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Buruli Ulcer Treatment & Management

  • Author: Aaron Z Hoover, MD, FAAD; Chief Editor: William D James, MD  more...
 
Updated: Jul 17, 2014
 

Medical Care

Since 2004, the medical management of Buruli ulcers has become an active area of research. Through the use of the mouse footpad model developed by Fenner, rifampicin, rifabutin, amikacin and streptomycin have demonstrated bactericidal activity and azithromycin, clarithromycin and moxifloxacin to have bacteriostatic activity.[39] Antibiotics not only destroy or inhibit the causative mycobacteria, they reverse the immunosuppression of the mycolactone.[30, 39] Antibiotics have reduced the rate of infection recurrence and reduced the need for surgical intervention.

In 2004, the WHO recommended a treatment protocol that divided lesions into 3 categories (see Table 2 below). The WHO recommended that all categories receive a course of rifampicin and streptomycin. Recurrence rates after antibiotic treatment are reported to be 2-3%.[9, 40, 41] This regimen has been reported to heal lesions without requiring surgery in 47% of patients in a series of 224 and 95% in a series of 160.[40, 42] The median healing times for category I, II, and III were 8, 10, and 20 weeks, respectively.[42] The use of rifampicin and streptomycin remains the criterion standard of care; however, current research is looking for an all-oral regimen. The 2 options at this point are combining rifampin with clarithromycin or a fluoroquinolone (moxifloxacin/ciprofloxacin). Fluoroquinolones are not recommended in pregnant women or children.

Table 2. Categories of Treatment[43] (Open Table in a new window)

Category Form of Disease Treatment Primary Aim Secondary Aim level of Health Care System Diagnosis
I Small early lesion (eg, nodules, papules, plaques, ulcers < 5 cm in diameter) Complete antibiotics



If at or near a joint, maintain same movement as on unaffected side



If surgery is needed in noncritical areas, consider this after 8 weeks of antibiotic treatment



Cure without surgery



Cure without movement limitations



Reduce or prevent recurrence Community health centers and district hospitals Strong clinical diagnosis (with or without laboratory confirmation)
II Nonulcerative and ulcerative plaque and edematous forms



Single large ulcerative lesion 5-15 cm in diameter



Complete antibiotics, before surgery (if possible)



If at or near a joint, maintain same movement as on unaffected side



Cure without surgery



Reduce extent of the surgical debridement when needed



Cure without movement limitations



Reduce or prevent recurrence Health centers, district and tertiary hospitals Strong clinical diagnosis (with or without laboratory confirmation)
III Lesions in the head and neck region, particularly the face



Disseminated/mixed forms (eg, osteitis, osteomyelitis, joint involvement)



Multiple lesions and



osteomyelitis



Extensive lesion >15 cm



Complete antibiotics, before surgery (if possible)



If at or near a joint, maintain same movement as on unaffected side



Cure without surgery



Cure without movement limitations



Reduce or prevent recurrence District and tertiary hospitals Strong clinical diagnosis (with or without laboratory confirmation)

Nienhuis et al compared the efficacy of 2 antibiotic regimens for M ulcerans infection. In Ghana, patients aged 5 years or older were randomly assigned to receive streptomycin (15 mg/kg IM qd) plus rifampicin (10 mg/kg PO qd) for 8 weeks (n = 76) or streptomycin and rifampin for 4 weeks followed by rifampin and clarithromycin (7.5 mg/kg PO qd) for 4 weeks (n = 75). No significant difference was observed for each treatment regimen (healed lesions at 1 y were 96% for 8-wk streptomycin vs 91% for 4-wk streptomycin); however, the number of streptomycin injections was able to be reduced by switching to oral clarithromycin after 4 weeks.[44]

In 2007, the Australian Victorian Department of Human Services recommended the combination of rifampicin and clarithromycin or ciprofloxacin or moxifloxacin for 3 months.[45] It has proven effective in small case series.[37] Friedman et al demonstrated a successful treatment in 42 of 43 patients using rifampin (10 mg/kg PO qd) combined with either ciprofloxacin (500 mg twice daily) or clarithromycin(500 mg twice daily). The majority of these patients had WHO category I lesions.[46] In severe disease, oral rifampicin with intravenous amikacin is the treatment of choice.

While further research is needed to determine optimal duration of treatment of an all-oral antibiotic regimen, the existing research has led the WHO to summarize its stance on treatment as follows[43] :

  • "In summary, there is now overwhelming evidence that 8 weeks of streptomycin–rifampicin or 4 weeks of rifampicin–streptomycin followed by 4 weeks of rifampicin–clarithromycin or 8 weeks of other oral regimens all achieve recurrence-free healing with an acceptable level of side-effects. This is true for ulcers of all sizes, even without additional surgery to remove necrosis or skin grafting to accelerate healing."

Rifampicin at 10 mg/kg body weight by mouth daily for 8 weeks and streptomycin at 15 mg/kg body weight by intramuscular injection daily for 8 weeks (contraindicated in pregnancy) remains the WHO recommended standard antibiotic treatment.

While awaiting further confirmation of efficacy, the WHO has stated that an alternative regimen based on vast clinical practice is (1) rifampicin at 10 mg/kg by mouth daily for 8 weeks and clarithromycin at 7.5 mg/kg by mouth twice daily for 8 weeks or (2) rifampicin at 10 mg/kg by mouth once daily for 8 weeks and moxifloxacin at 400 mg by mouth once daily for 8 weeks (for adults only).[43]

With the increase in the use of antibiotics as the primary treatment, a paradoxical reaction during antibiotic therapy has been recognized. O'Brien et al first reported this phenomenon in patients with M ulcerans in whom there is clinical deterioration of lesions after initial improvement on antibiotics or the appearance of new lesions.[47] A similar process has been well documented in M tuberculosis infection, M leprae infection, and HIV infection among patients who are undergoing antiviral treatment.

Antibiotic treatment leads to a reversal of the immune suppression, which can lead to a brisk inflammatory response and release mycobacterial antigens from dead organisms. This immune response can be misinterpreted as treatment failure or secondary infection and lead to unnecessary medical or surgical intervention if a paradoxical reaction is not considered. Paradoxical reactions occur in9-23% of patients treated with antibiotics.[46, 48, 49, 50]

They can occur anywhere from the first week of treatment until 8 months after initiation of antibiotics, and most occur 3-10 weeks after the start of treatment. Reactions can occur after the completion of antibitoics and should not be assumed to signal a treatment failure or a reason to restart antibiotics.

An increased risk was associated with patients with an edematous lesion or if amikacin was the part of the initial antibiotic regimen.[49]

If a paradoxical reaction is suspected, a specimen should be sent for histopathological examination and culture. It should be cautioned that PCR and AFB stains can be positive because of the detection of nonviable M ulcerans.

Treatment strategies include clinical observation, needle aspiration of fluctuant lesions, minimal debridement if necessary, and adjunctive corticosteroid administration to settle inflammation in severe reactions. Prednisone is used at a dose of 0.5-1 mg/kg for 2-3 weeks with gradual tapering for a course of 4-8 weeks.[50] Prolonging the antibiotic course to 12 weeks can be considered.

Other treatment options have been explored. Hyperthermia with a 40°C water bath, such as a circulating water jacket, has shown some success.[51, 52] The use of hyperbaric oxygen has also been reported as effective in a small number of patients.[53] The use of ozone therapy is being explored after initially encouraging results.[54]

Studies of the effectiveness of the BCG vaccine against M ulcerans have been disappointing, with most studies demonstrating no lasting benefit. The BCG vaccine may provide some protection against the onset of disease, although this effect does not last past a year.[55, 56] Individuals who were previously immunized were less likely to have ulcers that cause osteomyelitis. Despite the disappointing results with the BCG vaccine, a new vaccine is an active area of research (http://www.burulivac.eu/ ).

Now that it is known that mycolactone affects WASP and N-WASP, suppression of this pathway could be a strategy to treat Buruli ulcers.[10]

Guidelines

The Infectious Diseases Society of America recently updated their guidelines for the diagnosis and management of skin and soft tissue infections. For the full guidelines, see Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America.[57, 58]

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Surgical Care

Excision was the treatment of choice in the past, but recurrence rates after surgery alone are 6-30%. With the use of antibiotics, 40% of patients do not require surgery. In conjunction with antibiotics, surgery is used to remove devitalized tissue, cover open wounds with a skin graft, and correct or minimize deformities.[59] Note the images below.

An edematous Buruli ulcer in a 9-year-old Togolese An edematous Buruli ulcer in a 9-year-old Togolese girl. Courtesy of Wayne M. Meyers, MD.
Photo of Tongolese girl taken 5 years after the Bu Photo of Tongolese girl taken 5 years after the Buruli ulcer had been excised and repaired with autologous split-skin graft by G.B. Priuli, MD. Courtesy of Wayne M. Meyers, MD.

For those who refuse or cannot tolerate antibiotics, surgeries can have excellent cure rates in certain cases. Small subcutaneous nodules or small ulcerations younger than 6 months and smaller than 10 cm in diameter may be excised en bloc with primary closure. Risk factors for recurrence in surgery-alone patients include immunosuppression, positive histologic margins for inflammation or infection, patients older than 60 years, and clinical symptoms present longer than 75 days.[48] Use of PCR to evaluate surgical margins may reduce recurrences.[60]

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Contributor Information and Disclosures
Author

Aaron Z Hoover, MD, FAAD Staff Dermatologist/Dermatopathologist, Front Range Dermatology Associates

Aaron Z Hoover, MD, FAAD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Christian Medical and Dental Associations, International Society of Dermatopathology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Humira.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Franklin Flowers, MD Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine

Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Surgery

Disclosure: Nothing to disclose.

Acknowledgements

Special thanks to Ms Carmen Urich for helping me obtain articles needed to update this publication.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of the following previous authors, Brian P. Green, DO, MS, PA-C; Sean T. Gunning, MD; and Mary K. Mather, MD, to the development and writing of this article.

The authors and editors of Medscape Reference would also like to thank Wayne M. Meyers, MD, for his clinical images from his article with Douglas S. Walsh, MD, in Transactions of the Royal Society of Tropical Medicine and Hygiene.[3]

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Buruli ulcer can extend to 15% of a person's skin surface and may destroy nerves and blood vessels. Metastatic bone lesions may develop.
An edematous Buruli ulcer in a 9-year-old Togolese girl. Courtesy of Wayne M. Meyers, MD.
Photo of Tongolese girl taken 5 years after the Buruli ulcer had been excised and repaired with autologous split-skin graft by G.B. Priuli, MD. Courtesy of Wayne M. Meyers, MD.
Table 1. Pros and Cons of Sampling Techniques From the WHO [18]
Method Pros Cons
Direct smear examination • Easy to perform at local level



• Does not require expensive materials and equipment



• Rapid results



• Uses swabs, fine-needle aspiration, and biopsy samples



• Low sensitivity (< 60%)



• Needs trained personnel



• Needs external quality assurance



Polymerase chain reaction • Results fairly rapid



• Uses swabs, fine-needle aspiration, and biopsy samples



• High sensitivity (>95%)



• Requires a sophisticated laboratory



• Expensive to perform



• Needs trained personnel



• Requires strict quality control



Culture of M ulcerans • Uses swabs, fine-needle aspiration, and biopsy samples • Requires a sophisticated



laboratory



• Needs trained personnel



• Results take >8 weeks



• Low sensitivity (20-60%)



• Not useful for immediate patient management



Histopathology • Sensitivity is about 90%



• Results fairly rapid (if services are available)



• Useful in establishing differential diagnosis and monitoring unexpected response to treatment



• Requires a sophisticated laboratory



• Expensive to perform



• Needs trained personnel



• Requires invasive procedure (ie, biopsy)



Table 2. Categories of Treatment [43]
Category Form of Disease Treatment Primary Aim Secondary Aim level of Health Care System Diagnosis
I Small early lesion (eg, nodules, papules, plaques, ulcers < 5 cm in diameter) Complete antibiotics



If at or near a joint, maintain same movement as on unaffected side



If surgery is needed in noncritical areas, consider this after 8 weeks of antibiotic treatment



Cure without surgery



Cure without movement limitations



Reduce or prevent recurrence Community health centers and district hospitals Strong clinical diagnosis (with or without laboratory confirmation)
II Nonulcerative and ulcerative plaque and edematous forms



Single large ulcerative lesion 5-15 cm in diameter



Complete antibiotics, before surgery (if possible)



If at or near a joint, maintain same movement as on unaffected side



Cure without surgery



Reduce extent of the surgical debridement when needed



Cure without movement limitations



Reduce or prevent recurrence Health centers, district and tertiary hospitals Strong clinical diagnosis (with or without laboratory confirmation)
III Lesions in the head and neck region, particularly the face



Disseminated/mixed forms (eg, osteitis, osteomyelitis, joint involvement)



Multiple lesions and



osteomyelitis



Extensive lesion >15 cm



Complete antibiotics, before surgery (if possible)



If at or near a joint, maintain same movement as on unaffected side



Cure without surgery



Cure without movement limitations



Reduce or prevent recurrence District and tertiary hospitals Strong clinical diagnosis (with or without laboratory confirmation)
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