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Article

Carriage of Rifampicin- and Multidrug-Resistant Pseudomonas aeruginosa in Apparently Healthy Camels: A View Through a Zoonosis Lens

by
Dalia Hamza
and
Hala M. Zaher
*
Department of Zoonoses, Faculty of Veterinary Medicine, Cairo University, Cairo 12211, Egypt
*
Author to whom correspondence should be addressed.
Microbiol. Res. 2025, 16(6), 107; https://doi.org/10.3390/microbiolres16060107 (registering DOI)
Submission received: 2 April 2025 / Revised: 15 May 2025 / Accepted: 22 May 2025 / Published: 25 May 2025
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Abstract

:
Pseudomonas aeruginosa poses a significant global concern in human and veterinary medicine due to its resistance to multiple antimicrobials. Limited research has been carried out on rifampicin-resistant P. aeruginosa, particularly in food-producing animals such as camels. Therefore, the purpose of this study was to investigate the occurrence of rifampicin- and multidrug-resistant P. aeruginosa in apparently healthy camels. Nasal swabs and tissue samples were collected from one hundred apparently healthy slaughtered camels, and they were subjected to bacteriological isolation and identification of P. aeruginosa. Antimicrobial susceptibility testing was performed, followed by phenotypic and genotypic detection of ESBL-producing P. aeruginosa isolates. Twenty-two P. aeruginosa strains were investigated for the rpoB gene, including rifampicin-resistant isolates. P. aeruginosa was found in 16% (16/100) of the investigated apparently healthy slaughtered camels. P. aeruginosa was confirmed in sixteen and six isolates from nasal swabs and tissue samples, respectively, by pigment production on cetrimide agar. The most predominant beta-lactamase-encoding gene in twenty-two ESBL-producing isolates was blaPER (40.9%), followed by blaCTX-M (36.4%), blaTEM (31.8%), and blaSHV (27.3%). Multidrug resistance was identified in 54.5% (12/22) of P. aeruginosa isolates. The rpoB gene was detected in 11 (50%) out of 22 P. aeruginosa strains, with eleven positive isolates being regarded as rifampicin-resistant. Furthermore, phylogenetic analysis of a rifampicin- and multidrug-resistant P. aeruginosa rpoB gene sequence revealed a genetic relatedness to P. aeruginosa strains retrieved from human clinical cases. In conclusion, this study provides a snapshot on the occurrence of rifampicin- and multidrug-resistant P. aeruginosa among apparently healthy camels. In line with a possible risk of animal-to-human transfer, further molecular studies on rifampicin-resistant P. aeruginosa in animals are required to better understand and combat this serious zoonotic pathogen.

1. Introduction

Pseudomonas aeruginosa is a ubiquitous, Gram-negative, and opportunistic pathogen in human and veterinary medicine. In humans, severe P. aeruginosa infections are typically seen in immunocompromised patients and in nosocomial settings, resulting in pneumonia and septicemia [1]. P. aeruginosa can cause diseases in food-producing and companion animals, such as otitis externa in dogs [2], clinical and subclinical mastitis in dairy cattle [3], and endometritis in cows, camels, and mares [4]. Treatment of both community-acquired and nosocomial P. aeruginosa infections is a great challenge, as it can develop resistance to many classes of antimicrobial drugs [5]. The World Health Organization (WHO) designated carbapenem-resistant Enterobacterales (CRE), Acinetobacter baumannii (CRPA), Pseudomonas aeruginosa (CRPA), methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-resistant Enterococcus faecium (VRE) as critical or high-priority antimicrobial-resistant bacteria. These bacteria are significant pathogens worldwide, primarily causing healthcare-associated infections [6]. A primary resistance mechanism in P. aeruginosa is the production of beta-lactamase enzymes, including extended-spectrum beta-lactamases (ESBLs) encoded by genes such as blaPER, blaCTX-M, blaSHV, and blaTEM, which hydrolyze beta-lactam antibiotics [7,8]. Furthermore, multidrug-resistant (MDR) P. aeruginosa has grown rapidly over the last decades, rendering treatments of P. aeruginosa infection more challenging [9]. Camels contribute significantly to human life in the Middle East, Africa, and South Asia owing to cultural and economic bases. In Egypt, dromedary camels (Camelus dromedarius) are multipurpose animals that provide several benefits for humans, such as transportation, tourism, milk, meat, and hair. They have a major role in nomadic or pastoralist communities living in arid or semi-arid areas [10]; hence, camels represent an important source of zoonotic disease transmission to humans [11]. The asymptomatic carriage of multidrug-resistant P. aeruginosa in camels worsens the threat [12], as antibiotic-resistant strains can silently enter the food chain or the environment, posing a zoonotic risk [13].
As antimicrobial resistance continues to rise worldwide, rifampicin is regarded as the “last-resort” antibiotic that retains antibacterial activity against multidrug-resistant bacterial pathogens [14]. Rifampin was primarily employed as a key drug for tuberculosis due to its potent bactericidal effect against Mycobacterium tuberculosis [15]. Later on, rifampicin has been widely used for implant-associated staphylococcal infections since it has proven activity in staphylococcal biofilm-related infections [16]. Unfortunately, its efficiency is limited by the rapid development of resistant bacteria. Rifampicin resistance has been reported in many Gram-negative urinary tract pathogens [17,18,19], tuberculosis patients [20], and Staphylococcus aureus strains [21,22]. A few reports regarding rifampicin resistance in P. aeruginosa have been published so far [23,24,25], revealing an overlooked issue in camels. Also, from a public health perspective, it is imperative to predict rifampicin resistance and prevent its emergence. Therefore, the current study aimed to investigate the occurrence of rifampicin- and multidrug-resistant P. aeruginosa strains in apparently healthy slaughtered camels as well as conduct a phylogenetic analysis to clarify the public health relevance of such strains.

2. Materials and Methods

2.1. Sample Collection

This study included one hundred apparently healthy slaughtered camels selected from three local abattoirs (Bassitin, Imbaba, and Munib) in Cairo and Giza governorates. The selection criteria were apparently healthy camels that showed no obvious signs of illness upon physical examination or observation. They appeared normal in behavior, movement, and physical condition. Nasal swabs (n = 100) were collected just after slaughtering by inserting sterile cotton swabs into the nasal passage after thoroughly cleaning and disinfecting the external nares. Each nasal swab was placed into a screw-capped tube containing Cary–Blair transport media. After disinfecting the exterior surface of tissue samples (n = 100) with 70% alcohol to reduce surface contamination, a piece of fresh tissue from the thigh muscle was obtained using sterile scissors and tissue forceps and placed into sterile containers. All samples were transported in an icebox to the laboratory of Zoonoses, Faculty of Veterinary Medicine, Cairo University, for immediate bacteriological processing.

2.2. Isolation and Identification of Pseudomonas aeruginosa

Tissue samples were homogenized with a tissue grinder under aseptic conditions. The nasal and tissue samples were inoculated into brain heart infusion broth at 37 °C for 24 h. Subsequently, they were cultured on cetrimide agar plates and incubated at 37 °C for 18–24 h in aerobic conditions. Suspected colonies were identified by their pigmentation (either brown or green) and a musty smell. A subculture of a single colony was performed on blood agar to obtain a pure colony. The preliminary identification of isolates was based on the Gram staining, hemolysis on blood agar, pigment production, and biochemical characteristics, according to Quinn et al. [26]. All presumptive P. aeruginosa isolates were finally confirmed using the VITEK®2 automated system (bioMérieux).

2.3. Antimicrobial Susceptibility Testing

All P. aeruginosa strains were tested for antimicrobial susceptibility using the Kirby–Bauer disc diffusion method, as recommended by the Clinical and Laboratory Standards Institute (CLSI) guidelines [27]. Twelve antimicrobial agents were included: ceftazidime (CAZ; 30 µg), cefepime (CPM; 30 µg), ceftriaxone (CTR; 30 μg), cefotaxime (CTX; 30 μg), aztreonam (AT; 30 μg), imipenem (IPM; 10 µg), meropenem (MEM; 10 µg), amikacin (AK; 30 µg), gentamicin (GEN; 10 µg), ciprofloxacin (CIP; 5 µg), rifampicin (RIF; 30 μg), and trimethoprim/sulfamethoxazole (SXT; 1.25/23.75 μg). The diameter of the inhibitory zone surrounding antimicrobial discs was measured, and results were reported. Isolates resistant to at least one agent in three or more antimicrobial categories were regarded as multidrug resistant (MDR) [28].

2.4. Phenotypic Identification of ESBL-Producing P. aeruginosa Isolates

Twenty-two P. aeruginosa isolates were initially screened for ESBL production using a double-disc approximation test according to CLSI recommendations [27]. Briefly, the susceptibility to cefotaxime (30 μg), cefotaxime/clavulanate (30/10 μg), ceftazidime (30 μg), and ceftazidime/clavulanate (30/10 μg) was determined. ESBL-producing strains were recognized by a minimum 5 mm increase in zone diameter around cefotaxime/clavulanate and ceftazidime/clavulanate discs as compared to discs without clavulanic acid.

2.5. DNA Extraction

The genomic DNA was extracted from bacterial isolates by the boiling method [29]. The extracted DNA was preserved at −20 °C until further molecular analysis.

2.6. Genotypic Detection of Beta-Lactamase-Encoding Genes in ESBL-Producing P. aeruginosa Isolates

Polymerase chain reaction was carried out using specific primers to detect genes encoding ESBLs (blaTEM, blaSHV, blaCTX-M, and blaPER) in twenty-two ESBL-producing strains, as described previously [30,31,32].

2.7. Molecular Detection of the rpoB Gene in P. aeruginosa Isolates

All 22 P. aeruginosa strains, including 16 rifampicin-resistant and 6 rifampicin-susceptible isolates, were investigated for the P. aeruginosa rpoB gene using the following oligonucleotide primers: LAPS (5′-TGGCCGAGAACCAGTTCCGCGT-3′) and LAPS27 (5′-CGGCTTCGTCCAGCTTGTTCAG-3′) [33]. PCR amplification was carried out in a final volume of 50 μL containing 25 μL of EmeraldAmp GT PCR master mix (Takara, Japan), 0.5 µL of each primer (20 pmol), and 5 µL of DNA template and completed up to 50 μL with nuclease-free water. The PCR thermal profile was as follows: an initial denaturation at 94 °C for 10 min, followed by 40 cycles of denaturation at 94 °C for 30 s, annealing at 55 °C for 1 min, extension at 72 °C for 1 min, and a final extension step at 72 °C for 10 min.

2.8. Partial DNA Sequencing of the P. aeroginosa rpoB Gene and Phylogenetic Analysis

One PCR product of the rifampicin- and multidrug-resistant P. aeruginosa rpoB gene was selected and purified using a QIAquick purification kit (Qiagen, Hilden, Germany). Afterwards, sequencing was conducted on an ABI 3500 Genetic Analyzer (Applied Biosystems, Waltham, MA, USA) with the Big Dye Terminator V3.1 kit (Thermo Fisher, Waltham, MA, USA). The partial sequence of the P. aeruginosa rpoB gene was deposited in GenBank under the accession number PV287649. To determine the genetic relatedness between the P. aeruginosa rpoB gene sequence retrieved in this study and those isolated from human clinical cases on GenBank records, ClustalW multiple alignment was employed via BioEdit software version 7.0.9. MEGA 7 software was used to create a phylogenetic tree using a maximum likelihood method where a bootstrap consensus tree was achieved with 500 replicates (Figure 1).

3. Results

3.1. Occurrence of P. aeruginosa in Apparently Healthy Slaughtered Camels

Overall, P. aeruginosa was detected in 16% (16/100) of the examined apparently healthy slaughtered camels. Ten nasal swabs (10 isolates) from ten camels as well as six nasal swabs (6 isolates) and six tissue samples (6 isolates) from the same six camels were positive for P. aeruginosa infection, as shown in Table 1. All P. aeruginosa isolates were pyocyanin producers on cetrimide agar.

3.2. Antimicrobial Susceptibility Pattern of P. aeruginosa Isolates

Twenty-two isolates were resistant to ceftazidime, ceftriaxone, and cefotaxime (100%), followed by cefepime (95.5%). Rifampicin resistance was observed in 72.7% of P. aeruginosa strains, with 16 isolates being rifampicin-resistant and 6 isolates being rifampicin-susceptible. Sulfamethoxazole-trimethoprim and aztreonam resistance were found in 50% and 36.4%, respectively. A low level of resistance was detected towards meropenem (9.1%), gentamicin (4.5%), ciprofloxacin (4.5%), and imipenem (4.5%). On the other hand, all isolates were susceptible to amikacin. Multidrug resistance (MDR) was identified in 54.5% (12/22) of P. aeruginosa isolates, with ten and two isolates obtained from nasal swabs and tissue samples, respectively, displaying multidrug resistance patterns (Table 2).

3.3. Phenotypic and Genotypic Detection of ESBL-Producing P. aeruginosa Isolates

ESBL production was detected in all 22 P. aeruginosa isolates. All suspected ESBL producers were screened for beta-lactamase genes. The blaPER was the most predominant beta-lactamase gene (40.9%), followed by blaCTX-M (36.4%), blaTEM (31.8%), and blaSHV (27.3%), as exhibited in Table 3.

3.4. Occurrence of the rpoB gene in P. aeruginosa Isolates

In the current study, the rpoB gene was recognized in 11 (50%) out of 22 P. aeruginosa strains (Table 3). The eleven positive isolates were categorized as rifampicin-resistant.

4. Discussion

P. aeruginosa is one of the main causes of pneumonia in camels [34,35]; however, the published literature concerning the prevalence of P. aeruginosa in camels remains scarce [4]. In this study, the occurrence of P. aeruginosa in apparently healthy camels was higher than that documented by Abdelrahman et al. [12] (5.3%) and Gebru et al. [36] (1.8%) in apparently healthy camels in Egypt and Ethiopia, respectively, but it was lower than that identified by Elhariri et al. [37] in camel meat (22.5%). One of the predisposing stress factors for P. aeruginosa infection is animal transportation, which could accelerate P. aeruginosa growth and enhance its recovery rate [12]. In this study, nasal swabs (16 isolates) had a higher P. aeruginosa infection rate than tissue samples (6 isolates). P. aeruginosa infection may arise in camel slaughterhouses or farms and can be transmitted to camels through the following routes: P. aeruginosa is widespread in the environment, particularly in water, soil, and moist areas [38]. Therefore, camel slaughterhouses or farms with poor sanitation, standing water, or contaminated equipment could harbor the bacteria. Additionally, camels may become infected with P. aeruginosa through drinking contaminated water, especially if their immune system is compromised [39]. P. aeruginosa is often used as an indicator organism in quality control processes since its presence might indicate hygiene practices, inadequate sanitation, or water contamination [38,40], so contamination with P. aeruginosa may imply greater quality failures, affecting several operations along the supply chain. For example, contaminated raw materials, improper handling practices, poor packaging hygiene, and suboptimal storage conditions may introduce P. aeruginosa into the environment [41,42]. Furthermore, the identification of P. aeruginosa in an abattoir is critically important because it can be a reliable indicator of potential outbreaks. The presence of this pathogen in the abattoir environment (e.g., on equipment, in water supplies, or meat surfaces) serves as an early warning of contamination risk [43], enhancing bacterial growth and increasing the likelihood of an outbreak among workers. Moreover, P. aeruginosa is known to produce biofilm on surfaces [44,45]. Once established, these biofilms are difficult to remove and can cause persistent contamination, raising the risk of further outbreaks.
Importantly, P. aeruginosa is one of the top microorganisms requiring urgent novel antimicrobial intervention [46]. In the current study, there was a high resistance towards ceftazidime, ceftriaxone, cefotaxime, and cefepime. In a similar vein, P. aeruginosa strains isolated from apparently healthy camels demonstrated 100% resistance to cefotaxime and cefepime [12]. In addition, 100% of P. aeruginosa isolates obtained from camel meat were resistant to ceftazidime and ceftriaxone, followed by cefepime (95.2%) [37]. Ceftazidime is the most commonly prescribed cephalosporin for combating P. aeruginosa infections due to its specific anti-pseudomonal activity; nevertheless, ceftazidime resistance is rising [47]. Ceftazidime-resistant P. aeruginosa has been identified in clinical isolates globally [48,49], including Egypt [50]. Ceftazidime resistance is attributed to overexpression of the MexAB-OprM efflux pump, which is induced by mutations in the nalC, nalD or mexR regulatory genes [51,52]. Mutations in dacB, which encodes penicillin-binding protein 4 (PBP4); ampD, which encodes a peptidoglycan recycling enzyme; and ampR, which encodes a regulator of ampC production, may result in increased expression of AmpC β-lactamase [53]. While P. aeruginosa strains showed low resistance to meropenem, imipenem, gentamicin, and aztreonam in this study, Abdelrahman et al. [12] reported higher resistance to meropenem (88.2%), imipenem (82.4%), gentamicin (76.4%), and aztreonam (70.5%). Elhariri et al. [37] revealed higher resistance to aztreonam (76.1%) but lower resistance to meropenem (14.2%) and imipenem (23.8%). In this study, 50% of P. aeruginosa isolates were resistant to sulfamethoxazole/trimethoprim, whereas Abdelrahman et al. [12] and Elhariri et al. [37] recognized that 70.5% and 61.9% of isolates retrieved from apparently healthy camels were susceptible to sulfamethoxazole/trimethoprim, respectively. Variations in antibiotic use and antibiotic stewardship practices may account for the discrepancies in antibiotic resistance observed across studies [4]. Food-producing animals like cattle, camels, and sheep are exposed to antibiotics during their lives. Tetracyclines are a class of broad-spectrum antibiotics that are widely available, cheap, and effective in the treatment of respiratory, digestive, and septicemic diseases. Camel dairy farmers commonly use antibiotics such as oxytetracycline and tetracycline [54]. Quinolones and fluoroquinolones (FQs) are frequently implicated in the veterinary field due to their wide range of activity against both Gram-positive and Gram-negative pathogens. In addition, sulfonamides are widely used in livestock for prevention and control of many bacterial infections, including those associated with respiratory and genital diseases and mastitis [54]. Antibiotics may be employed in camel farming for disease treatment, prevention, and growth promotion [55]. According to a study conducted by Mohmed et al. [55], 80% of participants administered antibiotics without a prescription. Furthermore, their investigation revealed that the majority of camel farmers prefer self-administration over seeking veterinary assistance; notably, 88% of camel dairy farmers make their own decisions when providing antibiotics. As a result, antibiotic residues in dairy products are transmitted to consumers through ingestion, posing potential risks such as teratogenic effects, reproductive disorders, and the emergence of antimicrobial-resistant (AMR) bacteria [56].
P. aeruginosa is a multidrug-resistant opportunistic pathogen that causes acute or chronic infections in immunosuppressed people [9]. Multidrug resistance was detected in 54.5% of the retrieved P. aeruginosa isolates in this investigation; however, Elhariri et al. [37] reported MDR in all isolates. The emergence of MDR P. aeruginosa has also been reported worldwide [57,58], and it has recently become a public health concern since it usually occurs in patients with multiple underlying diseases, which may explain the worse outcome [59]. Moreover, antimicrobial resistance in P. aeruginosa infections in camels should be closely monitored in the future, in line with potential animal-to-human transfers between pets and owners [60,61] and similar to other zoonotic pathogens [62,63] because MDR Pseudomonas can be transmitted from various sources to humans via horizontal gene transfer, making the emergence and occurrence of MDR P. aeruginosa a hot topic [9]. It is known that pyocyanin, a blue phenazine pigment, is produced by 90–95% of P. aeruginosa strains [64]. It is employed in a variety of biological activities, involving biofilm formation, bacterial cell fitness, and gene expression [65]. It has been documented that P. aeruginosa isolates that produce pyocyanin have a higher prevalence of multidrug resistance and more virulence factors than non-producing strains [64]. Notably, food-producing and companion animals may be a major vehicle for the wide dissemination of ESBL-producing Enterobacteriaceae [66,67] and P. aeruginosa [68]. In this work, the most prevalent genotype for ESBL production was blaPER, followed by blaCTX-M, blaTEM, and blaSHV. Abdel-Rahman et al. [12] determined that blaTEM (64.7%) was the most frequently detected β-lactamase gene in P. aeruginosa isolates obtained from apparently healthy camels, followed by blaSHV (47.0%) and blaCTX-M (29.4%). However, the most common ESBL gene found in P. aeruginosa strains isolated from camel meat was blaCTX-M (38%), followed by blaSHV (33.3%) and both blaTEM and blaPER-1 at 28.5% [37]. In 1993, a Turkish patient at a French hospital provided the first evidence of PER-1, which is produced only by P. aeruginosa [69]. Most penicillins and cephalosporins, such as cefoperazone, cefuroxime, ceftriaxone, and cefazidime, are hydrolyzed effectively by this enzyme, yet PER-1 was not able to hydrolyse oxacillin, cephamycins, or imipenem [70]. In the last decade, CTX-M-type enzymes have become the most frequently distributed ESBLs worldwide, which prevail in community-acquired infections [71] and confer resistance to penicillins, extended-spectrum cephalosporins, and monobactams [72]. Consequently, camels could be a reservoir for ESBL-producing P. aeruginosa [12,37], posing a potential risk to human contacts.
Interestingly, in this study, 72.7% of the retrieved P. aeruginosa isolates were resistant to rifampicin, whereas Elhariri et al. [37] found that 100% of P. aeruginosa strains obtained from camel meat were rifampicin-resistant. To the best of the authors’ knowledge, there are no available data on the occurrence of rifampicin-resistant P. aeruginosa in other livestock, but there have been reports of rifampicin-resistant Mycobacterium tuberculosis in cattle [73] and rifampicin-resistant Brucella spp. in cattle, sheep, goats, and buffalo [74]. Rifampicin-resistance has also been detected in multi-resistant porcine livestock-associated methicillin-resistant Staphylococcus aureus (MRSA) [75] and in Escherichia coli in feedlot cattle [76]. Rifampicin is not a first-line treatment for P. aeruginosa infections; however, there are scientific and clinical reasons for investigating rifampicin resistance in P. aeruginosa. It provides a model for studying rifampicin resistance mechanisms [24,77], and rifampicin is sometimes studied in combination with other antibiotics like colistin to explore synergistic effects, particularly for multidrug-resistant P. aeruginosa strains [78,79]. In addition, the fitness cost associated with rifampicin resistance in P. aeruginosa has been described [23,25]. The DNA-dependent RNA polymerase β-subunit, which is encoded by the rpoB gene, is the target of rifampicin [80]. Mutated rpoB induces a conformational change that affects the binding affinity of rifampicin to the β-subunit of the RNA polymerase; therefore, the drug becomes inactive without proper binding to the target site. In the current work, the P. aeruginosa rpoB gene was identified in 50% of P. aeruginosa strains, all of which were rifampicin-resistant. This may be attributed to the genetic variability in the target region [80]. Certain mutations or structural variations in some strains might alter the regions where primers bind. Sequence comparisons of the rpoB regions harboring rifampicin mutations reveal a high level of conservation among different bacterial species [81]. For instance, the molecular characterization of mutations resulting in rifampicin resistance has shown that the rpoB gene is a target of these mutations in E. coli [82]. This has also been demonstrated in many other bacteria, encompassing Bacillus anthracis [83], Mycobacterium tuberculosis [15], Streptococcus pyogenes [84], Staphylococcus aureus [21], Helicobacter pylori [85], and P. aeruginosa [24]. Furthermore, the rpoB gene has been employed to simultaneously identify bacteria and determine rifampicin resistance [86]. In the current study, we carried out partial DNA sequencing of the rpoB gene in one rifampicin- and multidrug-resistant P. aeruginosa isolate, and phylogenetic analysis revealed that this strain was enclosed in the same cluster with P. aeruginosa isolates recovered from human clinical cases with 99% matching identity, pointing out the potential public health significance of this strain.

5. Conclusions

The current study highlights the occurrence of rifampicin- and multidrug-resistant P. aeruginosa in nasal swabs and tissue samples of apparently healthy slaughtered camels, opening a gate for further studies concerning molecular and genetic characterization of rifampicin-resistant P. aeruginosa in animals. Given the potential zoonotic transmission of this pathogen, implementation of the One Health approach is crucial for continuous monitoring and limiting the spread of rifampicin and MDR P. aeruginosa strains at the human-animal-environment interface.

Author Contributions

D.H., study design, supervising the work, and writing manuscript; D.H., methodology; H.M.Z., writing manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Institutional Review Board Statement

The research was conducted according to the guidelines of the ethical committee of the Faculty of Veterinary Medicine, Cairo University, Egypt (Vet CU 110520251074). All methods were approved by the Institutional Animal Care and Use Committee (IACUC) of the Faculty of Veterinary Medicine, Cairo University, Egypt.

Informed Consent Statement

Not applicable.

Data Availability Statement

All data generated or analyzed during this study are included in this published article. The partial P. aeruginosa rpoB gene sequence generated in this study from apparently healthy camel was deposited in GenBank under the following accession number: PV287649.

Conflicts of Interest

The authors declare that they have no competing interests.

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Microbiolres 16 00107 g001
Figure 1. A phylogenetic consensus tree was constructed using the maximum likelihood method via Mega 7 software to reveal the genetic relationship between P. aeruginosa rpoB sequence in this study and those retrieved from humans available on GenBank.
Figure 1. A phylogenetic consensus tree was constructed using the maximum likelihood method via Mega 7 software to reveal the genetic relationship between P. aeruginosa rpoB sequence in this study and those retrieved from humans available on GenBank.
Microbiolres 16 00107 g001
Table 1. Occurrence of Pseudomonas aeruginosa in apparently healthy slaughtered camels.
Table 1. Occurrence of Pseudomonas aeruginosa in apparently healthy slaughtered camels.
No. of Examined CamelsNo. of Positive Camels Total
10 camels 6 camels 16 camels (16%)
10010 nasal swabs (10 isolates)6 nasal swabs (6 isolates)16 isolates
6 tissue samples (6 isolates)6 isolates
Table 2. Antimicrobial susceptibility pattern of Pseudomonas aeruginosa isolates.
Table 2. Antimicrobial susceptibility pattern of Pseudomonas aeruginosa isolates.
Sample TypeIsolate No.CAZCPMCTRCTXATAKGENRIFCIPSXTMRPIPMMDR
Pattern
Nasal swab1RRRRRSSRSRRRMDR
Nasal swab2RRRRRSSRSRSSMDR
Nasal swab3RRRRRSSRSRSSMDR
Nasal swab4RRRRSSSRSRSSMDR
Nasal swab5RRRRSSSRSRSSMDR
Nasal swab6RRRRSSSRSSSS-
Nasal swab7RRRRSSSSSSSS-
Nasal swab8RRRRSSSSSSSS-
Nasal swab9RRRRRSRRSRRSMDR
Nasal swab10RRRRRSSRSRSSMDR
Nasal swab11RRRRRSSRSRSSMDR
Nasal swab12RRRRRSSRSRSSMDR
Nasal swab13RRRRSSSRSRSSMDR
Nasal swab14RRRRSSSSSSSS-
Nasal swab15RRRRSSSSSSSS-
Nasal swab16RRRRSSSSRSSS-
Tissue sample17RRRRSSSRSSSS-
Tissue sample18RSRRRSSRSSSSMDR
Tissue sample19RRRRSSSSSSSS-
Tissue sample20RRRRSSSRSRSSMDR
Tissue sample21RRRRSSSRSSSS-
Tissue sample22RRRRSSSRSSSS-
Total (22) 22/22
(100%)		21/22
(95.5%)		22/22 (100%)22/22
(100%)		8/22
(36.4%)		0/22
(0%)		1/22
(4.5%)		16/22
(72.7%)		1/22
(4.5%)		11/22
(50%)		2/22
(9.1%)		1/22
(4.5%)		12/22 (54.5%)
Ceftazidime (CAZ); cefepime (CPM); ceftriaxone (CTR); cefotaxime (CTX); aztreonam (AT); imipenem (IPM); meropenem (MEM); amikacin (AK); gentamicin (GEN); ciprofloxacin (CIP); rifampicin (RIF); and trimethoprim/sulfamethoxazole (SXT). R: resistant; S: susceptible; MDR: multidrug resistance.
Table 3. Occurrence of beta-lactamase-encoding genes and rpoB gene in Pseudomonas aeruginosa isolates.
Table 3. Occurrence of beta-lactamase-encoding genes and rpoB gene in Pseudomonas aeruginosa isolates.
Isolate No.Beta-Lactamase-Encoding Genes rpoB Gene
blaPERblaCTX-MblaTEMblaSHV
1+++ +
2+ ++
3++ +
4+++ +
5+ + +
6
7 +
8
9+ + +
10 ++
11+ + +
12+ ++
13 +
14 +
15
16 +
17 + +
18++ +
19 +
20 + +
21
22 +
Total9/22 (40.9%)8/22 (36.4%)7/22 (31.8%)6/22 (27.3%)11/22 (50%)
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Hamza, D.; Zaher, H.M. Carriage of Rifampicin- and Multidrug-Resistant Pseudomonas aeruginosa in Apparently Healthy Camels: A View Through a Zoonosis Lens. Microbiol. Res. 2025, 16, 107. https://doi.org/10.3390/microbiolres16060107

AMA Style

Hamza D, Zaher HM. Carriage of Rifampicin- and Multidrug-Resistant Pseudomonas aeruginosa in Apparently Healthy Camels: A View Through a Zoonosis Lens. Microbiology Research. 2025; 16(6):107. https://doi.org/10.3390/microbiolres16060107

Chicago/Turabian Style

Hamza, Dalia, and Hala M. Zaher. 2025. "Carriage of Rifampicin- and Multidrug-Resistant Pseudomonas aeruginosa in Apparently Healthy Camels: A View Through a Zoonosis Lens" Microbiology Research 16, no. 6: 107. https://doi.org/10.3390/microbiolres16060107

APA Style

Hamza, D., & Zaher, H. M. (2025). Carriage of Rifampicin- and Multidrug-Resistant Pseudomonas aeruginosa in Apparently Healthy Camels: A View Through a Zoonosis Lens. Microbiology Research, 16(6), 107. https://doi.org/10.3390/microbiolres16060107

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