Oophoritis

Oophoritis, also known as ovaritis, is an inflammatory condition affecting one or both ovaries, often occurring as a component of pelvic inflammatory disease (PID) and characterized by swelling, cysts, or abscess formation in the affected organs.^[1][2] This uncommon disorder primarily arises from bacterial infections, such as those caused by Chlamydia trachomatis or Neisseria gonorrhoeae, which ascend from the lower genital tract, though it can also stem from viral causes like mumps or, rarely, autoimmune processes leading to primary ovarian insufficiency.^[1][3][4][5] Symptoms typically include lower abdominal or pelvic pain, fever, and abnormal vaginal discharge, though the condition can be asymptomatic in mild cases.^[1][2][3] Diagnosis involves medical history, physical examination, laboratory tests, imaging, and sometimes laparoscopy.^[1][2] Treatment focuses on addressing the underlying cause, such as antibiotics for bacterial infections or hormone replacement therapy for autoimmune cases to manage symptoms and prevent long-term health complications.^[1][3][2][5] Untreated oophoritis can lead to scarring, infertility (affecting up to 1 in 8 women with a history of PID), ectopic pregnancy, chronic pelvic pain, and rarely, sepsis.^[3][2] Prevention includes safe sexual practices, treatment of sexually transmitted infections, and mumps vaccination.^[3][4]

Overview

Definition

Oophoritis, also termed ovaritis, refers to the inflammation of one or both ovaries.^[6] This condition is characterized by inflammatory changes within the ovarian tissue, distinguishing it as a targeted involvement of the ovaries rather than adjacent structures.^[7] The term originates from the Greek "oophoron," meaning ovary or egg-bearing, combined with the suffix "-itis," indicating inflammation.^[8] It first appeared in medical literature in the early 19th century, around 1833, and was initially described in contexts associated with infectious processes affecting the reproductive organs.^[8] Oophoritis frequently manifests as part of pelvic inflammatory disease (PID), an ascending infection of the upper female genital tract that commonly incorporates the fallopian tubes, resulting in salpingo-oophoritis.^[9] In this context, PID represents a broader syndrome where oophoritis contributes to the overall pathology but is not isolated.^[10] This ovarian-specific inflammation must be differentiated from related conditions such as salpingitis, which primarily affects the fallopian tubes, or endometritis, involving the uterine lining, to accurately identify the site of involvement in pelvic disorders.^[10]

Classification

Oophoritis is primarily classified into infectious and autoimmune types, with infectious oophoritis being the most common form, typically resulting from bacterial or viral pathogens.^[1] Infectious oophoritis often overlaps with pelvic inflammatory disease (PID), particularly in cases involving ascending genital tract infections.^[11] Within the infectious category, subtypes include acute oophoritis, characterized by sudden onset and frequently associated with sexually transmitted infections, and chronic oophoritis, which involves persistent or recurrent inflammation leading to long-term ovarian damage.^[12] Autoimmune oophoritis represents a rare immune-mediated variant, where the body's immune system targets ovarian tissue, often manifesting as a cause of primary ovarian insufficiency (POI).^[13] This condition is sometimes integrated into broader autoimmune polyendocrine syndromes, such as type I or type II, alongside other endocrine disorders like Addison's disease or thyroiditis.^[13] Other rare infectious forms of oophoritis include tuberculous oophoritis, a chronic granulomatous inflammation due to Mycobacterium tuberculosis, typically arising from hematogenous spread or extension from salpingitis.^[14] Another uncommon presentation is post-mumps oophoritis, a viral complication following mumps infection that can lead to transient or, less frequently, permanent ovarian dysfunction.^[15]

Causes

Infectious Causes

Infectious oophoritis primarily arises from bacterial infections that ascend from the lower genital tract to the ovaries, often as a component of pelvic inflammatory disease (PID).^[16] The most common causative agents are sexually transmitted bacteria, particularly Neisseria gonorrhoeae (responsible for gonorrhea) and Chlamydia trachomatis, which account for approximately 85% of PID cases involving oophoritis.^[16] These pathogens typically originate from cervical infections and spread upward through the endometrium and fallopian tubes, leading to ovarian involvement.^[16] Other bacterial causes include opportunistic pathogens such as Escherichia coli and anaerobic bacteria (e.g., Bacteroides species or Peptostreptococcus), which can facilitate infection in the presence of disrupted vaginal flora.^[16] These are frequently associated with practices like vaginal douching, which may propel normal vaginal or enteric bacteria into the upper genital tract, or the use of intrauterine devices (IUDs), where insertion can introduce contaminants, elevating risk particularly within the first three weeks post-placement.^[17][3] Viral causes are less common but significant, with the mumps virus (Rubulavirus) being a notable example, causing oophoritis in approximately 5% of postpubertal women infected with the disease.^[18] Transmission occurs via respiratory droplets, and the virus disseminates hematogenously or through ascending routes to inflame the ovaries, potentially unilaterally or bilaterally.^[18] Key risk factors for infectious oophoritis mirror those for PID and include having multiple sexual partners, untreated sexually transmitted infections (STIs), and poor hygiene practices such as douching, which disrupt the protective cervical mucus barrier.^[3][17] Immunocompromised states, such as those from HIV or chemotherapy, further heighten susceptibility to opportunistic bacterial or viral pathogens like cytomegalovirus, though these are rare.^[16] Individuals with a history of STIs or recent IUD insertion face elevated risks due to facilitated microbial ascension.^[3] Pathophysiologically, infectious agents breach the cervical barrier, often during menstruation or due to mucosal disruption, ascending via the fallopian tubes to directly infect ovarian tissue or induce secondary inflammation through immune response.^[16] This process can result in acute inflammation, abscess formation, or chronic scarring, commonly within the context of broader PID.^[16]

Autoimmune Causes

Autoimmune oophoritis represents a rare form of ovarian inflammation driven by aberrant immune responses, in which autoreactive T-lymphocytes and autoantibodies specifically target the theca and granulosa cells of the ovary, culminating in the progressive destruction of developing ovarian follicles. This immune-mediated attack disrupts normal folliculogenesis without involving infectious agents, distinguishing it from pathogen-induced variants. The condition primarily affects women of reproductive age and is a recognized contributor to primary ovarian insufficiency (POI).^[19][20] The disorder frequently manifests as part of autoimmune polyendocrine syndrome type 1 (APS-1), a monogenic condition resulting from mutations in the AIRE gene, which encodes a transcription factor essential for promoting immune tolerance in the thymus by facilitating the expression of tissue-specific antigens. In APS-1, ovarian involvement occurs in 45-60% of affected females, often alongside adrenal insufficiency and hypoparathyroidism. Autoimmune oophoritis can also present in isolation or in association with other autoimmune conditions, including systemic lupus erythematosus (SLE), Addison's disease, and pernicious anemia, reflecting a broader breakdown in self-tolerance that may involve polygenic factors such as specific HLA alleles in autoimmune polyendocrine syndrome type 2 (APS-2).^[20][19][21] Pathophysiologically, the process begins with the infiltration of the ovarian stroma by mononuclear lymphocytes, predominantly CD4+ and CD8+ T cells, which mediate direct cytotoxicity against steroid-producing cells while initially sparing primordial follicles. This selective targeting leads to the depletion of the ovarian follicle reserve, ovarian atrophy, interstitial fibrosis, and elevated gonadotropin levels, ultimately causing premature ovarian failure before age 40. The presence of autoantibodies against steroidogenic enzymes, such as 21-hydroxylase and 17-hydroxylase, further exacerbates tissue damage by impairing hormone synthesis.^[20][19] As a primary autoimmune etiology, oophoritis accounts for approximately 4% of POI cases, with histological confirmation often revealing lymphocytic oophoritis in association with adrenal autoimmunity. Early detection through autoantibody screening can identify at-risk individuals, particularly those with polyglandular syndromes.^[22][21]

Signs and Symptoms

Symptoms of Infectious Oophoritis

Infectious oophoritis, often occurring as a component of pelvic inflammatory disease (PID), typically presents with acute symptoms that signal an underlying bacterial infection. Patients commonly experience sudden onset of lower abdominal or pelvic pain, which may be unilateral or bilateral depending on the pathogen involved, accompanied by fever and chills indicative of systemic inflammation. Additional gastrointestinal symptoms such as nausea and vomiting frequently occur, while foul-smelling vaginal discharge is a hallmark sign due to concurrent cervicitis or endometritis. Associated symptoms related to PID extension include dyspareunia, or pain during intercourse, which arises from inflamed adnexal structures, as well as irregular menstrual bleeding and urinary discomfort from bladder irritation. These manifestations can vary in intensity but often prompt medical evaluation due to their impact on daily activities. In chronic or recurrent cases, symptoms may evolve to persistent pelvic pain, exacerbated by adhesions that form as a result of repeated inflammation and can lead to bowel or bladder dysfunction. Notably, up to 50% of mild infections caused by Chlamydia trachomatis may remain asymptomatic, allowing silent progression without initial clinical signs. The pattern of ovarian involvement differs by etiology; bilateral oophoritis is more prevalent in gonococcal infections, whereas mumps-associated oophoritis tends to be unilateral. Symptoms often overlap with salpingo-oophoritis when the fallopian tubes are concurrently affected.

Symptoms of Autoimmune Oophoritis

Autoimmune oophoritis primarily manifests through symptoms arising from estrogen deficiency, as the autoimmune attack targets ovarian theca and granulosa cells, leading to progressive ovarian failure. Common presentations include primary or secondary amenorrhea and oligomenorrhea, which often result in infertility during the reproductive years.^[23][19] Patients frequently experience vasomotor symptoms such as hot flashes and night sweats, alongside signs of hypoestrogenism like vaginal dryness, dyspareunia, and vulvovaginal atrophy.^[23][5] In contrast to more acute inflammatory conditions, autoimmune oophoritis typically involves minimal pelvic pain, though ovarian enlargement or cystic structures may be detected on physical examination or imaging, reflecting lymphocytic infiltration without significant acute discomfort.^[23] Additional endocrine effects can include reduced libido, sleep disturbances, mood alterations such as irritability or emotional lability, and general fatigue due to hormonal imbalance.^[23][5] When autoimmune oophoritis occurs as part of a polyglandular autoimmune syndrome, such as type 1 or 2, associated symptoms from coexisting conditions may emerge, including hyperpigmentation and hypotension if Addison's disease is present, or thyroid-related signs like enlargement or skin changes.^[19] Neurological manifestations, such as those from myasthenia gravis in rare cases, can also accompany the ovarian symptoms.^[19] The onset is usually insidious in adolescence or early adulthood, progressing to premature ovarian insufficiency (POI), with symptoms often mimicking early menopause and thereby delaying diagnosis due to their subtlety and rarity.^[23][19]

Diagnosis

Diagnostic Approaches for Infectious Oophoritis

Diagnosis of infectious oophoritis, often occurring as part of pelvic inflammatory disease (PID), relies on a combination of clinical evaluation, laboratory testing, imaging, and exclusion of alternative conditions to confirm ovarian inflammation due to infectious agents such as Neisseria gonorrhoeae or Chlamydia trachomatis.^[24][16] The process begins with assessing clinical suspicion in sexually active individuals, particularly those at risk for sexually transmitted infections (STIs), to guide presumptive treatment while pursuing confirmatory tests.^[25] A thorough clinical history is essential, emphasizing sexual history, including the number of partners, use of barrier contraception, and recent STI exposure, as well as risk factors for PID such as age under 25 years or prior infections.^[16] Patients may report lower abdominal or pelvic pain, often bilateral, accompanied by vaginal discharge, dyspareunia, or abnormal uterine bleeding, though symptoms can be subtle or absent often.^[24][25] Physical examination involves a bimanual pelvic exam to detect cervical motion tenderness, uterine tenderness, or adnexal tenderness, which are minimum criteria for suspecting PID and associated oophoritis.^[24] Adnexal masses or fullness may indicate ovarian involvement, such as tubo-ovarian abscess, while additional findings like mucopurulent cervical discharge or fever greater than 38.3°C increase diagnostic specificity.^[16] A pregnancy test is routinely performed to exclude ectopic pregnancy.^[25] Laboratory tests support the diagnosis by identifying infection or inflammation. Nucleic acid amplification tests (NAATs) on cervical, vaginal, or urine samples are recommended to detect N. gonorrhoeae and C. trachomatis, the most common pathogens, with sensitivities exceeding 90%.^[24] A complete blood count (CBC) may reveal leukocytosis in approximately 60% of cases, while elevated erythrocyte sedimentation rate (ESR >15 mm/h) occurs in about 75%, indicating systemic inflammation.^[25] Saline microscopy of vaginal discharge showing abundant white blood cells further corroborates lower genital tract involvement.^[16] Imaging modalities aid in visualizing ovarian pathology. Transvaginal ultrasound is the initial choice, detecting ovarian enlargement, fluid-filled structures, or abscesses with a complex adnexal mass in cases of advanced infection, though sensitivity for early oophoritis is limited.^[24][25] In ambiguous or severe cases, laparoscopy provides direct visualization of inflamed ovaries or fallopian tubes, allowing for sampling and culture to identify pathogens, serving as the gold standard with positive predictive value around 65% for salpingitis.^[16] Differential diagnosis is critical to rule out non-infectious mimics. Conditions such as appendicitis, ectopic pregnancy, ovarian torsion, or cyst rupture must be excluded through history, exam, labs (e.g., beta-hCG for pregnancy), and imaging (e.g., ultrasound or CT for appendicitis).^[24][25] Empirical antibiotic therapy may be initiated based on clinical suspicion in high-risk patients while awaiting confirmatory results.^[16]

Diagnostic Approaches for Autoimmune Oophoritis

Diagnosis of autoimmune oophoritis typically follows exclusion of infectious etiologies through appropriate clinical evaluation.^[21] Serological testing plays a central role in identifying autoimmune involvement, focusing on the detection of anti-ovarian antibodies (AOAs) and autoantibodies targeting steroid-producing cells. AOAs, detected via indirect immunofluorescence or enzyme-linked immunosorbent assays, are present in approximately 20% of women with premature ovarian insufficiency (POI) suggestive of autoimmune oophoritis.^[26] Specific autoantibodies, such as those against 21-hydroxylase (a key steroidogenic enzyme), indicate immune-mediated destruction of ovarian theca cells and are particularly relevant in cases associated with autoimmune polyendocrine syndromes.^[27] A panel screening for multiple steroidogenic autoantibodies enhances diagnostic accuracy to 84.1%, outperforming single-antibody tests.^[27] Endocrine evaluation through hormone assays confirms ovarian failure and supports the autoimmune etiology. Elevated follicle-stimulating hormone (FSH) levels exceeding 40 IU/L, measured on at least two occasions, alongside low estradiol (<50 pg/mL), are hallmark findings in autoimmune POI, reflecting diminished ovarian reserve and feedback dysregulation.^[28] These assays, combined with luteinizing hormone measurements, help differentiate primary ovarian dysfunction from hypothalamic causes.^[21] Imaging modalities, particularly transvaginal pelvic ultrasound, provide structural insights into ovarian morphology. In autoimmune oophoritis, ultrasound often reveals small ovaries with reduced volume, cystic changes, and decreased antral follicle count, indicating chronic lymphocytic infiltration and follicular atresia.^[23] Ovarian biopsy, though rarely performed due to procedural risks and ethical concerns, remains the gold standard for histopathological confirmation. It demonstrates lymphocytic infiltration, predominantly of CD3+ T cells and CD20+ B cells, surrounding developing follicles in the theca layer.^[21] In suspected autoimmune polyendocrine syndrome type 1 (APS-1), genetic testing for mutations in the autoimmune regulator (AIRE) gene is recommended, as biallelic loss-of-function variants underlie up to 100% of familial cases with ovarian involvement.^[29] Screening for co-existing autoimmune conditions is essential, given the frequent polyautoimmune presentation. Tests for thyroid function (e.g., thyroid-stimulating hormone and anti-thyroid peroxidase antibodies) and adrenal antibodies (e.g., anti-21-hydroxylase) are routinely advised, as up to 30% of women with autoimmune POI have concurrent thyroiditis or Addison's disease.^[23] This comprehensive approach facilitates early detection and management of associated endocrinopathies.^[30]

Treatment

Treatment of Infectious Oophoritis

The treatment of infectious oophoritis, typically occurring as part of pelvic inflammatory disease (PID) caused by pathogens such as Neisseria gonorrhoeae or Chlamydia trachomatis, primarily involves broad-spectrum antibiotics to eradicate the infection. Outpatient regimens are recommended for mild to moderate cases and include a single intramuscular dose of ceftriaxone 500 mg (1 g if patient weight >150 kg) combined with oral doxycycline 100 mg twice daily for 14 days and oral metronidazole 500 mg twice daily for 14 days. Alternative outpatient options include cefoxitin 2 g intramuscularly with probenecid 1 g orally as a single dose, followed by the same doxycycline and metronidazole regimen. For severe cases requiring hospitalization—such as those with nausea, vomiting, high fever, or confirmed tubo-ovarian abscess—intravenous therapy is initiated, such as cefotetan 2 g every 12 hours plus doxycycline 100 mg orally or intravenously every 12 hours.^[24] Treatment duration is at least 14 days for all regimens to ensure complete pathogen clearance, with inpatient patients transitioning to oral antibiotics after 24-48 hours of clinical improvement. To prevent reinfection, sexual partners from the preceding 60 days should be evaluated, tested for gonorrhea and chlamydia, and treated empirically with ceftriaxone and doxycycline, often using expedited partner therapy if follow-up is uncertain.^[24] Surgical intervention is reserved for complications like tubo-ovarian abscesses unresponsive to antibiotics within 72 hours. For abscesses larger than 5 cm, image-guided percutaneous drainage or laparoscopic drainage is preferred to avoid rupture and peritonitis, with antibiotics continued post-procedure. In cases of recurrent infectious oophoritis with irreversible tubal damage, salpingectomy may be performed to remove the affected fallopian tube and prevent further episodes.^[31][32][33] Supportive care focuses on symptom relief and includes nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen for pain and fever management, bed rest to reduce pelvic congestion, and adequate hydration to support recovery. Patients are advised to abstain from sexual intercourse until treatment completion and symptom resolution to avoid spreading the infection.^[24][34] Follow-up evaluation is essential, with clinical reassessment within 72 hours to confirm improvement; if no response, hospitalization or alternative antibiotics are considered. Repeat testing for chlamydia and gonorrhea is recommended 3 months post-treatment to verify cure and detect reinfection, particularly in high-risk individuals.^[24]

Treatment of Autoimmune Oophoritis

Autoimmune oophoritis has no definitive cure, with treatment primarily aimed at symptom management, hormonal replacement, and modulation of the underlying autoimmune process to mitigate ovarian damage and associated primary ovarian insufficiency (POI).^[35] Hormone replacement therapy (HRT) forms the cornerstone of management, utilizing estrogen-progesterone combinations to alleviate menopausal symptoms such as hot flashes and vaginal dryness while preserving bone health and reducing cardiovascular risks. In women with POI due to autoimmune oophoritis, HRT is recommended until the typical age of natural menopause to mimic physiologic ovarian hormone production and prevent long-term complications like osteoporosis.^[36][37] Immunosuppressive therapies are considered in progressive cases to halt autoimmune destruction of ovarian tissue. Corticosteroids, such as alternate-day glucocorticoids, have induced return of menstrual cycles and improved ovarian function in select patients with histologically confirmed autoimmune oophoritis. Azathioprine has shown potential to restore ovarian function and fertility in cases associated with comorbid autoimmune conditions like Addison's disease. For patients with concomitant myasthenia gravis, thymectomy may resolve oophoritis and normalize ovarian function, as evidenced by case reports of menses resumption post-procedure.^[38]00249-4/fulltext)^[39] Fertility is significantly impaired due to follicular loss, but assisted reproductive technologies offer options for conception. Egg donation remains the most reliable method for achieving pregnancy in women with autoimmune oophoritis-related POI, involving in vitro fertilization with donor oocytes transferred to the patient's uterus.^[40] Ongoing monitoring is essential to assess treatment efficacy and complications. Regular measurement of follicle-stimulating hormone (FSH) and estradiol levels helps evaluate ovarian reserve and hormonal status, while bone density scans via dual-energy X-ray absorptiometry (DEXA) are recommended to detect and manage osteoporosis risk from estrogen deficiency.^[41][42] Experimental approaches, such as rituximab—a monoclonal antibody targeting CD20-positive B cells—have demonstrated promise in refractory antibody-mediated cases by restoring menstrual cycles and enabling oocyte retrieval for fertility preservation in autoimmune POI. Clinical trials are investigating its role in improving ovarian response, though broader efficacy data remain limited.^[43]

Complications

Complications of Infectious Oophoritis

Infectious oophoritis, often occurring as a component of pelvic inflammatory disease (PID), can lead to significant short- and long-term complications if untreated or recurrent, primarily due to inflammatory damage to the ovaries and adjacent structures like the fallopian tubes.^[16] These sequelae arise from scarring, adhesions, and persistent infection, affecting reproductive health and overall well-being.^[16] One major complication is infertility, resulting from scarring and obstruction of the fallopian tubes that impairs ovum transport. After a single episode of PID involving oophoritis, the risk of tubal infertility is approximately 10-15%, with the likelihood increasing to 20-50% after multiple episodes due to cumulative fibrosis and hydrosalpinx formation.^[44][16] Ectopic pregnancy risk is substantially elevated following infectious oophoritis, as tubal damage creates sites for abnormal implantation. Women with a history of PID, including oophoritis, face a 6- to 10-fold increased risk of ectopic pregnancy compared to those without, stemming from partial or complete tubal occlusion.^[17] Chronic pelvic pain is another common long-term outcome, affecting up to one-third of women post-PID with oophoritis, often due to intra-abdominal adhesions causing dyspareunia or dysmenorrhea. This persistent pain arises from ongoing inflammation and scar tissue distortion of pelvic organs.^[16][45] Abscess formation, particularly tubo-ovarian abscess (TOA), complicates 15% of cases involving salpingo-oophoritis, where pus accumulates in the adnexa and risks rupture, leading to peritonitis or further pelvic destruction. Untreated TOA can necessitate surgical intervention to prevent life-threatening intra-abdominal infection.^[10][31] In severe or untreated instances, infectious oophoritis can progress to systemic spread, culminating in sepsis through bacteremia from ruptured abscesses or disseminated infection. This occurs in advanced PID cases, potentially leading to septic shock and high mortality if not promptly managed.^[46][16]

Complications of Autoimmune Oophoritis

Autoimmune oophoritis primarily manifests through progressive destruction of ovarian follicles, culminating in primary ovarian insufficiency (POI), a condition characterized by irreversible loss of ovarian function before age 40. This leads to anovulation and estrogen deficiency, resulting in infertility in approximately 90% of affected individuals due to depleted follicular reserves. While spontaneous pregnancies occur in 5-10% of POI cases, the autoimmune-mediated follicular damage in oophoritis severely limits natural conception rates, often necessitating assisted reproductive technologies such as oocyte donation for fertility preservation.^[28] The inflammatory process in autoimmune oophoritis induces ovarian fibrosis and atrophy, where chronic immune infiltration replaces functional ovarian tissue with scar-like fibrotic changes, rendering the ovaries small and non-functional as observed on ultrasound or MRI imaging. This structural degeneration exacerbates POI by halting folliculogenesis entirely, contributing to the hypoestrogenic state that drives downstream complications. Estrogen deficiency from these ovarian changes significantly increases the risk of osteoporosis, with affected women experiencing accelerated bone mineral density loss and a 1.5-fold higher fracture risk compared to those with natural menopause. Similarly, cardiovascular disease risk elevates due to endothelial dysfunction and adverse lipid profiles, with ischemic heart disease mortality up to 80% higher in POI patients.^[47] In women with POI due to autoimmune oophoritis, approximately 2-3% have asymptomatic autoimmune adrenal insufficiency, and up to 24% test positive for thyroid peroxidase autoantibodies, with overt hypothyroidism in 8-20%. In the context of broader autoimmune syndromes such as autoimmune polyendocrine syndrome type 1 (APS-1), where oophoritis occurs, Addison's disease affects 80-90% of patients, and autoimmune thyroid disease occurs in approximately 10% of cases. The early onset of menopausal symptoms, including hot flashes and vaginal atrophy, also imposes substantial psychological burdens, with elevated rates of depression, anxiety, and diminished quality of life reported among patients. Comprehensive management, including hormone replacement therapy, is essential to mitigate these multifaceted impacts.^[47][48]

Prevention and Epidemiology

Prevention Strategies

Preventing oophoritis, particularly its infectious forms as a component of pelvic inflammatory disease (PID), involves strategies to mitigate sexually transmitted infections (STIs), which are the primary cause. Consistent use of condoms during sexual intercourse significantly reduces the risk of acquiring STIs like chlamydia and gonorrhea that can ascend to the ovaries.^[2] Practicing monogamy or limiting sexual partners further lowers exposure to these pathogens.^[2] Routine STI screening is recommended annually for all sexually active women under 25 years old, as well as for older women with risk factors such as new or multiple partners, to detect and treat infections early.^[49] Early treatment of STIs can reduce the progression to PID.^[2] Vaccination plays a key role in preventing viral causes of oophoritis, notably mumps, which can lead to ovarian inflammation in up to 5-7% of post-pubertal females with the disease.^[18] The measles-mumps-rubella (MMR) vaccine, administered in two doses—the first at 12-15 months and the second at 4-6 years—provides approximately 88% effectiveness against mumps and is the standard recommendation for immunization.^[50] Hygiene practices are essential to avoid disrupting the vaginal microbiome, which can facilitate bacterial ascent. Avoiding douching is critical, as it removes protective bacteria and increases PID risk by altering vaginal pH and flora balance.^[2] Prompt treatment of lower genital tract infections, such as bacterial vaginosis or urinary tract infections, with appropriate antibiotics like metronidazole for bacterial vaginosis, helps prevent their progression to upper reproductive tract involvement including oophoritis.^[51] For autoimmune oophoritis, often associated with autoimmune polyendocrine syndrome type 1 (APS-1) due to AIRE gene mutations, prevention focuses on risk assessment rather than direct intervention. Genetic counseling is advised for families with a history of APS-1 to evaluate inheritance risks, as the condition follows an autosomal recessive pattern, enabling informed family planning.^[48] Early screening for ovarian function, such as measuring anti-ovarian antibodies or follicle-stimulating hormone levels, is recommended in patients with known autoimmune disorders or APS-1 to detect premature ovarian insufficiency promptly.^[48] General preventive measures include regular gynecological examinations to monitor reproductive health and facilitate early detection of infections or abnormalities.^[52] Education on PID risks, emphasizing safe sex practices and the importance of vaccination and screening, empowers individuals to adopt protective behaviors.^[3]

Epidemiological Overview

Oophoritis, encompassing both infectious and autoimmune forms, exhibits varying prevalence depending on etiology and population. The infectious variant, typically arising as a component of pelvic inflammatory disease (PID), affects approximately 1-2% of women annually in high-risk groups, with over 1 million cases reported yearly in the United States alone. Globally, PID prevalence ranges from 0.28% to 1.67%, though oophoritis specifically occurs in a subset of these cases, often linked to ascending sexually transmitted infections. In contrast, autoimmune oophoritis is rare, accounting for approximately 4% of primary ovarian insufficiency (POI) cases, which themselves affect about 1% of women under 40 years old.^[53][54][22] Demographically, infectious oophoritis predominantly impacts women aged 15-35 years, with the highest incidence among sexually active adolescents and young adults, where up to 75% of PID cases occur under age 25. It is more prevalent in low socioeconomic groups facing barriers to sexually transmitted infection (STI) screening and treatment, as well as in developing regions with limited healthcare access and higher STI burdens. Autoimmune oophoritis primarily affects Caucasian females and shows familial clustering, particularly in autoimmune polyendocrine syndrome type 1 (APS-1), which has a prevalence of about 1 in 100,000 individuals.^{[55][17][56][22]} Epidemiological trends indicate declining rates of infectious oophoritis in high-income countries, attributed to widespread STI screening and vaccination programs that have reduced PID incidence. However, outbreaks of mumps virus continue to elevate cases, with oophoritis complicating up to 5% of infections in postpubertal women. On a global scale, oophoritis contributes significantly to infertility, accounting for approximately 20% of cases in women under 35, primarily through tubal damage from recurrent PID episodes.^[57][4][58]