Over one million cases of acute salpingitis are reported every year in the US, but the number of incidents is probably larger, due to incomplete and untimely reporting methods and that many cases are reported first when the illness has gone so far that it has developed chronic complications. For women age 16–25, salpingitis is the most common serious infection. It affects approximately 11% of females of reproductive age.

Salpingitis has a higher incidence among members of lower socioeconomic classes. However, this is thought of being an effect of earlier sex debut, multiple partners, and decreased ability to receive proper health care rather than any independent risk factor for salpingitis.

As an effect of an increased risk due to multiple partners, the prevalence of salpingitis is highest for people age 15–24 years. Decreased awareness of symptoms and less will to use contraceptives are also common in this group, raising the occurrence of salpingitis.

For the affected, 20% need hospitalization.

Regarding patients age 15–44 years, 0.29 per 100,000 dies from salpingitis.

However, salpingitis can also lead to infertility because the eggs released in ovulation can't get contact with the sperm. Approximately 75,000-225,000 cases of infertility in the US are caused by salpingitis. The more times one has the infection, the greater the risk of infertility. With one episode of salpingitis, the risk of infertility is 8-17%. With 3 episodes of salpingitis, the risk is 40-60%, although the exact risk depends on the severity of each episode.

In addition, damaged oviducts increase the risk of ectopic pregnancy. Thus, if one has had salpingitis, the risk of a pregnancy to become ectopic is 7 to 10-fold as large. Half of ectopic pregnancies are due to a salpingitis infection.

Other complications are:

- Infection of ovaries and uterus

- Infection of sex partners

- An abscess on the ovary

Regular testing for sexually transmitted infections is encouraged for prevention. The risk of contracting pelvic inflammatory disease can be reduced by the following:

- Using barrier methods such as condoms; see human sexual behavior for other listings.

- Seeking medical attention if you are experiencing symptoms of PID.

- Using hormonal combined contraceptive pills also helps in reducing the chances of PID by thickening the cervical mucosal plug & hence preventing the ascent of causative organisms from the lower genital tract.

- Seeking medical attention after learning that a current or former sex partner has, or might have had a sexually transmitted infection.

- Getting a STI history from your current partner and strongly encouraging they be tested and treated before intercourse.

- Diligence in avoiding vaginal activity, particularly intercourse, after the end of a pregnancy (delivery, miscarriage, or abortion) or certain gynecological procedures, to ensure that the cervix closes.

- Reducing the number of sexual partners.

- Sexual monogamy.

- Abstinence

PID can cause scarring inside the reproductive system, which can later cause serious complications, including chronic pelvic pain, infertility, ectopic pregnancy (the leading cause of pregnancy-related deaths in adult females), and other complications of pregnancy. Occasionally, the infection can spread to in the peritoneum causing inflammation and the formation of scar tissue on the external surface of the liver (Fitz-Hugh–Curtis syndrome).

Though urinary tract infections in men are rare, bacterial infection is the most common cause of acute epididymitis. The bacteria in the urethra back-track through the urinary and reproductive structures to the epididymis. In rare circumstances, the infection reaches the epididymis via the bloodstream.

In sexually active men, "Chlamydia trachomatis" is responsible for two-thirds of acute cases, followed by "Neisseria gonorrhoeae" and "E. coli" (or other bacteria that cause urinary tract infection). Particularly among men over age 35 in whom the cause is "E. coli", epididymitis is commonly due to urinary tract obstruction. Less common microbes include "Ureaplasma", Mycobacterium, and "cytomegalovirus", or "Cryptococcus" in patients with HIV infection. "E. coli" is more common in boys before puberty, the elderly, and men who have sex with men. In the majority of cases in which bacteria are the cause, only one side of the scrotum or the other is the locus of pain.

Non-infectious causes are also possible. Reflux of sterile urine (urine without bacteria) through the ejaculatory ducts may cause inflammation with obstruction. In children, it may be a response following an infection with enterovirus, adenovirus or "Mycoplasma pneumoniae". Rare non-infectious causes of chronic epididymitis include sarcoidosis (more prevalent in black men) and Behçet's disease.

Any form of epididymitis can be caused by genito-urinary surgery, including prostatectomy and urinary catheterization. Congestive epididymitis is a long-term complication of vasectomy. Chemical epididymitis may also result from drugs such as amiodarone.

Acute Endometritis is characterized by infection. The organisms most often isolated are believed to be because of compromised abortions, delivery, medical instrumentation, and retention of placental fragments. There is not enough evidence for the use of prophylactic antibiotics to prevent endometritis after manual removal of placental in vaginal birth. Histologically, neutrophilic infiltration of the endometrial tissue is present during acute endometritis. The clinical presentation is typically high fever and purulent vaginal discharge. Menstruation after acute endometritis is excessive and in uncomplicated cases can resolve after 2 weeks of clindamycin and gentamicin IV antibiotic treatment.

In certain populations, it has been associated with "Mycoplasma genitalium" and pelvic inflammatory disease.

Epididymitis makes up 1 in 144 visits for medical care (0.69 percent) in men 18 to 50 years old or 600,000 cases in males between 18 and 35 in the United States.

It occurs primarily in those 16 to 30 years of age and 51 to 70 years. As of 2008 there appears to be an increase in incidences in the United States that parallels an increase in reported cases of chlamydia and gonorrhea.

Oophoritis is an inflammation of the ovaries.

It is often seen in combination with salpingitis (inflammation of the fallopian tubes). It may develop in response to infection.

Chronic Endometritis is characterized by the presence of plasma cells in the stroma. Lymphocytes, eosinophils, and even lymphoid follicles may be seen, but in the absence of plasma cells, are not enough to warrant a histologic diagnosis. It may be seen in up to 10% of all endometrial biopsies performed for irregular bleeding. The most common organisms are Chlamydia trachomatis (chlamydia), Neisseria gonorrhoeae (gonorrhea), Streptococcus agalactiae (Group B Streptococcus), Mycoplasma hominis, tuberculosis, and various viruses. Most of these agents are capable of causing chronic pelvic inflammatory disease (PID). Patients suffering from chronic endometritis may have an underlying cancer of the cervix or endometrium (although infectious cause is more common). Antibiotic therapy is curative in most cases (depending on underlying cause), with fairly rapid alleviation of symptoms after only 2 to 3 days.

Chronic granulomatous endometritis is usually caused by tuberculous. The granulomas are small, sparse, and without caseation. The granulomas take up to 2 weeks to develop and since the endometrium is shed every 4 weeks, the granulomas are poorly formed.

In human medicine, pyometra (also a veterinary condition of significance) is regarded as a form of chronic endometritis seen in elderly women causing stenosis of the cervical os and accumulation of discharges and infection. Symptom in chronic endometritis is blood stained discharge but in pyometra the patient complaints of lower abdominal pain.

The annual prevalence in the general population of chronic pelvic pain syndrome is 0.5%. 38% of primary care providers, when presented with a vignette of a man with CPPS, indicate that they have never seen such a patient. However, the overall prevalence of symptoms suggestive of CP/CPPS is 6.3%. The role of the prostate was questioned in the cause of CP/CPPS when both men and women in the general population were tested using the (1) National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) —with the female homolog of each male anatomical term use on questionnaires for female participants— (2) the International Prostate Symptom Score (IPSS), and (3) additional questions on pelvic pain. The prevalence of symptoms suggestive of CPPS in this selected population was 5.7% in women and 2.7% in men, placing in doubt the role of the prostate gland. New evidence suggests that the prevalence of CP/CPPS is much higher in teenage males than once suspected.

In recent years the prognosis for CP/CPPS has improved with the advent of multimodal treatment, phytotherapy, protocols aimed at quieting the pelvic nerves through myofascial trigger point release and anxiety control, and chronic pain therapy.

Tubal factor infertility can be due to Chlamydia infection and testing for Chlamydia antibodies is one diagnostic tool. Women have difficulty getting pregnant or carrying a baby to term due to the buildup of scar tissue in the Fallopian tubes causing damage to the cilia on the epithelial cells. TFI can also be due to endometriosis.

Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.

In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.

Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.

Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.

Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.

Over time, the relapse rate is high, exceeding 50%. However, recent research indicates that combination therapies offer a better prognosis than antibiotics alone.

A 2007 study showed that repeated combination pharmacological therapy with antibacterial agents (ciprofloxacin/azithromycin), alpha-blockers (alfuzosin) and Serenoa repens extracts may eradicate infection in 83.9% of patients with clinical remission extending throughout a follow-up period of 30 months for 94% of these patients.

A 2014 study of 210 patients randomized into two treatment groups found that recurrence occurred within 2 months in 27.6% of the group using antibiotics alone (prulifloxacin 600 mg), but in only 7.8% of the group taking prulifloxacin in combination with Serenoa repens extract, Lactobacillus Sporogens and Arbutin.

Prognosis is highly variable. Spontaneous remission is common. Complete cure can be obtained with proper antibiotic treatments to kill the causative bacteria, such as tetracycline, doxycycline, or erythromycin. Prognosis is more favorable with early treatment. Bacterial superinfections may complicate course. Death can occur from bowel obstruction or perforation, and follicular conjunctivitis due to autoinoculation of infectious discharge can occur.

Tubal factor infertility (TFI) is female infertility caused by diseases, obstructions, damage, scarring, congenital malformations or other factors which impede the descent of a fertilized or unfertilized ovum into the uterus through the Fallopian tubes and prevents a normal pregnancy and full term birth. Tubal factors cause 25-30% of infertility cases. Tubal factor is one complication of Chlamydia trachomatis infection in women.

Sexually transmitted Chlamydia and genital mycoplasma infections are preventable causes of infertility and negative pregnancy outcomes. When the infections progress and ascend, they can result in TFI. Infertility can have multiple possible causes and may not be recognized for years after a gonorrhea, Chlamydia or Mycoplasma infection has caused tubal damage, as the affected woman may not have attempted to become pregnant until years later.

Genital elephantiasis or esthiomene, which is the dramatic end-result of lymphatic obstruction, which may occur because of the strictures themselves, or fistulas. This is usually seen in females, may ulcerate and often occurs 1–20 years after primary infection.

Fistulas of, but not limited to, the penis, urethra, vagina, uterus, or rectum. Also, surrounding edema often occurs. Rectal or other strictures and scarring. Systemic spread may occur, possible results are arthritis, pneumonitis, hepatitis, or perihepatitis.

If symptomatic, testing is recommended. The risk of contracting Micoplasma infection can be reduced by the following:

- Using barrier methods such as condoms

- Seeking medical attention if you are experiencing symptoms suggesting a sexually transmitted infection.

- Seeking medical attention after learning that a current or former sex partner has, or might have had a sexually transmitted infection.

- Getting a STI history from your current partner and insisting they be tested and treated before intercourse.

- Avoiding vaginal activity, particularly intercourse, after the end of a pregnancy (delivery, miscarriage, or abortion) or certain gynecological procedures, to ensure that the cervix closes.

- Abstinence

Mycoplasmas have a triple-layered membrane and lack a cell wall. Commonly used antibiotics are generally ineffective because their efficacy is due to their ability to inhibit cell wall synthesis. Micoplasmas are not affected by penicillins and other antibiotics that act on the cell wall. The growth of micoplasmas in their host is inhibited by other broad-spectrum antibiotics. These broad-spectrum antibiotics inhibit the multiplication of the mycoplasma but does not kill them. Tetracyclines, macrolides, erythromycin, macrolides, ketolides, quinolones are used to treat mycoplasma infections. In addition to the penicillins, mycoplasmas are resistant to rifampicin. Mycoplasmas may be difficult to eradicate from human or animal hosts or from cell cultures by antibiotic treatment because of resistance to the antibiotic, or because it does not kill the mycoplasma cell. Mycoplasma cells are able to invade the cells of their hosts.

Little is known about the cause of vestibulodynia. A number of causes may be involved, including sub-clinical human papillomavirus infection, chronic recurrent candidiasis, or chronic recurrent bacterial vaginosis. Muscular causes have been implicated as well, since chronic vulvar pain may be the result of chronic hypertonic perivaginal muscles, leading to vaginal tightening and subsequent pain. Some investigators have postulated the existence of neurological causes, such as vestibular neural hyperplasia. Finally, psychological factors may contribute to or exacerbate the problem, since the anticipation of pain often results in a conditioned spasmodic reflex along with sexual desire and arousal problems.

SIN is associated with infertility and ectopic pregnancy, and may present as either.

It is characterized by nodular thickening of the tunica muscularis of the narrow (isthmic) portion of the Fallopian tube. In severe cases, it leads to complete obliteration of the tubal lumen. It is uncommonly bilateral.

Diagnosis is readily made by the cotton-swab test, in which pressure is applied in a circular fashion around the vulvar vestibule to assess complaints of pain. Laboratory tests are used to exclude bacterial or viral infection, and a careful examination of the vulvo/vaginal area is conducted to assess whether any atrophy is present.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.