GRANULOMA VENEREO PDF

This page includes the following topics and synonyms: Granuloma Inguinale, da Calymmatobacterium granulomatis, Donovanosi, Granuloma venereo. Basta-Juzbasic A, Ceovic R. Chancroid, lymphogranuloma venereum, granuloma inguinale, genital herpes simplex infection, and molluscum. The diagnosis and treatment of donovanosis (granuloma inguinale). .. Guariento A, Delascio D, de Macedo OB, Luisi A. Granuloma venéreo e gestaço. Matern.

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Lymphogranuloma venereum is a sexually transmitted disease caused by L1, L2, and L3 serovars of Chlamydia trachomatis. In the last 10 years outbreaks have appeared in North America, Europe, and Australia in the form of proctitis among men who have sex with men. Three stages of disease have been described.

The disease in primary stage may go undetected when only a painless papule, pustule, or ulceration appears. The diagnosis is difficult to establish on clinical grounds alone and frequently relies upon either serologic testing, gganuloma, or more recently, nucleic acid amplification testing of direct specimens. A proper treatment regimen cures the infection and prevents further damage to tissues. Lymphogranuloma venereum causes potentially severe infections with possibly irreversible sequels if adequate treatment is not begun promptly.

Early and accurate diagnosis is essential. Doxycycline is the drug of choice. Pregnant and lactating women should be treated with erythromycin gfanuloma azithromycin. Patient must be followed up during the treatment, until disease signs and symptoms have resolved. Repeated testing for syphilis, hepatitis B and C, and HIV to detect early infection should be performed. Lymphogranuloma venereum LGV is a sexually transmitted disease STD caused by L1, L2, and L3 serovars of Chlamydia trachomatis that primarily infects the lymphatics and can be transmitted through unprotected vaginal, anal, or venereeo sexual contact.

The attachment process of the elementary body to a host cell is the event most crucial to a successful infection. Elementary bodies attach to columnar epithelial cells followed by endocytosis and inhibition of lysosomal fusion.

A number of chlamydial ligands have been identified and characterized. These include the major outer membrane protein MOMP as well as the cysteine-rich OmcB Omp2 protein, hsp70, the polymorphic outer membrane proteins, and the thermolabile granu,oma membrane protein. In addition to these proposed ligands, there venefeo a considerable amount of experimental evidence to suggest that the glycosaminoglycan, heparan sulfate, is involved in the chlamydial attachment-infectivity process.

Heparan sulfate acts as a host cell receptor for MOMP. LGV synonyms include lymphopathia venerea, tropical bubo, climatic bubo, strumous bubo, poradenitis inguinales, Durand-Nicolas-Favre disease, and lymphogranuloma inguinale. The incidence has been low in developed world, but in the last 10 years outbreaks have appeared in North America, Europe, venerel Australia in the form of proctitis among men who have sex with men MSM.

LGV probably affects both sexes equally, although it is more commonly reported in men because early manifestations of LGV are more apparent in men. Men typically present with the acute form of the disease, whereas women often present when they develop complications from later stages of the disease.

LGV may appear at any age, but the highest incidence is between 15 and 40 years sexually active population. Sincethere have been a series of LGV outbreaks reported across Europe. Seventy-seven percent of cases have been diagnosed in London, Brighton, and Manchester.

This is a major public health concern because grqnuloma shedding of HIV during clinical proctitis could increase the risk of HIV transmission to uninfected men. In these regions, a survey from Madagascar showed that C. From the beginning of the year until the end ofcases of LGV were notified in Barcelona.

This is in contrast to the cenereo circulating among MSM in the United States, which show more molecular diversity. Based on these findings, it is now speculated that the LGV epidemic among MSM in Europe caused by the L2b variant may have been imported to Europe from the United States by the end of the previous century via the highly internationalized network of sexual contacts among MSM.

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Between November and JanuaryLGV was identified in people, with 27 people identified as being obtained from homosexual males. LGV is predominantly a disease of the lymphatic tissue. LGV serovars and other strains of C. After lymphangitis, areas of necrosis occur within the nodes, followed by the formation of abscess.

The incubation period lasts 3—30 days, after which a primary lesion occurs in the form of a small painless papule, pustule, nodule, shallow erosion, or herpetiform ulcer Table 1.

The initial lesions may be differentiated from the more common herpetic lesions by the lack of pain associated with the lesion.

Granuloma venéreo – Heraclides Cesar de Souza Araujo – Google Books

Differentiation from a syphilitic chancre requires serologic testing. The lesion usually heals within 1 week and may go unnoticed in the urethra, vagina, or rectum. Mucopurulent discharge from urethra, cervix, or rectum may be present regarding the inoculation site.

Some ulcers in the recent MSM outbreak have been described as indurated and of variable tenderness; their duration has been as long as several weeks.

The new clinical picture is mostly seen among the MSM. Hemorrhagic proctitis in MSM is the primary manifestation of infection following direct transmission to the rectal mucosa. It might also occur in women with rectal exposure. However, patients may present to gastroenterologists or colorectal surgeons for persisting symptoms. These cases may present with an incomplete or undisclosed history of proctosigmoiditis, without the characteristic adenopathy syndrome.

During the initial evaluation and colonoscopy, there is a strong clinical and endoscopic suspicion of inflammatory bowel disease by virtue of presentation and endoscopic and histological findings. Genital ulcers and inguinal symptoms were less common.

LGV serovars can cause symptomatic ulceration and pharyngitis but also asymptomatic carriage at this site. Secondary LGV begins within 2—6 weeks after the onset of primary lesion.

Lymphogranuloma venereum

Depending on the site of inoculation, LGV can cause inguinal syndrome after primary lesion of the anterior vulva, penis, or urethra or anorectal syndrome usually after primary lesion of the posterior vulva, vagina, or anus.

It is the most common clinical manifestation of genital LGV among heterosexuals. In two-thirds of cases, this produces unilateral enlargement, inflammation, suppuration, and abscesses.

The disease process may involve one or many lymph nodes, and if adjacent to one another, they may coalesce. The central areas of such lymph nodes may venerei undergo necrosis. In other cases, they may develop into hard, nonsuppurative masses. Women often have primary involvement of upper vagina, cervix, or posterior urethra; however, if venero are receptive to anal sex they may have primary involvement of the rectum. These regions drain to the deep iliac or perirectal nodes and cause intra-abdominal or retroperitoneal lymphadenopathy that may lead to symptoms of lower abdominal pain or low-back pain.

The systemic spread of LGV C. In addition, systemic spread occasionally results in arthritis, pneumonitis, abnormal hepatic enzymes, granhloma perihepatitis. Rare systemic complications include cardiac involvement, aseptic vensreo, and ocular inflammatory disease.

In the rare pharyngeal syndrome affecting the mouth and throat, cervical lymphadenopathy and buboes can occur. This stage manifests predominantly in women, but also in homosexual men, because of the location of the involved lymphatics. It is characterized by a chronic inflammatory response and the destruction of tissue, which is followed by the formation of perirectal abscess, fistulas, strictures, and stenosis of rectum. Lymphorroids are hemorrhoid-like swellings of obstructed perirectal, and intestinal lymphatics may also occur.

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If it is not treated, chronic progressive lymphangitis leads to chronic edema and sclerosing fibrosis. This results in strictures and fistulas that can cause elephantiasis of the genitals, esthiomene chronic ulcerative disease of vulva leading to disfiguring fibrosis and scarringand frozen pelvis syndrome. Finally, regarding clinical features, it has to be noted that in the present LGV epidemic among MSM, UK cohorts showed almost all LGV to be symptomatic, 314 but Dutch studies had a significant proportion of asymptomatic infection detected.

Modern techniques now rely on nucleic acid amplification tests NAATs in well-equipped laboratories. For the detection of LGV serovars of C. The first step includes C.

NAATs are not approved for testing samples from extra-genital sites, but studies have demonstrated high sensitivity and specificity in rectal chlamydial infections. PCR, strand displacement amplification, or transcription-mediated amplification. The second step is performed only if the first step test detects C. Two tests for the second step are available: For patients with genital disease, genital and lymph node specimens lesion swabs and bubo aspirate may be tested for C.

It is not always possible to culture the organism. Culture at primary stage is not often possible because the primary lesion often goes unnoticed. Four techniques are available: With appropriate clinical presentation, a complement fixation antibody titer of higher than 1: Titers that are greater than 1: In addition, a four-fold increase in the complement fixation titer of blood samples taken 2 weeks apart is indicative. The test has Histology of the lymph nodes is not specific: LGV causes potentially severe infections with possibly irreversible sequels if adequate treatment is not begun promptly.

Therefore, the rapid C. In general, intracellular-acting agents such as doxycycline, erythromycin, and azithromycin and certain quinolones are advised. He subsequently responded to treatment with moxifloxacin mg daily for 10 days; no isolate was available for resistance testing. A recent paper suggests that inguinal LGV may require prolonged courses of doxycycline, exceeding the currently advised day regimen. These data suggest that doxycycline may be more effective than azythromycin in the treatment of rectal chlamydial infections.

As adjunctive therapy, the aspiration of fluctuant buboes is recommended for pain relief and prevention of rupture or chronic sinus formation, in contrast to surgical incision of buboes due to potential complications. The pharynx is a reservoir for chlamydia and LGV and may play a role in ongoing transmission. Although spontaneous clearance may occur in untreated patients with pharyngeal chlamydia, in high-risk STD clinic patients, testing the pharynx for chlamydia should be considered.

A recent study suggests that HIV seropositivity was the strongest risk factor for LGV and that proctoscopic findings and elevated WBC counts in anorectal smear specimens were the only clinically relevant predictors for LGV infection. For all MSM reporting receptive anorectal intercourse, rectal chlamydia screening is recommended.

If the anorectal chlamydia test result is negative, no treatment should be administered or doxycycline treatment should be stopped after a minimum of 7 days.

If the anorectal chlamydia test result is positive and LGV testing is available, doxycycline treatment mg twice per day should be started or continued until LGV is rejected. A 7-day course of doxycycline is effective for treatment of a non-LGV chlamydia. Therapy should be continued until 21 days after confirmation of LGV.