Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (723 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the epididymis. Its clinical features include enlarged epididymis, a swollen scrotum; PAIN; pyuria; and fever. It is usually related to infections in the urinary tract, which likely spread to the epididymis through either the vas deferens or the lymphatics of the spermatic cord.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Epididymitides.
Where it fits in the MeSH classification
- Broader topics
- Genital Diseases, Male
Related concepts
- Epididymis
- Scrotum
- Pyuria
- Fever
- Urinary Tract
- Vas Deferens
- Spermatic Cord
Research landscape
PubMed indexes 2,564 records tagged with the MeSH heading “Epididymitis” (counts retrieved 2026-11-04). 192 of them (7.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,648 records.
Reviews account for 224 records (8.7%) and meta-analyses for 4. Randomized controlled trials number 23 (0.9%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,648 |
| 2000-2009 | 361 |
| 2010-2019 | 363 |
| 2020 onward | 192 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 224 | 8.7% |
| Meta-analyses | 4 | 0.2% |
| Randomized controlled trials | 23 | 0.9% |
Method: PubMed query "Epididymitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Lipopolysaccharide and lipotheicoic acid differentially modulate epididymal cytokine and chemokine profiles and sperm parameters in experimental acute epididymitis | 2018 | Research article Design not recorded in structured metadata | 54 | cc by PMID 29311626 · DOI · PMC5758752 |
| Necrosis is the dominant cell death pathway in uropathogenic Escherichia coli elicited epididymo-orchitis and is responsible for damage of rat testis | 2013 | Research article Design not recorded in structured metadata | 49 | cc by PMID 23301002 · DOI · PMC3534655 |
| Differential Immune Response to Infection and Acute Inflammation Along the Epididymis | 2020 | Review article Design not recorded in structured metadata | 47 | cc by PMID 33329594 · DOI · PMC7729520 |
| Old disease, new twist | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42806674 · DOI · PMC13728528 |
Lipopolysaccharide and lipotheicoic acid differentially modulate epididymal cytokine and chemokine profiles and sperm parameters in experimental acute epididymitis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Bacterial infections are the most prevalent etiological factors of epididymitis, a commonly diagnosed inflammatory disease in the investigation of male infertility factors.
- Closing excerpt
- Our study provides evidence that early epididymal inflammatory signaling events to bacterial activators of innate immunity may contribute to the detrimental effects of epididymitis upon male fertility.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Bacterial infections are the most prevalent etiological factors of epididymitis, a commonly diagnosed inflammatory disease in the investigation of male infertility factors. The influence of early pathogenic mechanisms at play during bacterial epididymitis on reproductive outcomes is little understood. We report here that experimental epididymitis induced in rats by Gram-negative (LPS) and Gram-positive (LTA) bacterial products resulted in differential patterns of acute inflammation in the cauda epididymis. LPS elicited a strong inflammatory reaction, as reflected by upregulation of levels of mRNA for seven inflammatory mediators (Il1b, Tnf, Il6, Ifng, Il10, Nos2 and Nfkbia), and tissue concentration of six cytokines/chemokines (IL1A, IL1B, IL6, IL10, CXCL2 and CCL2) within the first 24 h post-treatment. Conversely, LTA induced downregulation of one (Nfkbia) and upregulation of six (Il1b, Il6, Nos2, Il4 Il10 and Ptgs1) inflammatory gene transcripts, whereas increased the tissue concentration of three cytokines/chemokines (IL10, CXCL2 and CCL2). The stronger acute inflammatory response induced by LPS correlated with a reduction of epididymal sperm count and transit time that occurred at 1, 7, and 15 days post-treatment. Our study provides evidence that early epididymal inflammatory signaling events to bacterial activators of innate immunity may contribute to the detrimental effects of epididymitis upon male fertility.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29311626 · DOI · PMC5758752
Necrosis is the dominant cell death pathway in uropathogenic Escherichia coli elicited epididymo-orchitis and is responsible for damage of rat testis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Male infertility is a frequent medical condition, compromising approximately one in twenty men, with infections of the reproductive tract constituting a major etiological factor.
- Closing excerpt
- Substantial necrotic changes seen in Sertoli cells will contribute to impaired spermatogenesis by loss of function in supporting the dependent germ cells.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (252 words)
Male infertility is a frequent medical condition, compromising approximately one in twenty men, with infections of the reproductive tract constituting a major etiological factor. Bacterial epididymo-orchitis results in acute inflammation most often caused by ascending canalicular infections from the urethra via the continuous male excurrent ductal system. Uropathogenic Escherichia coli (UPEC) represent a relevant pathogen in urogenital tract infections. To explore how bacteria can cause damage and cell loss and thus impair fertility, an in vivo epididymo-orchitis model was employed in rats by injecting UPEC strain CFT073 into the vas deference in close proximity to the epididymis. Seven days post infection bacteria were found predominantly in the testicular interstitial space. UPEC infection resulted in severe impairment of spermatogenesis by germ cell loss, damage of testicular somatic cells, a decrease in sperm numbers and a significant increase in TUNEL (+) cells. Activation of caspase-8 (extrinsic apoptotic pathway), caspase-3/-6 (intrinsic apoptotic pathway), caspase-1 (pyroptosis pathway) and the presence of 180 bp DNA fragments, all of which serve as indicators of the classical apoptotic pathway, were not observed in infected testis. Notably, electron microscopical examination revealed degenerative features of Sertoli cells (SC) in UPEC infected testis. Furthermore, the passive release of high mobility group protein B1 (HMGB1), as an indication of necrosis, was observed in vivo in infected testis. Thus, necrosis appears to be the dominant cell death pathway in UPEC infected testis. Substantial necrotic changes seen in Sertoli cells will contribute to impaired spermatogenesis by loss of function in supporting the dependent germ cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23301002 · DOI · PMC3534655
Differential Immune Response to Infection and Acute Inflammation Along the Epididymis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The epididymis is a tubular structure connecting the vas deferens to the testis.
- Closing excerpt
- Improved understanding of the different immunological microenvironments is the basis for an improved therapy and counseling of patients with epididymal infections.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (175 words)
The epididymis is a tubular structure connecting the vas deferens to the testis. This organ consists of three main regions-caput, corpus, and cauda-that face opposing immunological tasks. A means of combating invading pathogens is required in the distally located cauda, where there is a risk of ascending bacterial infections originating from the urethra. Meanwhile, immune tolerance is necessary at the caput, where spermatozoa with immunogenic neo-antigens originate from the testis. Consistently, when challenged with live bacteria or inflammatory stimuli, the cauda elicits a much stronger immune response and inflammatory-inflicted damage than the caput. At the cellular level, a role for diverse and strategically positioned mononuclear phagocytes is emerging. At the mechanistic level, differential expression of immunoprotective and immunomodulatory mediators has been detected between the three main regions of the epididymis. In this review, we summarize the current state of knowledge about region-specific immunological characteristics and unveil possible underlying mechanisms on cellular and molecular levels. Improved understanding of the different immunological microenvironments is the basis for an improved therapy and counseling of patients with epididymal infections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33329594 · DOI · PMC7729520
Old disease, new twist [4]
Abstract reading summary — source excerpts
- Opening excerpt
- An 81-year-old man with a history of high-grade urothelial carcinoma of the bladder and ureter on treatment with atezolizumab and tiragolumab presented to the emergency department with 5 months of malaise, generalized weakness, and fatigue and 2 weeks of subjective fevers.
- Closing excerpt
- He was admitted for further evaluation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (96 words)
An 81-year-old man with a history of high-grade urothelial carcinoma of the bladder and ureter on treatment with atezolizumab and tiragolumab presented to the emergency department with 5 months of malaise, generalized weakness, and fatigue and 2 weeks of subjective fevers. One month prior to presentation, he received an empiric 9-day course of levofloxacin for possible epididymitis based on scrotal pain and an ultrasound showing mild bilateral epididymal prominence. Blood and urine cultures were negative. His constitutional symptoms persisted, and he developed a subjective fever 2 weeks prior to presentation. He was admitted for further evaluation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42806674 · DOI · PMC13728528
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Immunophysiology and pathology of inflammation in the testis and epididymis [5]
- Research article Epididymitis and orchitis: an overview [6]
- Research article Relevance of male accessory gland infection for subsequent fertility with special focus on prostatitis [7]
- Research article Chronic epididymitis: impact on semen parameters and therapeutic options [8]
- Research article Epididymitis: revelations at the convergence of clinical and basic sciences [9]
- Research article Ovine contagious epididymitis: a review [10]
References
- Silva EJR, Ribeiro CM, Mirim AFM, Silva AAS, Romano RM, Hallak J, et al.. Lipopolysaccharide and lipotheicoic acid differentially modulate epididymal cytokine and chemokine profiles and sperm parameters in experimental acute epididymitis. . 2018. PMID 29311626 · DOI · PMC5758752
- Lu Y, Bhushan S, Tchatalbachev S, Marconi M, Bergmann M, Weidner W, et al.. Necrosis is the dominant cell death pathway in uropathogenic Escherichia coli elicited epididymo-orchitis and is responsible for damage of rat testis. . 2013. PMID 23301002 · DOI · PMC3534655
- Pleuger C, Silva EJR, Pilatz A, Bhushan S, Meinhardt A. Differential Immune Response to Infection and Acute Inflammation Along the Epididymis. . 2020. PMID 33329594 · DOI · PMC7729520
- Roudsari H, Dhaliwal G, Jagannath AD, Baik AH, Brondfield S. Old disease, new twist. . 2026. PMID 42806674 · DOI · PMC13728528
- Hedger MP. Immunophysiology and pathology of inflammation in the testis and epididymis. J Androl. 2011. PMID 21764900 · DOI · PMC7166903
- Trojian TH, Lishnak TS, Heiman D. Epididymitis and orchitis: an overview. Am Fam Physician. 2009. PMID 19378875
- Weidner W, Krause W, Ludwig M. Relevance of male accessory gland infection for subsequent fertility with special focus on prostatitis. Hum Reprod Update. 1999. PMID 10582781 · DOI
- Haidl G, Allam JP, Schuppe HC. Chronic epididymitis: impact on semen parameters and therapeutic options. Andrologia. 2008. PMID 18336457 · DOI
- Michel V, Pilatz A, Hedger MP, Meinhardt A. Epididymitis: revelations at the convergence of clinical and basic sciences. Asian J Androl. 2015. PMID 26112484 · DOI · PMC4577585
- Burgess GW. Ovine contagious epididymitis: a review. Vet Microbiol. 1982. PMID 6762755 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.