Impact of bacteriospermia on sperm DNA fragmentation: a narrative review

Introduction

Infertility is defined as the failure to achieve a clinical pregnancy after 12 months or more of regular, unprotected sexual intercourse (1). It is a global health issue affecting approximately 15% of couples worldwide, with a male factor contributing to nearly 50% of these cases (2). Beyond the biological inability to conceive, male infertility imposes a significant psychological burden on affected individuals and leads to substantial socio-economic costs, including the high expenses associated with repeated cycles of assisted reproductive technology (3). Given the declining birth rates in many developed nations, the management and diagnosis of male infertility have become a critical public health priority.

Traditionally, semen analysis—measuring sperm count, motility, and morphology—has been the gold standard for assessing male fertility. However, conventional semen analysis has inherent limitations in predicting male reproductive potential (4,5). Approximately 15% of infertile men exhibit completely “normal” semen parameters according to World Health Organization (WHO) criteria (4). Consequently, there has been a growing shift toward identifying more specialized molecular markers, among which sperm DNA fragmentation has emerged as a crucial indicator. High levels of sperm DNA fragmentation are associated with reduced natural conception rates, impaired embryo development, and increased risks of miscarriage (4). Notably, elevated sperm DNA fragmentation can be observed even in men with normal conventional semen profiles, explaining many cases of previously “idiopathic” infertility (5).

Emerging evidence suggests that bacteriospermia can impair sperm integrity through various mechanisms, including the induction of oxidative stress and the release of reactive oxygen species (ROS) (6,7). In addition to the direct impact of ROS, bacterial pathogens trigger an inflammatory response characterised by the production of inflammatory cytokines, most notably interleukin (IL)-6, which can drive sperm DNA fragmentation (8-10). Recently, several studies have reported a significant correlation between bacteriospermia and increased DNA fragmentation (6,11-13). Despite these findings, the relationship between bacteriospermia and sperm DNA fragmentation remains a subject of ongoing debate (14). Furthermore, to the best of our knowledge, no comprehensive review article has yet been published to synthesize the evidence on this specific association. Considering the high incidence of infertility and its associated socio-economic impact, clarifying the role of bacteriospermia in DNA damage is essential for developing more targeted therapeutic interventions.

Therefore, the purpose of this narrative review is to synthesize the currently available literature regarding the impact of bacteriospermia on sperm DNA fragmentation, address the existing controversies, and provide a comprehensive overview of how microbial factors influence male reproductive health. We present this article in accordance with the Narrative Review reporting checklist (available at https://tau.amegroups.com/article/view/10.21037/tau-2026-1-0135/rc).

Methods

The search was conducted on Jan 1^st, 2026 by both authors. Prior to conducting the literature search, the inclusion and exclusion criteria were established. A search was conducted on the PubMed/MEDLINE database using the following search terms: “DNA fragmentation”, “bacteria”, “semen”. A comprehensive search of the Google Scholar database was conducted, utilizing the search terms “DNA fragmentation”, “bacteria”, and “semen” (Table 1). The literature search and selection process were guided by specific inclusion criteria to ensure scientific relevance. We included original research articles that primarily focused on the association between bacterial infection in semen (bacteriospermia) and sperm DNA fragmentation. The scope was limited to studies involving human subjects and published in peer-reviewed journals to maintain the quality of the narrative review.

A meticulous search of additional pertinent literature was undertaken within the bibliographies of the selected papers. Two authors (J.H.L. and M.C.C.) independently performed the initial screening of titles and abstracts to identify potentially relevant studies. Following this, the full-text versions of the selected articles were independently assessed for final eligibility. In cases of disagreement or ambiguity regarding the inclusion of a specific study, the two authors engaged in detailed discussions to reach a mutual consensus. This independent dual-review process was implemented to minimize selection bias and ensure the academic integrity of the literature included in this narrative review. The study encompassed articles published from 2008 to 2025. A total of 129 articles were identified; however, 118 of these were excluded on the following grounds: they were not research articles; the study population comprised fewer than 50 individuals; they were duplicate records; they did not involve human subjects; or no English version was available. Following a thorough examination of the extant literature, a total of 11 articles (6,11-20) (Table 2) were deemed to be relevant to the present review.

Prevalence and diversity of microorganisms in semen

A study utilizing polymerase chain reaction (PCR)-based analysis (6) identified at least one organism in 20.1% of infertile participants, with Enterococcus faecalis (21.8%) emerging as the most prevalent species. Similarly, another PCR-based investigation of 510 subfertile males reported a 35.1% bacteriospermia rate, identifying Prevotella bivia (41.3%) and Ureaplasma urealyticum (13.4%) as the most frequent pathogens (15), while semen PCR screening in a separate cohort showed high positivity rates for Chlamydia trachomatis (24.3%) and Ureaplasma urealyticum (23.2%) (16). Another PCR screening for Chlamydia trachomatis revealed a positive rate of 13.75% (17).

Studies utilizing traditional semen culture have also reported a substantial microbial burden; for instance, standard culture methodologies identified at least one species in 34.88% of subfertile patients, with Enterococcus faecalis (25%) being the most frequent isolate (11), and 30% of patients in another culture-based study yielded bacterial growth, predominantly Staphylococcus (15%) (14). Furthermore, another study identified infections in 34.52% of men undergoing intracytoplasmic sperm injection, with Staphylococcus aureus being the most prevalent bacterium (12). For the detection of specific organisms, specialized Ureaplasma urealyticum semen cultures revealed infection rates ranging from 21.6% to 23.2% among infertile couples undergoing intrauterine insemination or in vitro fertilization (18,19). Finally, a large-scale culture-based investigation involving 7,852 subfertile men observed an overall bacteriospermia rate of 15.28%, where Enterococcus faecalis accounted for 56% of all positive cases (13).

Impact of bacteriospermia on conventional semen parameters

Patients with confirmed bacterial infections exhibited significantly lower sperm concentrations (33.8±35.1 ×10⁶/mL) and reduced motility (32.7%±19.8%) compared to the healthy control group (69.3±48.3 ×10⁶/mL and 47.3%±19.0%, respectively) (14). These findings are corroborated by another research (12), which reported a similar substantial decline in both concentration (24.74±15.86 vs. 76.08±50.96 ×10⁶/mL) and motility (25.74%±19.11% vs. 50.52%±18.53%) in the presence of bacterial infection.

Specific bacterial species are also closely linked to these declines (8). Enterococcus faecalis has been significantly associated with increased tail defects and non-progressive motility (6), while pathogens such as Streptococcus agalactiae, Escherichia coli, and Staphylococcus aureus have been shown to compromise the entire triad of concentration, motility, and morphology (11). Furthermore, infections involving Chlamydia trachomatis and Ureaplasma urealyticum markedly reduce reproductive metrics; patients with Chlamydia trachomatis, Ureaplasma urealyticum, or co-infections showed significantly lower motility (46.8%, 46.3%, and 41.2%, respectively, vs. 72.2%) and lower sperm counts (102.0, 93.1, and 91.6 vs. 136.6 million/mL) as compared to healthy controls (16). Similarly, Chlamydia trachomatis or Mycoplasma infections were associated with significantly lower relative values for concentration, motility, and morphology compared to controls (20). In bacteriospermic males, overall motility was significantly lower at 20.4%±10.0% compared to 36.0%±8.6% in non-infected individuals, with Prevotella bivia identified as a key independent predictor of poor concentration and vitality (15). Despite these findings, some reports on Ureaplasma urealyticum suggest a lack of significant impact, with studies showing no statistical difference in motility or concentration between positive and negative groups (18,19).

Correlation between bacteriospermia and sperm DNA fragmentation

Research has shown that semen samples infected with bacteria often exhibit a markedly higher DNA fragmentation index (DFI) than uninfected samples [20.5%, interquartile range (IQR): 17.0–38.8% vs. 15.0%, IQR: 10.0–23.0%] (6). The presence of Enterococcus species in particular was significantly associated with a higher DFI (6). Similar deterioration in DNA integrity was reported in cases of co-existing bacteriospermia and elevated seminal leukocytes, where the DFI increased compared to the control group (28.1% vs. 21.8%) (13). Furthermore, specific pathogens such as Chlamydia trachomatis and Ureaplasma urealyticum have been linked to significantly increased DNA damage. For example, patients diagnosed with Chlamydia trachomatis or Mycoplasma showed a higher DFI than controls (35.2%±13.6% vs. 10.8%±5.6%, P<0.001) (20). In other cohorts, while Chlamydia trachomatis alone did not always show a significant difference, patients with Ureaplasma urealyticum only (26.5%±12.3%) or co-infections of Chlamydia trachomatis and Ureaplasma urealyticum (30.3%±15.6%) exhibited significantly higher DFI compared to the control group (15.6%±8.9%) (16).

Other investigations confirm that a wide range of bacteria—including Enterococcus faecalis, Streptococcus agalactiae, Escherichia coli, Staphylococcus aureus, and Klebsiella pneumoniae—significantly increase DNA fragmentation compared to controls (11), with Prevotella bivia identified as an independent predictor of increased DNA fragmentation (15).

However, some studies have noted more nuanced results; for example, one report found that the increase in mean DFI (18.84%±0.94% in infected vs. 14.52%±0.76% in non-infected) did not reach statistical significance (P=0.07) (12). Similarly, several studies specifically targeting Ureaplasma urealyticum reported no significant differences in DFI between positive and negative groups, with median values remaining comparable at 14.28% vs. 12.79% (18,19). A study of Chlamydia trachomatis-infected patients revealed that the presence of sperm DNA fragmentation was not correlated with a positive diagnosis of the infection (17). Other bacterial strains, including certain Staphylococcus and Escherichia coli infections in specific cohorts, also showed no significant disparity in fragmentation rates compared to uninfected controls (16.8%±12.6% vs. 14.1%±7.6%) (14).

Impact of bacteriospermia on assisted reproductive technology

Recent studies have demonstrated that bacteriospermia has a detrimental effect on the outcomes of intrauterine insemination, particularly with regard to the success of fertilization. Research indicates a significant disparity in fertilization rates between bacteriospermic (67.13%±19.39%) and non-bacteriospermic (78.00%±17.71%) patients (P<0.05) (18), with other studies corroborating a general decline in fertilization efficiency among infected individuals (12). With regard to pregnancy outcomes associated with in vitro fertilization, studies have indicated that while certain data on Ureaplasma urealyticum suggest a marginal increase in miscarriage rates among infected individuals, the overall clinical pregnancy rate, live birth rate, and neonatal outcomes, encompassing birth weight and gestational age, did not attain statistical significance between the Ureaplasma urealyticum-positive and Ureaplasma urealyticum-negative cohorts (19).

Impact of antibiotic therapy on DNA fragmentation in patients with bacteriospermia

Following initial antibiotic treatment in patients with bacteriospermia, substantial improvements have been observed in semen parameters: sperm concentration increased from 43.3±17.4 to 54.1±15.3 ×10⁶/mL, total motility rose from 20.4%±10.0% to 35.8%±8.2%, and leukocytospermia decreased from 2.8±1.9 to 0.4±0.2 ×10⁶/mL (15). Most notably, antibiotic therapy significantly reduced DNA fragmentation levels from 43.2%±13.8% to 37.6%±10.4% (15). Another study also showed that after 3.8±2.2 months of antibiotic treatment, DNA fragmentation decreased from 37.7%±13.6% to 24.2%±11.2% (20).

Discussion and outlook

This narrative review aimed to evaluate the impact of bacteriospermia on sperm DNA fragmentation. Large-scale studies (6,11,13) consistently demonstrate a significant association between general bacteriospermia and elevated sperm DNA fragmentation. However, when examining specific pathogens, the results remain controversial and vary across different strains. These discrepancies indicate that the extent of DNA damage may be influenced by the unique characteristics of each bacterial species and the sensitivity of the diagnostic methods used.

The reported prevalence of bacteriospermia varies considerably, reflecting differences in study populations and microbiological detection methods. In studies utilizing PCR-based assays, the prevalence of at least one microorganism among subfertile men ranged from 20.1% to 35.1% (6,15). In contrast, culture-based investigations reported a wider range of prevalence, from 15.28% to 34.88% (11-14). Studies specifically targeting Ureaplasma species reported prevalence rates between 21.6% and 23.2% (16,18,19).

The identification of the most prevalent bacterial strains in infected semen exhibits considerable variation across the literature, reflecting differences in diagnostic techniques and patient cohorts. According to PCR-based investigations, Enterococcus faecalis was identified as the most predominant strain in one study, accounting for 21.8% of all infectious isolates (6). However, another PCR-based study reported a markedly different microbial profile, where Prevotella bivia emerged as the most frequent pathogen (41.3%), while Enterococcus faecalis was identified in only 9.5% of cases and Staphylococcus aureus was notably absent (15). Results from semen culture studies further highlight this diversity. Enterococcus faecalis consistently appears as a major pathogen in culture-based research, with reported prevalence rates of 25% (11) and as high as 56% in a large-scale analysis (13). In contrast, other culture-based reports found Staphylococcus aureus to be the most common isolate, with prevalence rates of 9.5% (12) and 15% (14), respectively. These discrepancies underscore the complex and heterogeneous nature of the seminal microbiome in subfertile men, where the dominance of specific strains like Enterococcus faecalis, Prevotella bivia, or Staphylococcus aureus may be influenced by the sensitivity of the detection method employed.

Bacteriospermia has been found to correlate with impaired conventional semen parameters in the majority of studies conducted to date. Patients with confirmed infections exhibited significantly lower sperm concentrations or motility compared to uninfected controls (8,11,14,15). Regarding specific pathogens, Enterococcus faecalis was associated with abnormal morphology and non-progressive motility, while Chlamydia trachomatis significantly compromised both count and motility (6,16,20). While some studies found no association between Ureaplasma urealyticum and conventional parameters (18,19), others reported a significant decline in sperm motility and sperm count in Ureaplasma urealyticum-positive cohorts (16).

Three distinct studies established a significant association between general bacterial infection in semen and higher sperm DNA fragmentation levels (6,11,13). However, one study reported no significant disparity in DNA fragmentation rates between infected and uninfected groups (14). Previous studies demonstrating a significant correlation between bacteriospermia and elevated sperm DNA fragmentation involved relatively large cohorts of 740, 172, and 4,935 participants, respectively (6,11,13). In contrast, the study that reported no significant disparity was limited by a smaller sample size of 120 subjects (14), suggesting that these conflicting outcomes may stem from differences in statistical power associated with study scale.

When examining specific pathogens, the presence of Enterococcus spp. in semen was significantly associated with increased DFI (6), and Prevotella bivia was identified as an independent predictor of DNA fragmentation (15). In contrast, the data regarding Ureaplasma urealyticum remain controversial. Results from certain semen culture studies indicated that neither the median DFI nor the proportion of patients with DFI >15% differed significantly between Ureaplasma urealyticum-positive and -negative groups (18,19). Conversely, other research has demonstrated a significantly higher DFI in patients harboring Ureaplasma (16). Similarly, findings for Chlamydia trachomatis vary based on the diagnostic approach. While PCR-confirmed seminal Chlamydia trachomatis infection showed no significant correlation with DNA fragmentation in one cohort (17), a significantly higher rate of fragmentation was observed when Chlamydia trachomatis was diagnosed via urethral smear or seminal pellet using direct immunofluorescence (20). These discrepancies suggest that the observed impact of bacteriospermia on sperm DNA fragmentation may be influenced by the specific bacterial strain and the sensitivity of the diagnostic methodology.

Sperm DNA fragmentation is a marker of chromatin damage in spermatozoa. Chromatin damage includes DNA strand breaks, cross-linkage of DNA, base modifications or deletions, and protamine deficiency (21). High sperm DNA fragmentation is associated with an increased risk of miscarriage following both in vitro fertilization and intracytoplasmic sperm injection, as well as a lower chance of achieving a natural pregnancy, a significantly lower success rate with intrauterine insemination, recurrent pregnancy loss (spontaneous loss of two or more pregnancies), and idiopathic male infertility (4). It is thought that oxidative stress levels are the main mechanism resulting in sperm DNA fragmentation when exposed to known risk factors such as radiation, heat, cigarette smoke, airborne pollutants, advanced male age, a high body mass index and insulin-dependent diabetes (4). ROS are produced by spermatozoa in small quantities under normal conditions, playing a role in processes such as capacitation, the acrosomal reaction and sperm-oocyte fusion (22). However, excessive production of ROS can impair the antioxidant defense of spermatozoa and seminal plasma, resulting in oxidative stress (23). ROS can disrupt the membrane of sperm cells through a process called lipoperoxidation. ROS are also known to attack the bases of DNA and its phosphodiester backbone. This leads to DNA fragmentation (24). In addition, ROS activate the caspases and nucleases involved in apoptotic pathways, which indirectly causes sperm DNA fragmentation (25). A study has demonstrated that higher levels of malondialdehyde, a marker of membrane lipid peroxidation caused by free radical damage, are associated with a concomitant increase in sperm DNA fragmentation (26), suggesting that oxidative pathways are major contributors to DNA instability.

The mechanism by which bacterial infection triggers sperm DNA fragmentation is widely hypothesized to be mediated by oxidative stress. Compelling laboratory evidence has established a direct correlation between the presence of bacteria in semen and elevated levels of ROS. Specifically, in vitro studies using 37 healthy volunteers demonstrated that exposure to lipopolysaccharide—a potent endotoxin found in the outer membrane of Gram-negative bacteria—resulted in significantly higher ROS production compared to control groups (7). These experimental findings are further corroborated by clinical data; for instance, PCR-based screening of subfertile men revealed a significant association between Enterococcus species and seminal ROS levels (6). Notably, the microbial burden appears to have a cumulative effect, as patients with detectable microorganisms in both semen and urine exhibited the highest ROS concentrations—exceeding normal reference ranges and reaching levels at least ten times higher than those of uninfected individuals (6). The biochemical impact of this oxidative environment induced by bacterial infection involves DNA fragmentation. In vitro models have shown that co-incubation of spermatozoa with species such as Bacteroides ureolyticus, Staphylococcus haemolyticus, and Escherichia coli induces severe damage to sperm membrane lipids. This lipid peroxidation is evidenced by a concomitant rise in malondialdehyde levels within sperm lysates (27), providing a mechanistic link between bacterial presence, membrane lipid destruction, and subsequent DNA fragmentation.

In addition to the direct impact of ROS, bacterial pathogens trigger an inflammatory response characterised by the production of inflammatory cytokines, which can drive sperm DNA fragmentation (8-10). The presence of seminal pathogens, such as gram-positive cocci and gram-negative bacilli, has been significantly associated with elevated levels of IL-6 in seminal plasma (8). This inflammatory mediator, often found in higher concentrations in patients with chronic male genital tract inflammation, shows a significant correlation with sperm DNA integrity (8). Furthermore, previous studies (9,10) have demonstrated that exposure to pro-inflammatory cytokine combinations, including IL-6 and IL-8, can directly induce sperm DNA fragmentation. This suggests that IL-6 may serve as a potential driver of DNA damage, potentially through the activation of apoptotic pathways or the further recruitment of leukocytes that amplify the release of ROS. Given that seminal IL-6 levels are often a more sensitive marker of inflammation than traditional leukocyte counts alone, these results underscore the critical role of the cytokine-mediated inflammatory environment in compromising the genomic integrity of human spermatozoa.

It has been demonstrated by certain retrospective studies that the administration of antibiotics has the capacity to restore the DNA fragmentation that is associated with bacteriospermia (15,20,28). These findings could provide a clinical rationale for initiating antibiotic therapy in patients presenting with concurrent bacteriospermia and elevated sperm DNA fragmentation. In order to verify this hypothesis, it is necessary to conduct a better-designed prospective study.

Finally, it is imperative to distinguish between true seminal infection and simple bacterial contamination, as the presence of bacteria in semen (bacteriospermia) does not invariably indicate a clinical infection. Our clinical perspective is supported by evidence that many microorganisms isolated from semen may originate from the normal flora of the male urethra rather than from the accessory glands (29,30). For instance, studies on the microbiologic flora of the normal male urethra have shown that species such as coagulase-negative staphylococci, Corynebacterium, and viridans streptococci are frequently present even in asymptomatic men, suggesting that these organisms often represent contamination from the distal urethra during ejaculation (29,30).

Therefore, the diagnosis of male adnexitis should not rely solely on the presence of bacteria, but should be carefully integrated with inflammatory markers and clinical symptoms. This distinction is clinically crucial because the indiscriminate use of antibiotic therapy for asymptomatic bacteriospermia poses significant risks. Not only can inappropriate antibiotic use lead to the emergence of multidrug-resistant bacterial strains, but certain antibiotics may also exert direct paradoxical deleterious effects on sperm parameters, including motility and morphology. Consequently, antibiotic treatment in andrological practice should be administered with great caution, reserved only for cases where a clear pathogenic role and infection are established.

Conclusions

This review suggests that bacteriospermia is a contributing factor in male infertility, primarily driven by its significant correlation with increased sperm DNA fragmentation. Therefore, screening for bacteriospermia and assessing sperm DNA fragmentation appear to be helpful in the evaluation of idiopathic male infertility. To further refine clinical protocols, large-scale prospective studies are warranted to confirm the benefits of antimicrobial therapy on genomic stability.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://tau.amegroups.com/article/view/10.21037/tau-2026-1-0135/rc

Peer Review File: Available at https://tau.amegroups.com/article/view/10.21037/tau-2026-1-0135/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://tau.amegroups.com/article/view/10.21037/tau-2026-1-0135/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Vander Borght M, Wyns C. Fertility and infertility: Definition and epidemiology. Clin Biochem 2018;62:2-10. [Crossref] [PubMed]
2. Agarwal A, Mulgund A, Hamada A, et al. A unique view on male infertility around the globe. Reprod Biol Endocrinol 2015;13:37. [Crossref] [PubMed]
3. Inhorn MC, Patrizio P. Infertility around the globe: new thinking on gender, reproductive technologies and global movements in the 21st century. Hum Reprod Update 2015;21:411-26. [Crossref] [PubMed]
4. Agarwal A, Majzoub A, Baskaran S, et al. Sperm DNA Fragmentation: A New Guideline for Clinicians. World J Mens Health 2020;38:412-71. [Crossref] [PubMed]
5. Osman A, Alsomait H, Seshadri S, et al. The effect of sperm DNA fragmentation on live birth rate after IVF or ICSI: a systematic review and meta-analysis. Reprod Biomed Online 2015;30:120-7. [Crossref] [PubMed]
6. Ho CLT, Vaughan-Constable DR, Ramsay J, et al. The relationship between genitourinary microorganisms and oxidative stress, sperm DNA fragmentation and semen parameters in infertile men. Andrologia 2022;54:e14322. [Crossref] [PubMed]
7. Urata K, Narahara H, Tanaka Y, et al. Effect of endotoxin-induced reactive oxygen species on sperm motility. Fertil Steril 2001;76:163-6. [Crossref] [PubMed]
8. Aghazarian A, Huf W, Klingler HC, et al. The effect of seminal pathogens on standard semen parameters, sperm kinematics and seminal inflammatory markers. J Reprod Immunol 2024;161:104183. [Crossref] [PubMed]
9. Fraczek M, Szumala-Kakol A, Dworacki G, et al. In vitro reconstruction of inflammatory reaction in human semen: effect on sperm DNA fragmentation. J Reprod Immunol 2013;100:76-85. [Crossref] [PubMed]
10. Haidl F, Haidl G, Oltermann I, et al. Seminal parameters of chronic male genital inflammation are associated with disturbed sperm DNA integrity. Andrologia 2015;47:464-9. [Crossref] [PubMed]
11. Eini F, Kutenaei MA, Zareei F, et al. Effect of bacterial infection on sperm quality and DNA fragmentation in subfertile men with Leukocytospermia. BMC Mol Cell Biol 2021;22:42. [Crossref] [PubMed]
12. Zeyad A, Hamad M, Amor H, et al. Relationships between bacteriospermia, DNA integrity, nuclear protamine alteration, sperm quality and ICSI outcome. Reprod Biol 2018;18:115-21. [Crossref] [PubMed]
13. Domes T, Lo KC, Grober ED, et al. The incidence and effect of bacteriospermia and elevated seminal leukocytes on semen parameters. Fertil Steril 2012;97:1050-5. [Crossref] [PubMed]
14. Zeyad A, Hamad MF, Hammadeh ME. The effects of bacterial infection on human sperm nuclear protamine P1/P2 ratio and DNA integrity. Andrologia 2018; [Crossref]
15. Chang SB, Kim TJ, Kim TH, et al. Impact of Microbial Infection on Sperm Parameters of Seminal Bacteria in Asymptomatic Subfertile Males. Urogenital Tract Infection 2023;18:82-92.
16. Liu KS, Mao XD, Pan F, et al. Effect and mechanisms of reproductive tract infection on oxidative stress parameters, sperm DNA fragmentation, and semen quality in infertile males. Reprod Biol Endocrinol 2021;19:97. [Crossref] [PubMed]
17. Dehghan Marvast L, Talebi AR, Ghasemzadeh J, et al. Effects of Chlamydia trachomatis infection on sperm chromatin condensation and DNA integrity. Andrologia 2018; [Crossref]
18. Wan YY, Shi XY, Liu WJ, et al. Associations of Ureaplasma urealyticum infection with male infertility and intrauterine insemination outcomes. Asian J Androl 2025;27:219-24. [Crossref] [PubMed]
19. Wan Y, Chen X, Chen Z, et al. Impact of Ureaplasma urealyticum infection on semen parameters and in vitro fertilization outcomes in infertile men. Front Endocrinol (Lausanne) 2024;15:1484007. [Crossref] [PubMed]
20. Gallegos G, Ramos B, Santiso R, et al. Sperm DNA fragmentation in infertile men with genitourinary infection by Chlamydia trachomatis and Mycoplasma. Fertil Steril 2008;90:328-34. [Crossref] [PubMed]
21. Esteves SC, Sharma RK, Gosálvez J, et al. A translational medicine appraisal of specialized andrology testing in unexplained male infertility. Int Urol Nephrol 2014;46:1037-52. [Crossref] [PubMed]
22. Agarwal A, Allamaneni SS. Role of free radicals in female reproductive diseases and assisted reproduction. Reprod Biomed Online 2004;9:338-47. [Crossref] [PubMed]
23. Henkel RR. Leukocytes and oxidative stress: dilemma for sperm function and male fertility. Asian J Androl 2011;13:43-52. [Crossref] [PubMed]
24. Villegas J, Schulz M, Soto L, et al. Influence of reactive oxygen species produced by activated leukocytes at the level of apoptosis in mature human spermatozoa. Fertil Steril 2005;83:808-10. [Crossref] [PubMed]
25. Sinha K, Das J, Pal PB, et al. Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis. Arch Toxicol 2013;87:1157-80. [Crossref] [PubMed]
26. Chen CS, Chao HT, Pan RL, et al. Hydroxyl radical-induced decline in motility and increase in lipid peroxidation and DNA modification in human sperm. Biochem Mol Biol Int 1997;43:291-303. [Crossref] [PubMed]
27. Fraczek M, Szumala-Kakol A, Jedrzejczak P, et al. Bacteria trigger oxygen radical release and sperm lipid peroxidation in in vitro model of semen inflammation. Fertil Steril 2007;88:1076-85. [Crossref] [PubMed]
28. Moskovtsev SI, Lecker I, Mullen JB, et al. Cause-specific treatment in patients with high sperm DNA damage resulted in significant DNA improvement. Syst Biol Reprod Med 2009;55:109-15. [Crossref] [PubMed]
29. Cottell E, Harrison RF, McCaffrey M, et al. Are seminal fluid microorganisms of significance or merely contaminants? Fertil Steril 2000;74:465-70. [Crossref] [PubMed]
30. Montagnini Spaine D, Mamizuka EM, Pereira Cedenho A, et al. Microbiologic aerobic studies on normal male urethra. Urology 2000;56:207-10. [Crossref] [PubMed]