Donovanosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]; Nate Michalak, B.A.

Donovanosis, a genital ulcer disease, is a sexually transmitted disease caused by the fastidious Gram-negative bacterium Klebsiella granulomatis. Aragão & Vianna classified the agent as Calymmatobacterium granulomatis in 1913. However, sequencing analysis by Carter et al. revealed that the agent should be reclassified to Klebsiella granulomatis. Donovanosis is rare in developed countries but is endemic in tropical and developing areas, including India, Papua New Guinea, the Caribbean, central Australia, and southern Africa. Donovanosis must be differentiated from other diseases that cause genital ulcers without lymphadenopathy including: primary or secondary syphilis, chancroid, herpes simplex, amoebiasis, and squamous cell carcinoma. Sexually transmitted diseases characterized as genital ulcer diseases may present with similar manifestations and lesion characteristics. Pathogenesis of K. granulomatis is poorly characterized. The incubation period of Klebsiella granulomatis is debated and ranges from 1 to 360 days with a median time of 50 days. Donovanosis starts as a papule or subcutaneous nodule which eventually ulcerates. The ulcer progresses to create areas of granulomatous tissue. Typical lesion characteristics include: beefy red color, nontender, emitting rank odor, elevated above skin, smooth and rolled edge, serpiginous outline. Physical examination of lesions can classify donovanosis into ulcerogranulomatous, hypertrophic, necrotic, and sclerotic variants. The standard method for identifying K. granulomatis and suggesting donovanosis as the diagnosis is a smear and stain of ulcer material. Microscopy of the stain reveals Donovan bodies within monocytes that may or may not be capsulated. Antimicrobial therapy is the mainstay of treatment for donovanosis. Azithromycin 1 g PO once per week for at least 3 weeks and until all lesions have completely healed is the preferred regimen. Since there is no vaccine for donovanosis, methods of primary prevention include: abstaining from sexual activity, limiting number of sexual partners and using a male or female condom. The goal of secondary prevention is to stop the spread of disease. Therefore infected individuals should abstain from sexual intercourse until symptoms reside.

Donovanosis was first called “serpiginous ulcer” in 1882. Charles Donovan first identified the cause of these genital lesions in 1905, which he called “Donovan bodies,” since the etiologic agent was unknown. Aragão & Vianna classified the agent as Calymmatobacterium granulomatis in 1913. However, sequencing analysis by Carter et al. revealed that the agent should be reclassified to Klebsiella granulomatis.

Klebsiella granulomatis may be transmitted through sexual contact, direct contact, or fecal contamination. K. granulomatis may also autoinoculate, resulting in multiple lesions. The pathogenesis of K. granulomatis is not well characterized. K. granulomatis replicates intracellularly within monocytes after being phagocytosed. Monocytes eventually rupture, recruiting additional monocytes and causing the formation of granulomas. On microscopic examination, pleomorphic Donovan bodies can be seen within the cytoplasm or phagosomes of monocytes.

Klebsiella granulomatis, originally classified as Calymmatobacterium granulomatis, is a fastidious Gram-negative pleomorphic bacteria causing donovanosis, a gential ulcer disease.

Donovanosis may be classified by four different clinical appearances of the lesion: ulcerogranulomatous, hypertrophic or verrucous, nectrotic, or sclerotic. Ulcerogrnulomatous is the most common.

Donovanosis must be differentiated from other diseases that cause genital ulcers without lymphadenopathy including: primary or secondary syphilis, chancroid, herpes simplex, amoebiasis, and squamous cell carcinoma. Sexually transmitted diseases characterized as genital ulcer diseases may present with similar manifestations and lesion characteristics.

A true incidence of donovanosis is difficult to determine due to limited knowledge of the disease, limited diagnostic tests, infrequency of disease compared to other sexually transmitted diseases, and occurrence of the disease in areas with limited resources. Most infections occur in people who’s ages range from 20 to 40 years. Sex and race are not a predilection for acquiring the disease. Donovanosis is rare in the United States and other developed countries. Donovanosis is endemic in tropical and developing areas, including India, Papua New Guinea, the Caribbean, central Australia, and southern Africa.

Risk factors for donovanosis include: multiple sex partners, unprotected sexual intercourse, travel to endemic areas, lack of circumcision in males, and poor genital hygiene.

The incubation period of Klebsiella granulomatis is debated and ranges from 1 to 360 days with a median time of 50 days. Donovanosis starts as a papule or subcutaneous nodule which eventually ulcerates. The ulcer progresses to create areas of granulomatous tissue. Pseudoepitheliomatous hyperplasia of lesion borders often occurs. Ulcers autoinoculate creating multiple lesions. “Pseudobuboes” may also develop. Chronic ulcers leads to fibrosis and eventually Elephantiasis-like swelling. K. granulomatis may disseminate causing extragenital lesions and systemic infection. Complications include: genital damage and scarring, elephantiasis, phimosis in men, [strictures]] or fistulas of the urethra, vagina, or anus, foinfection with other sexually transmitted infections and carcinoma (in 0.25% of cases). Prognosis is poor without treatment because the disease has a high morbidity; untreated disease leads to damage of the genital tissue, scarring, and elephantiasis. Donovanosis may reoccur after 6 to 18 months after treatment.

Patients develop the following local symptoms, typically 3 to 40 days after sexual contact: painless papules, painless ulcers of granulomatous tissue that spread and bleed easily, periadenitis, “pseudobuboes”, and absent lymphadenopathy. If the disease disseminates as a result of chronic ulcers, systemic symptoms may develop including: fever, malaise, anemia, night sweats, weight loss and toxemia.

Donovanosis is commonly characterized as painless, progressive ulcerative lesions without regional lymphadenopathy. Patients in later stages may present with scarring, elephantiasis-like swelling of genitals or perianal area, or stenosis of the urethra, vagina, or anus. Typical lesion characteristics include: beefy red color, nontender, emitting rank odor, elevated above skin, smooth and rolled edge, serpiginous outline. Physical examination of lesions can classify donovanosis into ulcerogranulomatous, hypertrophic, necrotic, and sclerotic variants. Common locations in males include: coronal sulcus, subpreputial region, and anus. Common locations in females include: labia minora, cervix, and fourchette.

The standard method for identifying K. granulomatis and suggesting donovanosis as the diagnosis is a smear and stain of ulcer material. Microscopy of the stain reveals Donovan bodies within monocytes that may or may not be capsulated. If swabs are taken for other diagnostic tests, the smear for Donovan bodies should be taken first to ensure there is adequate material to detect the Donovan bodies. K. granulomatis has been isolated via culture methods but is difficult and not practical as a tool for diagnosis.

Antimicrobial therapy is the mainstay of treatment for donovanosis. Azithromycin 1 g PO once per week for at least 3 weeks and until all lesions have completely healed is the preferred regimen. Alternative regimens include doxycycline, ciprofloxacin, erythromycin, and trimethoprim-sulfamethoxazole. Pregnant women should be treated with erythromycin. Sexual partners should also be evaluated and treated.

Since there is no vaccine for donovanosis, methods of primary prevention include: abstaining from sexual activity, limiting number of sexual partners and using a male or female condom. The goal of secondary prevention is to stop the spread of disease. Therefore infected individuals should abstain from sexual intercourse until symptoms reside.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Donovanosis was first called “serpiginous ulcer” in 1882. Charles Donovan first identified the cause of these genital lesions in 1905, which he called “Donovan bodies,” since the etiologic agent was unknown. Aragão & Vianna classified the agent as Calymmatobacterium granulomatis in 1913. However, sequencing analysis by Carter et al. revealed that the agent should be reclassified to Klebsiella granulomatis.

• Donovanosis was first called “serpiginous ulcer“, dating back to 1882.^[1]
• In 1905, Charles Donovan discovered intracellular bodies as the cause of this ulcer; the nature of the bodies was unknown and they were referred to as “Donovan bodies.”^[2]
• Calymmatobacterium granulomatis was presumed to be the causative agent of donovanosis by Aragão & Vianna in 1913.
• However, gene sequencing of bacteria in Donovan bodies by Carter et al. revealed that the caustive agent should be reclassified to Klebsiella granulomatis.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]; Nate Michalak, B.A.

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Klebsiella granulomatis may be transmitted through sexual contact, direct contact, or fecal contamination. K. granulomatis may also autoinoculate, resulting in multiple lesions. The pathogenesis of K. granulomatis is not well characterized. K. granulomatis replicates intracellularly within monocytes after being phagocytosed. Monocytes eventually rupture, recruiting additional monocytes and causing the formation of granulomas. On microscopic examination, pleomorphic Donovan bodies can be seen within the cytoplasm or phagosomes of monocytes.

• Klebsiella granulomatis may be transmitted through sexual contact.
• Although donovanosisis is typically considered a sexually transmitted disease, studies indicate it may also develop through fecal contamination or direct contact.
• K. granulomatis may also autoinoculate, resulting in multiple lesions that appear to be mirror images of each other.^[1]

• The pathogenesis of K. granulomatis is not well characterized.
• K. granulomatis is phagocytosed by macrophages.
• K. granulomatis is able to avoid destruction and replicates intracellularly within these monocytes.
• Monocytes eventually rupture, recruiting additional monocytes and causing the formation of granulomas.^[1][2]

• Donovan bodies (K. granulomatis) are seen within phagosomes or in the cytoplasm of monocytes or histocytes.
• Morphology of Donovan bodies:

• Pleomorphic ranging from coccus to bacillus
• 1-2 X 0.5-0.7 μm
• May or may not be capsulated
• Non-motile

• Epidermis of lesion borders show a degree of hyperplasia.
• A dense infiltrate of plasma cells is seen in the dermis.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A.;

Klebsiella granulomatis, originally classified as Calymmatobacterium granulomatis, is a fastidious Gram-negative pleomorphic bacteria causing donovanosis, a gential ulcer disease.

• Aragão and Vianna classified the bacteria causing donovanosis as Calymmatobacterium granulomatis in 1913. However, DNA sequencing of 16S rRNA and phoE genes revealed similarity to Klebsiella.^[1]

• There is 99% homology between the etiologic agent of donovanosis and members of Klebsiella.^[2]
• A proposal has been put forth to reclassify the bacteria to Klebsiella granulomatis.

• K. granulomatis morphology:^[3]

• Pleomorphic ranging from coccus to bacillus
• 1-2 X 0.5-0.7 μm
• May or may not be capsulated
• Non-motile

• K. granulomatis is an obligate, intracellular human pathogen.
• K. granulomatis is typically transmitted through sexual contact but may also be transmitted through direct contact and fecal contamination.^[4]

• 
  This image reveals some of the cytoarchitectural features seen in a lymph node specimen that had been extracted from a patient suspected of a Hantavirus illness. Note the concentration of lymphohistiocytic infiltrates, almost all cases have expanded paracortical regions, or T-cell regions with immunoblasts, which sometimes extend into the cortex and into the medulla. From Public Health Image Library (PHIL). ^[5]
• 
  “Donovan bodies” in a tissue sample used to diagnose granuloma inguinale. From Public Health Image Library (PHIL). ^[5]
• 
  “Donovan bodies” in a tissue sample used to diagnose granuloma inguinale. From Public Health Image Library (PHIL). ^[5]
• 
  Dieterle’s silver stain under photomicrographic examination, image reveals presence of numerous Donovan bodies. From Public Health Image Library (PHIL). ^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Donovanosis may be classified by four different clinical appearances of the lesion: ulcerogranulomatous, hypertrophic or verrucous, nectrotic, or sclerotic. Ulcerogrnulomatous is the most common.

Donovanosis may be classified by four different clinical appearances of the lesion:^[1]

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Donovanosis must be differentiated from other diseases that cause genital ulcers without lymphadenopathy including: primary or secondary syphilis, chancroid, herpes simplex, amoebiasis, and squamous cell carcinoma. Sexually transmitted diseases characterized as genital ulcer diseases may present with similar manifestations and lesion characteristics.

Donovanosis must be differentiated from other diseases that cause genital ulcers without lymphadenopathy:^[1]

• Primary or secondary syphilis
• Chancroid
• Herpes simplex
• Amoebiasis
• Squamous cell carcinoma

Other diseases that causes specifically granulomatous ulcers include:

• Cutaneous tuberculosis
• Paracoccidioidomycosis
• Leishmaniasis
• Pyoderma gangrenosum

Sexually transmitted diseases characterized as genital ulcer diseases may present with similar manifestations and lesion characteristics. A diagnosis based only on the patient’s medical history and physical examination frequently is inaccurate. Patients who have genital, anal, or perianal ulcers should be evaluated with laboratory tests to make a definitive diagnosis.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]; Nate Michalak, B.A.

A true incidence of donovanosis is difficult to determine due to limited knowledge of the disease, limited diagnostic tests, infrequency of disease compared to other sexually transmitted diseases, and occurrence of the disease in areas with limited resources. Most infections occur in people who’s ages range from 20 to 40 years. Sex and race are not a predilection for acquiring the disease. Donovanosis is rare in the United States and other developed countries. Donovanosis is endemic in tropical and developing areas, including India, Papua New Guinea, the Caribbean, central Australia, and southern Africa.

• A true incidence of donovanosis is difficult to determine due to limited knowledge of the disease, limited diagnostic tests, infrequency of disease compared to other sexually transmitted diseases, and occurrence of the disease in areas with limited resources.

• Most infections occur in people ages 20-40. The disease is rarely seen in children or the elderly.

• Although more males present with the disease, sex does not appear to be a risk factor.

• Donovanosis is more common among African-Americans but this is most likely due to socioeconomic disparities.^[1]

• Donovanosis is rare in the United States and other developed countries.^[2][1]

• Donovanosis is endemic in tropical and developing areas, including India, Papua New Guinea, the Caribbean, central Australia, and southern Africa.^[3][2]
• The largest epidemic occurred between 1922 and 1952 in Papua New Guinea where 10,000 cases were identified in a population of 15,000.
• Between 1993 and 1997 in southern India, 14% of genital ulcer cases were identified as donovanosis.
• 3,153 cases of donovanosis were recorded in Durban, South Africa during the late 1980s through late 1990s.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Risk factors for donovanosis include: multiple sex partners, unprotected sexual intercourse, travel to endemic areas, lack of circumcision in males, and poor genital hygiene.

• Multiple sex partners
• Unprotected sexual intercourse^[1]
• Travel to endemic areas in India, Papua New Guinea, the Caribbean, central Australia, and southern Africa^[2]
• Lack of circumcision in males
• Poor genital hygiene^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]; Nate Michalak, B.A.

The incubation period of Klebsiella granulomatis is debated and ranges from 1 to 360 days with a median time of 50 days. Donovanosis starts as a papule or subcutaneous nodule which eventually ulcerates. The ulcer progresses to create areas of granulomatous tissue. Pseudoepitheliomatous hyperplasia of lesion borders often occurs. Ulcers autoinoculate creating multiple lesions. “Pseudobuboes” may also develop. Chronic ulcers leads to fibrosis and eventually Elephantiasis-like swelling. K. granulomatis may disseminate causing extragenital lesions and systemic infection. Complications include: genital damage and scarring, elephantiasis, phimosis in men, [strictures]] or fistulas of the urethra, vagina, or anus, foinfection with other sexually transmitted infections and carcinoma (in 0.25% of cases). Prognosis is poor without treatment because the disease has a high morbidity; untreated disease leads to damage of the genital tissue, scarring, and elephantiasis. Donovanosis may reoccur after 6 to 18 months after treatment.

• The incubation period of Klebsiella granulomatis is debated and ranges from 1 to 360 days with a median time of 50 days.^[1]
• Donovanosis begins with a firm papule or subcutaneous nodule which eventually ulcerates.^[2]
• The ulcer slowly progresses centrifugally, without pain, to form areas of granulomatous tissue.^[3]
• Pseudoepitheliomatous hyperplasia of lesion borders, resembling squamous cell carcinoma, often occurs.
• Ulcers may autoinoculate creating multiple lesions.
• “Pseudobuboes” may develop, which are nodular lesions that resemble lymphadenitis.^[4]
• Fibrosis may occur leading to elephantiasis-like swelling as a result of chronic ulcers.
• K. granulomatis may disseminate causing extragenital lesions in the following areas:^[4]

• mouth
• cheek
• neck
• pharynx
• larynx
• nose
• thorax

• K. granulomatis may also disseminate to the abdomen, intestines, liver, lungs, uterus, and ovaries causing systemic infection.^[3]

• Genital damage and scarring
• Elephantiasis-like swelling^[4]
• Phimosis in men
• Strictures or fistulas of the urethra, vagina, or anus^[3]
• Coinfection with other sexually transmitted infections including: syphillis, chancroid, and Human Immunodeficiency Virus (HIV)
• Carcinoma (in 0.25% of cases)^[2]

• Treating this disease early decreases the chances of tissue damage or scarring. Untreated disease leads to damage of the genital tissue.
• Donovanosis may reoccur after 6 to 18 months even after successful treatment.^[3]

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