level, the calculated t-test value (4.366) was greater than the critical t-test value (2.015), indicating that the result was statistically significant and unlikely to be due to random chance.
Infections acquired in hospitals or other healthcare facilities are a significant public health issue (1). In developed nations, the prevalence of healthcare-associated infections (HAIs) is already high, affecting between 5% and 15% of patients admitted to standard wards and up to 50% of critically ill patients in intensive care units (ICUs) (2,3).
It is obvious that monitoring the hospital environment is crucial for preventing nosocomial infections. Although hand-to-hand contact is likely the greatest risk, surface contamination may also serve as a potential source of infection. Multidrug-resistant (MDR) microorganisms may contaminate high-contact communal items, such as telephones and medical charts, as well as the surfaces of frequently used medical equipment, necessitating laborious, expensive, and complicated operations to improve patient safety (4,5). The problem of environmental contamination presents an even greater challenge in the intensive care unit (ICU), where critically ill patients have multiple risk factors for nosocomial infections (6).
This issue becomes especially significant when multiresistant bacteria, such as non-fermenting rods, methicillin-resistant Staphylococcus, and vancomycin-resistant enterococci, arise in hospital settings (7-9).
MRSA, methicillin-resistant S. aureus, is among the most prevalent bacterial strains causing hard-to-control infections in hospital settings (10).
Coagulase-positive staphylococci (Such as S. aureus) and coagulase-negative staphylococci (S. epidermidis and S. saprophyticus) are germs that readily contaminate the hospital environment. People with venous catheters, individuals with diabetes, and healthcare workers are more susceptible to S. aureus. However, methicillin-resistant S. aureus (MRSA) poses the greatest threat because it causes nosocomial infections with exceptionally high rates of morbidity and mortality (11). S. aureus was one of the frequently isolated pathogens between 2006 and 2007 linked to nosocomial infections reported to the National Healthcare Safety Network. Of hospital supplies and equipment contaminated with S. aureus, 56% involved MRSA. Colonized or infected individuals are the most significant source of MRSA in hospitals because they can readily contaminate nearby electronic and medical equipment. MRSA can persist on dry surfaces for several months (12,13). Although the contaminated hands of healthcare workers are the main route by which MRSA is spread to patients, evidence indicates that patient infections can also result from exposure to MRSA-contaminated surfaces (14,15).
According to evidence from the literature review, S. aureus can survive on dry surfaces for anywhere from one week to three years (16). Although there is evidence that S. aureus may survive in both home and clinical environments, the dissemination of these organisms, especially MRSA, across the population has received less attention (17). According to certain studies, S. aureus may survive on a wide range of inanimate surfaces, including polyethylene for 90 days, sterile packaging for 266 days, screw-cap bottles for 318 days, and polypropylene for more than 1097 days (18). However, these results appear to be based on optimization of the experimental setup. These studies employed an inoculum of 107-109 CFU and staphylococcal strains that were highly resistant to desiccation. Although these findings were clear and consistent in the laboratory, they may not truly represent S. aureus survival in the general population. Because of their limited survival on dry surfaces for longer than 24 hours, dangerous and pathogenic S. aureus strains, such as MRSA, which cause hospital-associated infections, are rarely isolated from environmental fomites (19).
The epidemiology of MRSA, particularly on inanimate surfaces, has remained understudied in Abia State, Nigeria, and this may have contributed to its increase in hospital-acquired infections. The main aim of this study was to detect MRSA among S. aureus isolates and to detect the presence of the mecA gene among selected MRSA isolates.
This study was necessary because the majority of isolates recovered from inanimate surfaces, nostrils, and palms of the hands of healthcare workers in tertiary hospitals in Abia State were S. aureus.
Methods
This cross-sectional study was carried out in selected hospital wards in Federal Medical Centre, Umuahia, and Abia State University Teaching Hospital, Aba. Ethical approval was obtained from the healthcare facilities before sampling and analysis. Informed consent was obtained from the participating healthcare workers with utmost confidentiality.
The present study focused on 206 S. aureus isolates collected from inanimate surfaces, palms of the hands, and nostrils of healthcare workers after laboratory analysis. One hundred and twenty-two S. aureus isolates were collected from inanimate surfaces, while 84 S. aureus isolates were collected from the palms of the hands and nostrils of healthcare workers. A total of 14 S. aureus isolates were collected from the palms of the hands, while 70 S. aureus isolates were collected from nostrils. Sterile swab sticks dampened with sterile water were used to swab the surfaces of mattresses, tables, footwear, clinical coats, bed sheets, and pillows. These inanimate surfaces were selected based on their frequent use and direct contact with patients, healthcare workers, and visitors. Sterile swab sticks dampened with sterile water were used to swab the palms of the hands of healthcare workers, and sterile swab sticks were used to swab the nostrils of healthcare workers. To ensure that each surface area was well covered, the swab sticks were rotated.
Gram-stained isolates were identified using standard biochemical tests after the swab sticks were inoculated onto appropriate media (Blood agar and mannitol salt agar) and incubated for 24 to 48 hours at 37°C. Pigment production, acid production, coagulase, and catalase tests were the biochemical tests used to confirm S. aureus isolates from mannitol salt agar (20).
The disk diffusion method was used to test antibiotic susceptibility, and the results were interpreted in accordance with Clinical Laboratory Standards Institute guidelines (21). Sterile cotton wool swabs were dipped into a suspension of the organism's overnight growth prepared to the density of a 0.5 McFarland opacity standard to inoculate Mueller-Hinton culture plates. Any excess liquid from the swab was then expressed using the spread plate procedure before inoculation.
The antibiotic disks (Biomark, India) used had the following concentrations: tetracycline, 30 µg; ampicillin, 10 µg; meropenem, 10 µg; gentamicin, 10 µg; erythromycin, 5 µg; ciprofloxacin, 5 µg; cotrimoxazole, 25 µg; cefuroxime, 10 µg; augmentin, 30 µg; cefalexin, 10 µg; vancomycin, 30 µg; ceftazidime, 10 µg; chloramphenicol, 10 µg; ceftriaxone, 30 µg; cefotaxime, 30 µg; and amikacin, 30 µg.
To ensure that the growth was confluent or near confluent, the control and test plates were examined after overnight incubation. The diameter of each zone of inhibition was measured in mm using a ruler on the underside of the plate. Growth began at the endpoint of inhibition (22).
The Clinical and Laboratory Standards Institute criteria (23) were followed when conducting the test. Each isolate was suspended to a turbidity of 0.5 McFarland standard before being plated onto a Mueller-Hinton agar plate (Hardy Diagnostics, USA). On each plate, a 30 µg cefoxitin disk (Oxoid) was placed. Zone sizes were assessed after a 24-hour incubation period at 35°C. Resistance was defined as an inhibitory zone size of less than or equal to 19 mm. ATCC 33591 (MRSA) and ATCC 29213 (MSSA) were used as control strains.
To provide a detailed explanation, each isolate was cultured in 1 mL of sterile water in different 1.5 mL microcentrifuge tubes. For one minute, the samples were centrifuged at 10,000 rpm, and the supernatants were discarded.
After adding 200 µL of lysis buffer to each tube containing the pelleted samples, a vortex mixer was used to mix it thoroughly for a few seconds. The samples were incubated in a heating block machine (Biobase) at 55°C for 10 minutes. The samples were allowed to cool after incubation and were then centrifuged at 10,000 rpm for 30 seconds.
After this step, 200 µL of absolute ethanol was added to each sample, and the supernatants were carefully transferred into well-labeled spin columns fitted into collection tubes without dislodging the pellets.
The spin columns were centrifuged at 10,000 rpm for 1 minute, and the flow collected in the collection tubes was discarded.
Using 500 µL of wash buffer 1 and 2, respectively, the DNA trapped on the silica membrane in the spin columns was washed.
At each washing stage, the spin columns were centrifuged at 10,000 rpm for 30 seconds to allow the wash buffer to pass into the collection tubes.
To remove any traces of ethanol, the spin columns were spin-dried at 14,000 rpm. DNA samples were eluted into well-labeled, nuclease-free 1.5 mL microcentrifuge tubes with 50 µL of elution buffer. After elution, the DNA samples were stored at -20°C until further analysis (24).
The mecA gene was amplified by polymerase chain reaction (PCR) using specific primer pairs (mecA-F: 5'-AAAATCGATGGTAAAGGTTGGC-3'; mecA-R: 5'-AGTTCTGCAGTA CCGGATTTGC-3') (24).
For each isolate's DNA samples, a total reaction volume of 25 µL was prepared using 5X HOT FIREPol Blend Master Mix with 7.5 mM MgCl2 (Solis Biodyne). This was diluted to 1X concentration using 1X Blend Master Mix buffer (Solis Biodyne), 1.5 mM MgCl2, 200 µM of each deoxynucleoside triphosphate (dNTP) (Solis Biodyne), 25 pMol of each forward and reverse primer (BIOMERS, Germany), 2 units of Hot FIREPol DNA polymerase (Solis Biodyne), proofreading enzyme, 5 µL of extracted DNA, and sterile distilled water.
After five minutes of initial denaturation at 95°C, 30 amplification cycles of 30 seconds at 95°C, 30 seconds at 58°C, and 45 seconds at 72°C were carried out using a PTC 200 gradient thermal cycler Eppendorf. A final extension phase of 10 minutes at 72°C followed. Electrophoresis was performed at 80 V for 60 minutes after the resultant amplicons were separated on a 1.5% agarose gel. After electrophoresis, ethidium bromide staining and a UV transilluminator were used to view the DNA bands. A 100 bp DNA ladder was used as the DNA molecular weight marker (24).
Statistical analysis
SPSS statistical software version 20.0 was used for data analysis. Categorical variables, such as the frequency of the bacterial isolates, were summarized using proportions expressed as percentages.
Results
The prevalence of S. aureus on inanimate surfaces is provided in Table 1. Of the 122 S. aureus isolates collected from inanimate surfaces, footwear harbored the highest proportion (39.34%, n = 48), followed by mattresses (38.52%, n = 47), while clinical coats had the lowest proportion (0.82%, n = 1). At a 95% confidence level, the calculated t-test value (4.366) was greater than the critical t-test value (2.015), indicating that the result was statistically significant and unlikely to be due to random chance.
|
Table 1. Prevalence of Staphylococcus aureus on inanimate surfaces
.PNG) |
When the prevalence of S. aureus on inanimate surfaces and among healthcare workers was compared, healthcare workers had a higher percentage (68.85%) than inanimate surfaces (45.69%).
The antibiotic susceptibility profile of S. aureus isolates is provided in Table 3. The isolates were more susceptible to meropenem, augmentin, tetracycline, ceftazidime, cefuroxime, and cephalexin. Of the 206 S. aureus isolates tested for MRSA using cefoxitin disk diffusion, 43.69% (n = 90) were methicillin-resistant (Table 4).
.PNG)
.PNG)
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.PNG) Figure 1. Agarose gel electrophoresis amplification of the mecA gene (532 bp) of S. aureus isolates. M, Marker (100 bp); lanes 1, 2, 3, 4, 6, and 7, negative; lanes 5, 8, 9, and 10, positive |
Discussion
S. aureus (45.69%) was the prevalent bacterium isolated from inanimate surfaces/fomites in this study. These results are comparable to those of the Brazilian study, which found that S. aureus was the primary organism isolated from fomites 53.3 percent of the time (25). The findings of Munveshyaka et al. (26) on inanimate surfaces and equipment are also consistent with these findings. S. aureus can form biofilms on inanimate surfaces/fomites, and these biofilms can be more resistant to disinfectants and cleaning efforts, making them a more persistent source of infection.
S. aureus was observed more frequently in the nostrils than on the palms of the hands in this study, which corresponds to the findings of Pant and Sharma (27) and Junu et al. (28). This result is consistent with the notion that S. aureus most frequently colonizes the nostrils. Compared with nasal carriers, there are fewer reports of hand carriers. Compared with Mukhiya et al. (29) and Pant and Sharma (27), the prevalence of palm-of-hand carriers was lower, which may suggest that the healthcare workers who took part in this study practiced better hand hygiene. In this investigation, every hand carrier was also a nasal carrier, and the isolates from both locations shared similar antibiograms, indicating that they were phenotypically identical. The notion that hands are the primary vector for spreading S. aureus from surfaces to the nostrils and from the nostrils to surfaces is further supported by the possibility that these carriers tend to pick their noses.
The bacterial isolates were resistant to frequently used antibiotics. Erythromycin (29.13%), cotrimoxazole (29.13%), gentamicin (33.98%), ampicillin (33.98%), and ciprofloxacin (36.41%) had low susceptibility rates against S. aureus. S. aureus was more resistant to these drugs. This could be due to their availability, cost, and misuse. This is in line with the findings of Sanusi et al. (30). Adam et al. (31), on the other hand, found that the highest rate of S. aureus resistance was to trimethoprim-sulfamethoxazole. This could be due to the development of resistance mechanisms such as reduced antibiotic accumulation within the bacteria and bypassing the antibiotic's inhibitory effects.
Of the 390 bacterial isolates obtained from the two tertiary hospitals in Abia State, 206 (52.82%) were positive for S. aureus. Mukhiya et al. (32) and Firesbhat et al. (33) reported the presence of S. aureus on hospital surfaces in Nepal and Ethiopia, respectively, despite the scarcity of data regarding the prevalence of MRSA in Nigeria. These results contradict those of this investigation. The findings of this study are in line with those of Anyadoh et al. (34) and Sanusi et al. (30), who found that more than 50% of hospital surfaces were contaminated with S. aureus.
The rise of MRSA, which is resistant to cephalosporins, a class of antibiotics commonly used to treat Staphylococcus infections, as well as monobactams and all beta-lactam drugs, has worsened the emergence of S. aureus infections (35). Identifying MRSA accurately requires prompt and early diagnosis because MRSA infections lead to treatment issues and spread (36).
In this study, 90 (43.69%) S. aureus isolates were found to be resistant by the cefoxitin disk diffusion test for MRSA. This is comparable to the study by Khairullah et al. (37), which revealed that 47.62% of the isolates tested positive for MRSA. In comparison, Adam et al. (31) and Oguzkaya-Artan et al. (38) reported 2.1% of MRSA positivity, while Sanusi et al. (30) reported 5.4%. According to this study, a number of variables, such as improper hand hygiene and failure to clean surfaces, might contribute to the development of MRSA contamination on fomites/inanimate surfaces and healthcare personnel. MRSA contamination raises the possibility of the spread of hard-to-treat Staphylococci, posing a major public health danger.
According to Miragaia (39), mecA genotyping by PCR remains the primary recommendation despite its inability to be carried out on a regular basis, and phenotypic detection of MRSA via disk diffusion has not yet yielded fully reliable results. Nevertheless, because of its speed and affordability, disk diffusion identification of MRSA is still often utilized (40).
Oxacillin and cefoxitin diffusion disks exhibit the same 100% sensitivity and 74.07% and 92.59% specificities, respectively (41). However, because there is still a high percentage of false positives with the oxacillin disk diffusion approach, a number of earlier investigations found that cefoxitin disk diffusion had a higher sensitivity level than oxacillin for identifying MRSA (42). According to Vyas et al. (41), beta-lactamase hyperproduction may contribute to false positives by causing oxacillin resistance to manifest phenotypically without a genotypic resistance mechanism.
A total of 20 suspected methicillin-resistant S. aureus isolates were tested for the mecA gene, and only 4 isolates (20% of all isolates tested by PCR) were mecA gene-positive. This might be due to false positives in the phenotypic analysis. Suspected MRSA isolates were found to have the mecA gene, as shown by the PCR results. This is similar to Khirullah et al. (37), where 30% of the MRSA isolates tested were mecA gene-positive. However, this contrasts with Sanusi et al. (30), who reported that 83.33% of MRSA isolates were positive for the mecA gene. These findings are in line with the study by Ramandinianto et al. (43). Because it can increase the expression of PBP2a, which the mecA gene encodes, cefoxitin is an effective inducer of mecA gene expression (44). This also agrees with Reichmann and Pinho (45).
Conclusion
This study was conducted to detect the mecA gene and MRSA from S. aureus isolated from inanimate surfaces, palms of the hands, and nostrils of healthcare workers in selected hospital wards in the two tertiary hospitals in Abia State. This study found an MRSA prevalence of 43.69% and mecA gene positivity of only 20%.
The hospital wards evaluated in this study showed the presence of bacterial pathogens on inanimate surfaces and in the nostrils of healthcare workers, with S. aureus being the prevalent bacterial isolate in this study. Nasal carriage was higher than hand carriage in this study.
The presence of MRSA in the two tertiary hospitals poses a risk to healthcare and community environments by contaminating healthcare workers, patients, visitors, and surrounding surfaces. This could ultimately lead to community exposure to resistant bacteria. Therefore, prevention and control measures are required to stop the spread of S. aureus infections on fomites/inanimate surfaces and among healthcare personnel at tertiary hospitals in Abia State.
However, the unavailability of molecular laboratories in close proximity to run the mecA gene analysis immediately limited this study.
Acknowledgement
We thank the management of the Federal Medical Centre, Umuahia, and the Abia State University Teaching Hospital, Aba, Abia State, for granting ethical approval. We are grateful to the healthcare workers who participated in this study for their informed consent. We also acknowledge Sir and Lady O. Mgbeokwere for their financial support.
Funding Sources
Not applicable.
Ethical Statement
The ethics committees of the Federal Medical Centre, Umuahia (Code: FMC/QEH/G.596/Vol.10/746), and Abia State University Teaching Hospital (Code: ABSUTH/MAC/117/VOL1/60) approved the study.
Conflicts of Interest
The authors have no competing interests.
Author Contributions
EUO: Conceptualization; Methodology; Data curation; Formal analysis; Funding acquisition; Investigation; Resources; Visualization; Writing-Original draft; Writing-Review and Editing. IO: Supervision; Methodology. EON: Methodology; Investigation; Interpretation.
Data Availability Statement
All data are available upon request from the corresponding author.
Use of Artificial Intelligence
The authors declare that no artificial intelligence tools were used in this work.
Research Article: Research Article |
Subject:
Microbiology
Received: 2025/03/21 | Accepted: 2025/10/28 | Published: 2026/04/25 | ePublished: 2026/04/25
Received: 2025/03/21 | Accepted: 2025/10/28 | Published: 2026/04/25 | ePublished: 2026/04/25
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