ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Cutaneous manifestations of gonorrhea

Cutaneous manifestations of gonorrhea
Literature review current through: Jan 2024.
This topic last updated: Apr 20, 2023.

INTRODUCTION — Gonorrhea is a common bacterial sexually transmitted disease caused by infection with Neisseria gonorrhoeae, a gram-negative aerobic diplococcus. Although gonorrhea primarily affects the mucosa, cutaneous manifestations also may occur, particularly in patients with disseminated gonococcal infection (DGI).

Early diagnosis and treatment of gonorrhea is desirable, as untreated infection may result in pelvic inflammatory disease, chronic pelvic pain, ectopic pregnancy, or infertility and may facilitate human immunodeficiency virus (HIV) transmission [1-3]. The recognition of gonorrhea-related skin manifestations may assist with early diagnosis, thereby decreasing transmission of the disease and reducing the risk for complications.

The clinical manifestations of primary cutaneous gonorrhea, secondary cutaneous gonorrhea, and disseminated gonococcemia will be reviewed here. The epidemiology, pathogenesis, extracutaneous manifestations, diagnosis, and management of gonococcal infection are discussed separately.

(See "Epidemiology and pathogenesis of Neisseria gonorrhoeae infection".)

(See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents".)

(See "Treatment of uncomplicated gonorrhea (Neisseria gonorrhoeae infection) in adults and adolescents".)

(See "Disseminated gonococcal infection".)

(See "Gonococcal infection in the newborn".)

BIOLOGY — N. gonorrhoeae is a gram-negative, intracellular aerobic diplococcus that exclusively infects humans. The bacterium is capable of colonizing various mucosal surfaces including genitourinary, rectal, and pharyngeal sites. The outer membrane proteins and pili structures of N. gonorrhoeae facilitate its attachment to host mucosal epithelial cells and allow for the penetration of the organism into the subepithelium [1,4,5]. (See "Epidemiology and pathogenesis of Neisseria gonorrhoeae infection", section on 'Pathogenesis'.)

The presence of N. gonorrhoeae in host tissue usually elicits an acute inflammatory response that can manifest clinically as purulent discharge, epithelial sloughing, or abscess formation. Infrequently, hematologic dissemination occurs. (See "Disseminated gonococcal infection".)

Gonorrheal infection is highly transmissible, with an infectious risk per contact estimated at 20 to 50 percent for men and 60 to 90 percent for women [1]. The incubation period is usually between two and five days, but initial signs of infection may occur up to two weeks after transmission.

CUTANEOUS MANIFESTATIONS — Cutaneous lesions related to gonorrheal infection may occur as results of direct inoculation (primary cutaneous gonorrhea), primary mucosal infections (secondary cutaneous gonorrhea), or disseminated disease (disseminated gonococcal infection [DGI]). The features of these clinical presentations are reviewed below. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents".)

Primary cutaneous gonorrhea — Primary cutaneous gonorrhea may occur in genital or extragenital sites. Because the clinical features are nonspecific, recognition of these lesions as manifestations of gonorrhea requires a high index of clinical suspicion.

Extragenital — Extragenital primary cutaneous gonorrhea is rare. It is usually preceded by a history of cutaneous trauma, which likely facilitates entry of the organism into the nonmucosal skin [6-8]. A variety of clinical presentations have been described in the literature, including herpetiform or nonherpetiform digital pustules, abscesses, chancriform lesions, and suprapubic ecthyma [6-8]. As an example, digital pustules with lymphangitis and regional lymphadenopathy have developed following contact with contaminated laboratory equipment [1]. In addition, a neonatal scalp abscess has occurred after the use of a fetal monitor contaminated by maternal cervical infection [9].

Genital — Though not as rare as extragenital primary cutaneous gonorrhea, primary gonorrhea of the genital skin is uncommon [10]. It most frequently occurs in the clinical absence of signs or symptoms of urethral or cervical infection, although concomitant involvement of these sites may occur [6,7]. Unlike extragenital primary cutaneous gonorrhea, a preceding history of trauma (aside from normal sexual activity) is usually absent.

Potential clinical features of this variant include penile, erythematous, 1 to 2 mm pustules; fluctuant, furuncle-like nodules up to 2 cm in diameter; indurated abscesses; shallow erosions several millimeters in diameter; sinus-like lesions; and punched-out, indurated ulcers of varying size (picture 1). In males, involvement of the ventral penoscrotal raphe is rare, representing either a primary infection or local complication of urethral gonorrhea [11]. (See 'Secondary cutaneous gonorrhea' below.)

Secondary cutaneous gonorrhea — Cutaneous involvement in gonorrhea may occur in association with genitourinary, anorectal, or pharyngeal infections.

Genital — Genitourinary gonococcal infections tend to be more symptomatic in men (90 percent) than women (50 percent) [12-14]. In addition to the dysuria and the spontaneous profuse and purulent penile discharge that typically characterizes gonococcal urethritis in men [12], edema and erythema commonly develop at the urethral meatus and less frequently occur on the glans or foreskin (picture 2A-C). In severe cases, phimosis may occur. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Infection of the male urogenital tract'.)

In women the cervix is the primary site of infection, and although many women are asymptomatic, symptoms such as dysuria, dyspareunia, blood-tinged vaginal discharge, and intercourse-induced vaginal bleeding may occur [13,14]. Infrequently, involvement of the genital skin may develop due to spread of the infection, manifesting as 1 to 2 mm pustules, tender fluctuant nodules, or small ulcers. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Infection of the female urogenital tract'.)

Infection of the glandular structures of the genital mucosa may also result in cutaneous lesions. Invasion of N. gonorrhoeae into Tyson's or Cowper's glands in men or Bartholin or Skene's glands in women occasionally presents with inflammatory papules or pustules on the genital skin [1].

Anal — Anorectal infections may result from anal intercourse or may occur secondary to perianal contamination from cervical infections in women, and are often asymptomatic [12-14]. When symptoms are present, anal pruritus is the primary symptom with occasional secondary erythema and lichenification. Other potential manifestations of anorectal infection include rectal discharge, painful bowel movements, and bloody stools. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Proctitis'.)

Oral — Rarely, small oral ulcers and mucosal erythema may occur in patients with pharyngeal gonorrheal infection [15]. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Pharyngitis'.)

Disseminated gonococcal infection — Disseminated gonococcal infection (DGI) occurs in less than 3 percent of patients with gonorrhea. Complement deficiencies, as may occur in systemic lupus erythematosus, may increase risk for DGI [16-19].

DGI is divided into two clinical syndromes: tenosynovitis-dermatitis syndrome (triad of dermatitis, tenosynovitis, and polyarthralgias without purulent arthritis) and purulent arthritis syndrome without associated skin lesions [1,20-23]. Patients with features of both syndromes have been observed, and thus, these variants are often considered to be on the ends of a continuous spectrum. (See "Disseminated gonococcal infection", section on 'Clinical manifestations'.)

Tenosynovitis, dermatitis, polyarthralgia syndrome — Tenosynovitis, dermatitis, polyarthralgia syndrome is characterized by the triad of oligoarthralgia, tenosynovitis, and dermatitis. In addition, constitutional symptoms such as fever, chills, and generalized malaise occur during the acute stage of illness [1,22,24]. (See "Disseminated gonococcal infection", section on 'Clinical manifestations'.)

Cutaneous involvement occurs in 60 to 90 percent of patients with tenosynovitis, dermatitis, polyarthralgia syndrome [1,20-22]. Skin lesions are believed to arise secondary to bacterial embolization and the formation of cutaneous microabscesses. Patients develop pinpoint petechial macules that progress to form papules, pustules, vesicles, or bullae, which may become hemorrhagic or necrotic (picture 3A-E). The hemorrhagic vesicles or pustules, approximately 2 to 5 mm in diameter, are considered to be a characteristic finding [1,20-22]. Lesions in an individual patient may be in multiple stages of evolution.

Cutaneous lesions are most likely to occur on the dorsal surfaces of the distal extremities near joints. Involvement of the trunk, scalp, or face is exceptionally rare. Usually, 2 to 10 asymptomatic lesions are present; infrequently, patients develop more than 40 lesions.

Unlike joint involvement, which usually progresses without treatment, skin lesions are often transient, lasting only for three to four days even without treatment [1,22]. The lesions heal without scarring. Rarely, urticarial, target-like, erythema nodosum-like, or vasculitic lesions occur [25,26].

Purulent arthritis syndrome without skin lesions — Purulent arthritis syndrome without skin lesions usually follows untreated tenosynovitis, dermatitis, polyarthralgia syndrome and is typified by suppurative arthritis, which results in pain, redness, swelling, and decreased range of motion of one or several joints. The knees, wrists, and ankles are most commonly affected [1,22]. Rarely, skin lesions similar to those observed in DGI are seen, supporting the concept that these disorders may represent two ends of a spectrum.

DIAGNOSIS — The accurate diagnosis of gonorrheal infection requires a thorough patient history, physical examination, and laboratory studies. Laboratory tests utilized for diagnosis include microscopy, culture, and nucleic acid amplification tests. The diagnosis of genitourinary, anorectal, and pharyngeal gonococcal infection is reviewed separately. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents".)

In patients with suspected disseminated gonococcal infection (DGI), in addition to cultures of blood and synovial fluid, cultures should be performed on skin lesions via swabbing of pustules or from tissue specimens if pustules are not present [1]. Urogenital, rectal, and pharyngeal specimens for culturing should also be performed, as patients with DGI often have evidence of urogenital, rectal, or pharyngeal infection despite absence of symptoms at those sites [27,28]. Only 10 to 20 percent of skin cultures are positive in patients with cutaneous lesions of DGI; however, culture results may be useful for identifying other infectious causes. The diagnosis of DGI is discussed in greater detail elsewhere. (See "Disseminated gonococcal infection", section on 'Evaluation'.)

The diagnostic utility of laboratory investigations in primary cutaneous gonorrhea has not been specifically studied. Diagnosis of primary cutaneous gonorrhea via Gram stain and culture of spontaneous or expressible purulent drainage from pustules or furuncular lesions has been reported [6,7].

In general, a presumptive clinical diagnosis of gonorrhea warrants therapy while the results of laboratory investigations are pending.

Histopathology — The histopathologic findings in cutaneous gonorrhea are typically nonspecific, limiting the use of skin biopsy for diagnosis. The epidermis may show mild spongiosis, intraepidermal vesiculation, exocytosis of neutrophils, pustulation, or necrosis. In the dermis, features of leukocytoclastic vasculitis with associated microthrombi within blood vessels are usually present [1,29-31].

The detection of diplococci on tissue Gram stain from lesions in DGI is rare. When found, bacteria are typically located in the walls and lumina of cutaneous vessels or within the dermal inflammatory infiltrate. Pustular lesions of primary cutaneous gonorrhea are much more likely to demonstrate diplococci on histopathologic examination [32].

Gonococcal antigens may be detected using direct immunofluorescence in more than 50 percent of cases of DGI [29-31]. However, direct immunofluorescence is not typically performed due to the presence of more highly specific and sensitive nucleic acid amplification tests (such as polymerase chain reaction [PCR]) that may be able to detect even the presence of one organism. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents".)

DIFFERENTIAL DIAGNOSIS — The cutaneous manifestations of gonorrheal infection are not pathognomonic. Thus, multiple other disorders share similar clinical features. Other cutaneous bacterial infections may present with pustules or furuncles similar to those seen in primary cutaneous gonorrhea, and the possibility of syphilis, herpes simplex, donovanosis, lymphogranuloma venereum, and mpox (previously referred to as monkeypox) [33] as well as noninfectious disorders (such as Behçet syndrome) must be considered in patients who present with genital ulcers.

The acral, hemorrhagic pustules of disseminated gonococcal infection (DGI) should be distinguished from the acral Janeway lesions and Osler nodes that may occur in infective endocarditis and the hemorrhagic petechiae or pustules that can occur in the setting of meningococcemia. Unlike DGI, frank arthritis and tenosynovitis are usually absent in meningococcemia. The possibility of infective endocarditis is suggested by the presence of additional clinical findings such as a new-onset heart murmur or splinter hemorrhages on the nails. (See "Clinical manifestations of meningococcal infection" and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

The differential diagnosis of DGI is discussed in greater detail separately. (See "Disseminated gonococcal infection", section on 'Differential diagnosis'.)

Anal pruritus in anorectal gonorrhea can be easily mistaken for contact dermatitis, candidiasis, nonspecific intertrigo, lymphogranuloma venereum in gay men, and other disorders. (See "Approach to the patient with anal pruritus", section on 'Etiology'.)

TREATMENT — The treatment of gonococcal infections is reviewed separately. (See "Treatment of uncomplicated gonorrhea (Neisseria gonorrhoeae infection) in adults and adolescents" and "Disseminated gonococcal infection", section on 'Management'.)

SUMMARY AND RECOMMENDATIONS

Overview – Gonorrhea is a common sexually transmitted disorder that primarily infects mucosal surfaces. Cutaneous lesions may occur as a result of direct inoculation (primary cutaneous gonorrhea), as a secondary feature of mucosal infection (secondary cutaneous gonorrhea), or as a manifestation of disseminated disease (disseminated gonococcal infection [DGI]). (See 'Introduction' above.)

Primary cutaneous gonorrhea – Primary cutaneous gonorrhea may occur in genital or extragenital sites. Pustules, abscess, erosions, or ulcers may develop as a result of direct inoculation (picture 1). (See 'Primary cutaneous gonorrhea' above.)

Secondary cutaneous gonorrhea – Depending on the site or primary infection, secondary cutaneous gonorrhea may manifest with features such as inflammation of the genital skin, anal pruritus, or oral ulcers (picture 2A-C). (See 'Secondary cutaneous gonorrhea' above.)

Disseminated gonococcal infection – Cutaneous lesions frequently occur in patients with the tenosynovitis, dermatitis, polyarthralgia syndrome of DGI. Acral, hemorrhagic vesicles or pustules are a characteristic finding of this variant of gonorrhea. Patients typically have only 2 to 10 skin lesions. (See 'Disseminated gonococcal infection' above.)

Diagnosis – The clinical findings of cutaneous lesions in patients with gonorrhea are nonspecific. The combination of a thorough patient history, a physical examination, and laboratory studies are beneficial for diagnosis. (See 'Diagnosis' above and 'Differential diagnosis' above.)

  1. Ghosn SH, Kibbi AG. Cutaneous gonococcal infections. Clin Dermatol 2004; 22:476.
  2. Laga M, Manoka A, Kivuvu M, et al. Non-ulcerative sexually transmitted diseases as risk factors for HIV-1 transmission in women: Results from a cohort study. AIDS 1993; 7:95.
  3. Cohen MS, Hoffman IF, Royce RA, et al. Reduction of concentration of HIV-1 in semen after treatment of urethritis: implications for prevention of sexual transmission of HIV-1. AIDSCAP Malawi Research Group. Lancet 1997; 349:1868.
  4. Hook EW 3rd, Holmes KK. Gonococcal infections. Ann Intern Med 1985; 102:229.
  5. Alcorn TM, Cohen MS. Gonococcal pathogenesis: Adaptation and immune evasion in the human host. Curr Opin Infect Dis 1994; 7:310.
  6. Rosen T. Unusual presentations of gonorrhea. J Am Acad Dermatol 1982; 6:369.
  7. Scott MJ Jr, Scott MJ Sr. Primary cutaneous Neisseria gonorrhoeae infections. Arch Dermatol 1982; 118:351.
  8. Siboulet AC, Majewski E. Manifestation Cutane´es de la gonococcie. Nouveaux Aspects. Chancre cutane´ gonococcique. Bull Soc Fr Dermatol Syphilol 1974; 81:159.
  9. Varady E, Nsanze H, Slattery T. Gonococcal scalp abscess in a neonate delivered by caesarean section. Sex Transm Infect 1998; 74:451.
  10. Lal A, Rapose A. Gonococcal cellulitis: an (un)friendly bite. Infection 2018; 46:569.
  11. Fan W, Zhang Q, Wei M, et al. Clinical Study on Gonococcal Infection of the Penile Raphe. Urol Int 2023; 107:510.
  12. Sherrard J, Barlow D. Gonorrhoea in men: clinical and diagnostic aspects. Genitourin Med 1996; 72:422.
  13. McNeeley SG Jr. Gonococcal infections in women. Obstet Gynecol Clin North Am 1989; 16:467.
  14. Stansfield VA. Diagnosis and management of anorectal gonorrhoea in women. Br J Vener Dis 1980; 56:319.
  15. Bruce AJ, Rogers RS 3rd. Oral manifestations of sexually transmitted diseases. Clin Dermatol 2004; 22:520.
  16. To U, Kim J, Chia D. Lupus flare: an uncommon presentation of disseminated gonorrhea. Case Rep Med 2014; 2014:626095.
  17. Dutertre M, Tomasevic D, Guillermin Y, et al. Gonococcemia mimicking a lupus flare in a young woman. Lupus 2014; 23:81.
  18. Ellison RT 3rd, Curd JG, Kohler PF, et al. Underlying complement deficiency in patients with disseminated gonococcal infection. Sex Transm Dis 1987; 14:201.
  19. Graciaa SH, Graciaa DS, Yildirim I, Chonat S. Risk of Disseminated Gonococcal Infections With Terminal Complement Blockade. J Pediatr Hematol Oncol 2022; 44:e493.
  20. Brown TJ, Yen-Moore A, Tyring SK. An overview of sexually transmitted diseases. Part I. J Am Acad Dermatol 1999; 41:511.
  21. Martin DH, Mroczkowski TF. Dermatologic manifestations of sexually transmitted diseases other than HIV. Infect Dis Clin North Am 1994; 8:533.
  22. O'Brien JP, Goldenberg DL, Rice PA. Disseminated gonococcal infection: a prospective analysis of 49 patients and a review of pathophysiology and immune mechanisms. Medicine (Baltimore) 1983; 62:395.
  23. Beatrous SV, Grisoli SB, Riahi RR, et al. Cutaneous manifestations of disseminated gonococcemia. Dermatol Online J 2017; 23.
  24. Newman CR, Joshi K, Brucks E, Ferreira JP. Disseminated Gonococcal Infection in an Immunosuppressed Patient. Am J Med 2021; 134:e123.
  25. Ostlere LS, Harris D, Johnson M, Rustin MH. Gastrointestinal and cutaneous vasculitis associated with gonococcal infection in an HIV-seropositive patient. J Am Acad Dermatol 1993; 29:276.
  26. Mastrolonardo M, Loconsole F, Conte A, Rantuccio F. Cutaneous vasculitis as the sole manifestation of disseminated gonococcal infection: case report. Genitourin Med 1994; 70:130.
  27. Belkacem A, Caumes E, Ouanich J, et al. Changing patterns of disseminated gonococcal infection in France: cross-sectional data 2009-2011. Sex Transm Infect 2013; 89:613.
  28. Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect Dis Clin North Am 2005; 19:853.
  29. Shapiro L, Teisch JA, Brownstein MH. Dermatohistopathology of chronic gonococcal sepsis. Arch Dermatol 1973; 107:403.
  30. Barr J, Danielsson D. Septic gonococcal dermatitis. Br Med J 1971; 1:482.
  31. Kahn G, Danielsson D. Septic gonococcal dermatitis. Demonstration of gonococci and gonococcal antigens in skin lesions by immunofluorescence. Arch Dermatol 1969; 99:421.
  32. Weedon D. Bacterial and rickettsial infections. In: Weedon's Skin Pathology, 3rd ed, Elsevier Limited, 2010. p.547.
  33. Griffiths-Acha J, Vela-Ganuza M, Sarró-Fuente C, López-Estebaranz JL. Monkeypox: a new differential diagnosis when addressing genital ulcer disease. Br J Dermatol 2022; 187:1050.
Topic 15867 Version 14.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟