A FEMALE PATIENT, AB, 37, presents to the ED reporting joint pain and a rash of 3 to 4 days' duration. The rash began on her lower extremities and was erythematous and painful but not pruritic. The rash progressed to her upper extremities but did not appear on her trunk. Following the rash, she developed progressive bilateral lower extremity pain that is interfering with ambulation.
AB also reports pain in her right shoulder and both wrist joints. She denies travel outside of the US during the previous 12 months. Her health history includes anemia, tubal ligation, and cigarette smoking. She denies any history of rheumatoid or osteoarthritis, systemic lupus erythematosus, and recent fever or chills.
AB complains of a foul-smelling yellow vaginal discharge of 3 months' duration. It is unknown when she was last seen by a gynecologist. She states that she and her sexual partner are both monogamous.
Her vital signs are: 99.7[degrees] F (37.6[degrees] C) (temporal); pulse, 86/min; respiratory rate, 18/min; BP, 133/56 mm Hg; and SpO2, 100% on room air. Physical assessment is significant for vesiculopustular skin lesions involving the bilateral lower and upper extremities but not present on palmar or plantar surfaces or trunk.
A urine pregnancy test is negative. Lab results are within normal limits except for an elevated white blood cell (WBC) count of 13.8 x 103/mm3 (normal, 4.5 to 11.0 x 103/mm3), with 74% neutrophils (normal, 45% to 65% of total WBC), suggesting a bacterial infection. HIV test results are negative. Blood cultures are obtained and test positive for Neisseria gonorrhoeae. The rapid plasma reagin test for syphilis is nonreactive. A DNA probe analysis for Candida species (yeast), Gardnerella vaginalis (bacterial vaginosis), Trichomonas vaginalis (trichomoniasis), Chlamydia trachomatis (chlamydia), and N. gonorrhoeae (gonorrhea) is obtained. The results are positive for G. vaginalis, T. vaginalis, and N. gonorrhoeae.
AB is diagnosed with acute disseminated gonococcal arthritis, bacterial vaginosis, and trichomoniasis.
While in the ED, AB is treated with oral azithromycin, oral metronidazole, and I.V. ceftriaxone. She is admitted to a medical-surgical unit with antibiotic orders to continue the daily I.V. ceftriaxone and metronidazole BID for 6 more days. A peripherally inserted central catheter is placed so she can complete her I.V. therapy at home. AB is extensively counseled about sexually transmitted infections (STIs) and given information about smoking cessation. Her partner is referred to the local health department for follow-up.
AB's condition improves and she is discharged to home with instructions for follow-up with her primary care provider, infectious disease practitioner, and home healthcare.
Three common STIs
G. vaginalis infection resulting in bacterial vaginosis occurs when this organism replaces the normal vaginal flora. Risk factors include having multiple male or female sexual partners, a new sexual partner, douching, lack of condom use, recent antibiotic use, decreased estrogen production, use of an intrauterine device, and a lack of vaginal lactobacilli (normal vaginal flora).1,2
Trichomoniasis is a genitourinary infection caused by infection with a protozoan parasite, T. vaginalis, which is transmitted from an infected person during sexual intercourse.3 It is rare for infection to occur in the mouth, anus, or hands. Signs and symptoms include a purulent, malodorous thin vaginal discharge associated with burning, pruritus, or dysuria. However, 70% to 85% of infected women are asymptomatic.4
N. gonorrhoeae, also known as gonococcus, is the bacterium responsible for gonorrhea. This STI is transmitted during vaginal, oral, or anal sex with an infected person. Gonorrhea can also be transmitted during childbirth. In 2016, 468,514 cases of gonorrhea were reported in the US, an 18.5% increase since 2015.5
N. gonorrhoeae can spread through the bloodstream and infect other parts of the body, including the joints, resulting in disseminated gonococcal infection (DGI), which occurs in 0.5% to 3% of patients infected with N. gonorrhoeae.6,7 The probability of the organism spreading to the joints and other tissues depends upon host, microbial, and possibly immune factors (see Risk factors for DGI). Presenting signs and symptoms may include fever, chills, malaise, polyarthralgia of small and/or large joints, tenosynovitis, and dermatitis. Symmetrical polyarthralgia is uncommon.7 As in AB's case, DGI can coexist with other STIs, such as bacterial vaginosis and trichomoniasis.
The patient should undergo a complete history and physical exam, including a sexual history. The skin should be examined for pustular or vesiculopustular lesions. The joints should be carefully assessed for erythema, pain, and warmth. Albeit rare, the patient must also be assessed for life-threatening complications of DGI including meningitis and endocarditis.8
Diagnosis
DGI should be suspected in any sexually active patient who presents with arthralgia. Lab studies should include blood cultures and specimens from mucosal sites (urogenital, rectal, pharyngeal) for N. gonorrhoeae testing.7 Synovial fluid should also be sent for analysis and culture in patients with DGI who have an accessible joint effusion. All patients with suspected DGI should be tested for other STIs such as HIV, C. trachomatis, and syphilis because, as in AB's case, coexistent infection with other sexually transmitted pathogens is common. A definitive diagnosis of DGI is made by identification of N. gonorrhoeae on a specimen of blood, synovial fluid or tissue, skin lesion, or other nonmucosal site.7,8 Standard precautions are used when caring for patients with DGI.9
Consultation with an infectious diseases expert is recommended to ensure optimal antibiotic therapy. Ceftriaxone, either I.V. or I.M. every 24 hours for at least 7 days, plus a single one-time dose of azithromycin, is the preferred initial regimen for DGI. Therapy with metronidazole is effective for bacterial vaginosis and trichomoniasis.10,11 The azithromycin dose will also treat chlamydia if present.7 Direct observation to ensure swallowing should accompany the oral medication administration to maximize patient adherence to therapy.12
Combination antibiotic therapy is recommended to address the potential emergence of gonococcal cephalosporin resistance.8 The different mechanisms of action with combined therapy are thought to improve treatment success and potentially slow down antimicrobial resistance.13
Whenever possible, partners who have had sexual contact with patients with DGI within the 60 days before diagnosis should be contacted, offered testing, and be presumptively treated for N. gonorrhoeae along with the patient, which may also prevent reinfection.7,13
N. gonorrhoeae has developed resistance to nearly all the antibiotics used for gonorrhea treatment except the cephalosporins. Bacteria have an inherent ability to resist antibiotics, with the CDC carefully monitoring for increased antimicrobial resistance.8 As a result, a positive N. gonorrhoeae lab finding is a national notifiable condition that must be reported to the department of health by the lab performing the testing.14 The Department of Health may also assist with sexual partner notification and treatment.
Gonorrhea and other STIs may be prevented by being in a long-term mutually monogamous relationship with a partner who has tested negative for STIs. Educate patients about safer sex practices. Correctly and consistently using latex condoms will reduce, but not eliminate, the risk of disease transmission.
Risk factors for DGI7
Host factors: asymptomatic mucosal infection, recent menstruation, pregnancy, congenital or acquired complement deficiencies, systemic lupus erythematosus.
Microbial factors:N. gonorrhoeae have a variety of virulence and growth factors associated with an increased ability to cause DGI.
Immune factors: Despite DGI, blood, skin, and synovial fluid cultures may be negative while specimens from the genitourinary tract can test positive for the organism.
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