Buruli ulcer (Mycobacterium ulcerans infection)
Buruli ulcer is a chronic debilitating disease caused by the bacteria Mycobacterium ulcerans.
It is considered noncontagious.
It often affects the skin and sometimes bone and can lead to permanent disfigurement and long-term disability.
At least 33 countries with tropical, subtropical, and temperate climates have reported Buruli ulcers in Africa, South America, and Western Pacific regions. It is most common in West Africa.
The transmission mode is not known, and there is no known prevention for the disease.
While the condition can be readily diagnosed with modern techniques like PCR, the challenge for many rural regions in Africa is that these diagnostic tools are not available there. In off-the-grid clinics, the diagnosis may have to be made by clinical evaluation alone.
Antibiotics are the primary treatment today. Surgical debridement only has a complementary role in select cases.
The WHO has Buruli ulcer as a focus area, and we advise you to keep checking their website for regular updates about this condition. Click on the image below to get to the WHO site. A lot of our text here is also based on the information provided by the WHO
Figure 1 The WHO has an up-to-date website for Buruli ulcers, and we advise you to check here regularly for new guidelines about this condition. We also advise you to subscribe to the newsletter of the WHO to stay as up-to-date as possible. The link to this newsletter is at the bottom of the WHO website (you have to scroll down all the way to the bottom of the page to find the link). image copyrights: WHO;
Buruli ulcer, caused by Mycobacterium ulcerans, is a chronic debilitating disease that mainly affects the skin and sometimes bone. The organism belongs to the family of bacteria that causes tuberculosis and leprosy. Buruli ulcer is the third most common mycobacterial infection in humans, next to tuberculosis and leprosy.
In 1962, the disease was named after Buruli County, Uganda, now called Nakasongola District, where the epidemic was documented first. Other names include Bairnsdale, Kakerifu, Kasongo, or Searls' ulcer. Although this is an ulcer that is mainly found in the tropics, we reserve the term "tropical ulcer" for other causes of ulcers than M. ulcerans.
M. ulcerans produces a unique potent toxin called mycolactone that leads to the extensive destruction of tissue. The mode of transmission to humans remains unknown. Early diagnosis and treatment are crucial to minimizing morbidity, costs and preventing long-term disability. Even though mortality is low, morbidity and subsequent functional disability can be severe. The disease affects both sexes equally and all age groups, but it is particularly common in children under the age of 15.
Scope of the problem
Buruli ulcer (BU) has been reported in 33 countries in Africa, the Americas, Asia, and the Western Pacific. Most cases occur in tropical and subtropical regions except in Australia, China, and Japan. Out of the 33 countries, 14 regularly report data to WHO. Imported BU is occasionally diagnosed in the United States, Canada, and Europe.
The annual number of suspected Buruli ulcer cases reported globally was around 5000 cases until 2010, when it started to decrease until 2016, reaching its minimum with 1961 cases reported. Since then, the number of cases has risen again every year, up to 2713 cases in 2018. In 2020 1258 cases were reported compared with 2271 cases in 2019. The reduction in 2020 could be linked to the impact of Covid-19 on active detection activities (WHO)
BCG ( against tuberculosis) vaccination may have some effect on BU. Several reports suggest that BCG vaccination provides some protection against BU for 6 to 12 months after vaccination and that neonatal BCG vaccination reduces the risk of BU osteomyelitis in those who acquire BU as children or adults. However, a case-control study concluded that BCG vaccination is probably not protective against BU, so we do not have a definite answer to this. Prophylactic and therapeutic vaccines based on DNA engineering and virulence factors, including mycolactone, are under study (BuruliVac Project). We have found no up-to-date information on the BuruliVac project's status today. An extensive internet search revealed little up-to-date information on the project's status today. If any of our readers know more about this project, please contact us via our email address.
Figure 2 The exact mode of transmission of M. ulcerans is still unknown. In some areas- for example, West Africa - peak incidences are found during March, typically in swampy regions, suggesting an association with rainy seasons. image copyright: Martchan,Shutterstock
Mycobacterium ulcerans grows at temperatures between 29–33 °C ( in comparison, Mycobacterium tuberculosis thrives best at 37 °C) and needs a low (2.5%) oxygen concentration. Because M.ulcerans prefers lower temperatures, this favors the development of lesions in cooler tissues like the skin and subcutaneous tissues. The organism produces a unique toxin (mycolactone) which causes tissue damage and inhibits the immune response.
The exact mode of transmission of M. ulcerans is still unknown. In some areas, for example, in West Africa, peak incidences are found during March, typically in swampy regions, suggesting an association with rainy seasons in that area. BU is considered noncontagious. A possible mode of transmission is local, minor, often unnoticed skin trauma that permits inoculation of M ulcerans. The estimated incubation period is 2 to 3 months before the first symptoms appear. Because M ulcerans DNA is detectable in some aquatic insects, the role of insects as vectors that infect humans by biting is under investigation. M ulcerans DNA has also been detected in mosquitoes.
Lesions frequently occur in the limbs: 35% on the upper limbs, 55% on the lower limbs, and 10% on the other parts of the body. Health workers should be careful in diagnosing Buruli ulcers in patients with lower leg lesions to avoid confusion with other common causes of ulceration such as diabetes, arterial and venous insufficiency lesions ( often in the elderly). More rare differential diagnoses are tropical phagedenic ulcers, cutaneous squamous cell carcinoma, actinomycosis, leprosy, cutaneous leishmaniasis, tuberculosis, pyoderma gangrenosum, yaws, and ulcers caused by Haemophilus ducreyi. This list of differential diagnoses is not complete, but it covers the most important other diagnoses you have to keep in the back of your mind. HIV infection complicates the management of the patient, making clinical progression more aggressive and resulting in poor treatment outcomes.
The disease has been classified into three categories of severity: Category I single small lesion (32%), Category II non-ulcerative and ulcerative plaque and oedematous forms (35%), and Category III disseminated and mixed forms such as osteitis, osteomyelitis and joint involvement (33%).
Clinical findings- the pre-ulcerative stage:
Buruli ulcers often start as painless nodules only about 1-2 cm in diameter. Early nodular lesions are occasionally confused with insect bites, boils, lipomas, ganglions, lymph node tuberculosis, onchocerciasis nodules, or deep fungal subcutaneous infections.
Less commonly, it presents as a larger painless area of induration (plaque). The disease may progress with no pain and fever. Because the initial lesion is usually painless, many patients do not seek immediate medical attention. Sometimes the condition may initially present as a diffuse painless swelling of the legs, arms, or face (edema). The latter is a more aggressive variant that has been seen more frequently in Australia. These variants can develop into severe, extensive ulcers and are commonly misdiagnosed as cellulitis. Cellulitis may look like edema caused by M. ulcerans infection, but in the case of cellulitis, the lesions are usually painful, and the patient is ill and febrile. Remember that the initial edema caused by M. ulcerans usually is without pain, and the patients are initially in good condition. Also, remember that tropical phagedenic ulcers often start with a painful nodule or pustule as opposed to the usually painless nodules at the start of M ulcerans infections. Therefore, asking the patient in detail how the ulceration started and whether it was very painful at the onset can give us essential clues to the diagnosis.
Figure 3 The WHO publication " Treatment of Mycobacterium ulcerans disease- Guidance for healthcare workers" is an excellent resource. It also includes highly educational images of different stages of Buruli ulcer presentations. We want to thank the WHO for generously allowing us to reprint these images on WoundsAfrica. We strongly recommend you download this publication and share this with your colleagues. You can click on the image above to get to this publication.
The two images on the left show the early pustule phase of the Buruli ulcer. The two images on the left show what we refer to as plaques.
All images copyright WHO: https://apps.who.int/iris/bitstream/handle/10665/77771/9789241503402_eng.pdf
Figure 4 These four images show the oedematous presentations of M ulcerans disease. Understandably, these types of oedemas may be confused with other infections. In areas where Buruli ulcer is endemic, you must always have a high suspicion rate as to the diagnosis. Remember also that most other causes of infection and edema are usually accompanied by quite a lot of pain. In the case of edema due to M ulcerans, this is more often associated with minor pain.
All images copyright WHO: https://apps.who.int/iris/bitstream/handle/10665/77771/9789241503402_eng.pdf
Figure 5 These four images show that the oedematous form of M ulcerans infections can present as swellings in the facial area. Again, this may easily be mistaken for other types of infection.
All images copyright WHO: https://apps.who.int/iris/bitstream/handle/10665/77771/9789241503402_eng.pdf
Clinical findings – the ulcerative stage
Without treatment, the pre-ulcerative phase goes into the ulcerative stage within days to weeks (usually 4-8 weeks). The skin covering the plaque or nodule slowly sloughs, leaving an extensive necrotic ulcer with undermined edges. These undermined edges are quite characteristic of Buruli ulcers and help with the diagnosis. Tropical phagedenic ulcers, in comparison, usually have little or no undermined edges. Subcutaneous necrosis may extend several centimeters beyond the edge of the ulcer; therefore, the lesion appears smaller than its actual size. The ulcers may appear yellow or green and have a characteristic smell. Pain and local lymphadenopathy suggest secondary infection.
Be aware that M ulcerans can spread through the lymph vessels and metastasize to other body areas. Osteitis and osteomyelitis are much more common in Buruli ulcers than in, for example, tropical phagedenic ulcers. It is thought that about 30% of patients have bone- or joint involvement, which can lead to crippling complications. Did you know that nearly 1/4 of patients with M ulcerans osteomyelitis did not have a history of a skin ulcer? Keep this in mind when you have a patient with bone- or joint pain - it may well be an M ulcerans infection, although the patient never had a skin ulceration.
Figure 6 These four images show smaller ulcerations of M ulcerans at various stages.
Figure 7 These four images show more extensive ulcerations of M ulcerans on different body areas. As the upper right image shows, ulcerations can also appear in the face area.
Rapid diagnosis and treatment are necessary when suspecting Buruli ulcers. However, the majority of these ulcers occur in remote rural areas where fast and accurate testing is unfortunately not available. If you are lucky, a laboratory assistant may be available at an off-grid clinic trained in identifying acid-fast bacilli under the microscope! We will discuss diagnosis by microscopy and other methods shortly.
Experienced health professionals in endemic areas may be able to make a reasonably reliable clinical diagnosis by inspecting the ulcer alone, but training is essential. The images of clinical findings provided by the WHO in their excellent publication " Treatment of M ulcerans disease- Guidance to healthcare workers" are an excellent aid to recognizing the disease.
Four standard laboratory methods can be used to confirm Buruli ulcers: polymerase chain reaction (PCR), direct microscopy, histopathology, and culture. Obviously, PCR is the most accurate way to detect M ulcerans and the method that is least available to most patients in Africa. A good laboratory technician who is trained at spotting acid-fast bacilli under the microscope will also be able to make an accurate diagnosis, as long as the swabs contain enough bacteria. Culturing M ulcerans is difficult, and since it is very slow-growing, this process may take up to 12 weeks!
It is generally recommended that for both PCR and direct microscopy, swabs should be collected by circling the entire undermined edge of ulcerative lesions to maximize cell collection as MU is not uniformly distributed in the ulcers. A good sample collection can be achieved by collecting at least two swabs per lesion.
Swabs are not appropriate specimens for nonulcerative or pre-ulcerative lesions (oedematous, plaques, or nodules), as they often produce false-negative results. Instead, fine-needle aspiration (FNA) size18 or punch, incisional or excisional biopsy is required to obtain tissue fluid or fresh tissue. FNA should be collected from the weakest part of the lesion to increase the chance of collecting M ulcerans cells.
Tissue samples from ulcerative lesions should be taken from the edge of the lesion, preferably below the end of the undermined edge, and should contain necrotic tissue. For nonulcerative lesions, tissue samples should be collected from the center of the lesion. Tissue samples must always contain subcutaneous adipose tissue.
So, in conclusion: if you are working in an area where no laboratory assistance is available, you may have to make the diagnosis based on clinical appearance and the patient's history alone. However, in many parts of rural Africa, there are laboratory technicians, even at remote dispensaries, who are trained to detect acid- fast-bacilli. You should at least try to get direct microscopy done. If you are working closer to urban settings, a PCR analysis or histopathological laboratory may be available to aid you with the diagnosis.
In 2019, WHO established the Buruli ulcer Laboratory Network for Africa to help strengthen PCR confirmation in 9 endemic countries in Africa. 13 laboratories participate in this network - supported by the American Leprosy Missions, Anesvad, Raoul Follereau Foundation, and the Foundation for Innovative Diagnostic and coordinated by the Pasteur Center of Cameroon. Also, due to the Covid-19 epidemic, the number of PCR machines in Africa has increased manifold, although most are located in the private health sector.
Figure 8 Even in pretty remote areas in Africa, you may find a laboratory technician working at an off-the-grid clinic who can perform a Ziehl- Nielsen stain to reveal acid-fast bacilli under direct microscopy. In the absence of readily- available PCR machines, direct microscopy is usually your best chance of diagnosing M ulcerans. Take several swabs of the ulcer as described above. If the direct microscopy does not show acid-fast bacilli, do a new swab before deciding on another diagnosis—left image copyright: Vic Josh, Shutterstock.
Previously- up to about 2005 - surgical revision was the primary treatment principle for treating Buruli ulcers, accompanied by antibiotic treatment. Today, antibiotic treatment is considered the primary treatment choice, whereas surgical debridement has a more secondary role. Surgical debridement still has an important function here, but it is no longer routinely done on all lesions.
The WHO publication "Treatment of mycobacterium ulcerans disease (Buruli ulcer)- Guidance for health workers" is an excellent and comprehensive resource. Ensure you subscribe to the WHO newsletters to be informed when these guidelines are updated.
Figure 9 The WHO publication Treatment of mycobacterium ulcerans disease (Buruli ulcer) is a comprehensive treatment guide. It also has an excellent collection of images to aid in the diagnosis of the condition, printable requests for laboratory tests, and follow-up forms after antibiotic treatment. Click the image above to get to the link. All images copyright WHO: https://apps.who.int/iris/bitstream/handle/10665/77771/9789241503402_eng.pdf
In our chapter here, we will give you a brief overview of the current treatment principles
Today, it is well established that when patients with Buruli ulcers are treated with antibiotic regimes as recommended, most lesions heal without requiring surgery and with low recurrence rates. Oedematous lesions, the most aggressive form of the disease, have also responded to antibiotic treatment.
In the last 15 years, the first-line antibiotic treatment in many regions has been combined with Rifampicin and streptomycin. The standard dosage recommendations are Rifampicin at 10 mg/kg body weight by mouth daily for eight weeks and streptomycin at 15 mg/kg body weight by intramuscular injection daily for eight weeks. The fact that streptomycin has to be administered as an injection over such a long time has obviously been a challenge. It challenges the logistics of the treatment – not all patients live close to a clinic where the injections can be given daily, which may lead to compliance issues because of socio-economic factors. Another disadvantage is that streptomycin is contraindicated during pregnancy.
A recent study suggests the combination of rifampicin (10 mg/kg once daily) and clarithromycin (7.5 mg/kg twice daily) - it appears that this is now the recommended treatment. Both antibiotics are administered together over a period of 8 weeks. One significant advantage is that both these antibiotics are given orally, making the treatment logistics a lot easier. Furthermore, clarithromycin can be given to pregnant women.
A combination of rifampicin (10 mg/kg once daily) and moxifloxacin (400 mg once daily) is routinely used with good results in Australia, but its effectiveness has not been proven.
Telacebec is a new anti-tuberculous drug developed by a Korean company Qurient. The drug has demonstrated extreme potent activity against Mycobacterium ulcerans in animal studies, reducing treatment duration from 8 to 2 weeks. In January 2021, the US Food and Drug Administration granted orphan drug designation (ODD) to Telacebec as Buruli ulcer treatment. A clinical trial is being planned to evaluate the drug in patients.
Until about 2004, wide surgical excision of infected tissue was deemed necessary to achieve microbiological cure in Buruli ulcers. Today, however, surgical debridement is no longer seen as a first-line treatment for Buruli ulcer disease. Antibiotics have shown to be fully effective in eradicating the mycobacteria without surgery in most cases. Today surgery has a more complimentary role, and we use a much more conservative surgical approach than previously.
If there is abundant necrosis, debridement of the wound bed will most likely speed up the healing process. When it comes to surgical debridement technique in Buruli ulcers, we generally apply the same principles as wounds of other etiologies. We have written a separate chapter on the debridement of wounds – please also refer to that. In that chapter, we also discuss alternative methods for debriding chronic wounds like using medicinal maggots, for example. While we have extensive experience using medicinal maggots for debridement in other ulcers, we do not have any hands-on experience in using this method in Buruli ulcers, and we have not found any documentation on this either. However, we would expect that medicinal maggots could be a useful method in debriding Buruli ulcers.
As with all debridement – it is not always feasible to debride the wound entirely in one sitting. While the primary lesions of Buruli ulcers usually are pain-free, the ulcerative stages are typically accompanied by quite a lot of pain, and debridement is often experienced as highly uncomfortable by the patient. Therefore it is usually necessary to do a staged debridement over several sessions. If you have local anesthesia available, you may apply this topically onto the wound bed ( drip it into the wound, not inject) and let it work for about 10-15 minutes before debriding gently.
When we debride in a hospital setting with the help of general or regional anesthesia, we usually do a more aggressive debridement since it can be done entirely pain-free.
In extensive ulcers, it is still advisable to consider split-thickness skin grafting to shorten the healing time considerably. This can first be done when the wound bed is clean and sufficiently granulated. As a rule of thumb, many advise that this should be done at the earliest, four weeks after the antibiotic treatment regime has started. This is probably a sensible approach. At four weeks into the antibiotic treatment, the activity of M ulcerans is probably negligible, and further deterioration of the ulcer is unlikely. The other reason for waiting for several weeks is the rare paradoxical reaction, which sometimes occurs a few weeks after starting antibiotic treatment. This refers to the phenomenon that, for unknown reasons, the ulcer suddenly deteriorates even though the antibiotic treatment has been going on for a few weeks.
Wound care principles for Buruli ulcers
There are very few guidelines on best wound care practices for BU, and the current guidance is based on expert advice. Basic principles involve maintaining a moist wound environment. Again, we have to be realistic regarding what types of dressings are available in areas with minimal resources. Therefore, a lot of our advice is aimed at healthcare workers who only have a minimal choice of dressings available and may have to improvise a lot.
In general, we treat these ulcers like many other chronic ulcers. Indeed our recommendations here are the same as in the chapter on tropical phagedenic ulcers. Remember, though, that M ulcerans, although also present on the surface of the wound bed, hides in deeper tissues. Topical antibacterial solutions or even topical antibiotics cannot eradicate the bacteria. The only cure is by prescribing systemic antibiotics. However, topical antibacterial solutions and dressings may prevent and treat some secondary bacterial infections.
If there are only moderate amounts of necrotic tissue, you may choose more conservative methods of debridement- processes that aid the autolytic debridement process. Covering the wound bed in honey and using moistened gauze dressings can be helpful here. We have also used granulated sugar to debride leg ulcerations in both the acute and chronic phases. Fill the entire ulcer cavity with white granulated sugar. This works best if applied daily, as the wound exudate quickly dissolves the sugar. It is essential to have a good absorbent dressing over this, as sugar draws fluid from the wound bed and causes an increase in exudate, at least in the initial phase of the treatment. The patient must be informed that both honey and sugar can attract ants, especially during the night. Another method of debridement is using papaya directly applied to the wound bed. Again, please refer to our chapter on debridement for more information about this and other methods.
If there is an abundance of necrotic tissue, this will not only delay the healing of the wound but can encourage secondary infection by other bacterial strains. A careful surgical debridement of the wound may not only reduce the healing time but also reduce the pain in the ulcer and reduce the length of the antibiotic treatment.
In ulcers with extensive necrosis and infection, a thorough debridement under sedation or even general anesthesia may have to be done, if that is available. We have written a separate chapter on debridement and refer to this. We also believe that debridement by medicinal maggots is a suitable method here ( although we do not have any hands-on experience with this in Buruli ulcer treatment yet) - we also refer to the chapter about medicinal maggots.
We generally like to use antibacterial rinse solutions to irrigate the ulcers at dressing changes to prevent secondary infections. It is generally recommended to let these substances soak into the wound for about 15-20 minutes. We usually saturate a cotton gauze pad with this ( dripping wet) and lay this into the ulcer bed. Depending on what you have available, you can use a 2% vinegar solution for this, super-oxidized water, or 3% hydrogen peroxide. Remember that you can make the vinegar rinsing solution yourself. After this rinse, we like to paint the entire wound bed with gentian violet - this normally penetrates a few millimeters into the wound's surface, and we believe it may lead to quicker eradication of bacteria. We only use the gentian violet during the first two or three dressing changes as it is unknown how beneficial ( or harmful) this substance is to healthy tissues.
It appears that filling the wound bed with activated charcoal, especially during the initial phases, may delay further bacterial growth and probably aids in neutralizing bacterial toxins, which cause tissue destruction. You will find more about the charcoal method under " Antibacterial dressings."
Once the ulcer has " stabilized" and is not growing anymore, we can go over to more regular dressing choices. If you have few resources, cotton gauze dressings can be used. If the wound has little exudate, you can premoisten the gauze with, for example, the 2% vinegar solution ( they should only be slightly moist, not dripping wet!). You can apply a thin layer of zinc paste mixed with petrolatum jelly ( 50:50 ratio) over the entire wound bed to prevent the gauze from sticking to the wound bed, making removal painful during dressing changes.
If you have access to more modern dressings, then most polyurethane foam dressings would be appropriate here, especially those with antibiotic properties like silver coatings or those containing iodine. Another excellent, modern dressing for this purpose is Sorbact gauze. Once the ulcer bed is clean from necrotic tissue and shows promising granulation tissue, negative pressure wound therapy (NPWT) can probably be safely utilized to speed up the formulation of granulation tissue. Although there are case reports about the successful use of NPWT in M ulcerans ulcerations, we have little knowledge about that subject matter. We strongly advise you not to start with NPWT in Buruli ulcers until the antibiotic treatment has been going on for at least four weeks. If available, NPWT with irrigation would be the preferred method, in our opinion, utilizing an antibacterial solution as the irrigation fluid. You should have some experience using NPWT before using this method in patients with Buruli ulcers.
Once the wound bed is covered in good granulation tissue, partial thickness skin grafting can be done to shorten the healing time and possibly lead to a better cosmetic result. Again, we recommend you to wait with skin grafting until at least four weeks of antibiotic treatment have been given. Remember that there are also simpler techniques for transferring epidermal cells like the " blister technique" and punch-grafting methods. Please refer to the chapter on skin grafting for more information about these methods. In most rural areas, however, these techniques are not available, and Buruli ulcers are left to heal by the natural process with the aid of antibiotics and good general wound care.
Remember, as always in wound care: nutrition plays a decisive role. Especially protein supplementation and vitamin supplements ( Vitamin C!) are advised.
If you have the resources and facilities, it is wise to get the patient hospitalized for the initial part of the treatment ( about seven days). In this way, we can better control what is going on in the wound, do careful serial debridements (which are less painful), and frequent dressing changes. Furthermore, we can use those days to supply the patients with extra proteins and vitamins. During that time, the patient should also be taught how to change the dressing by themself or teach a caregiver. We are, of course, aware that many rural hospitals do not have the resources to take in all patients with ulcerations, or even more commonly, that the nearest hospital is a day's travel away. In most cases in rural areas, patients will therefore need to be treated as out-patients.
In summary, there are a number of treatment modalities you can apply here. It really depends on what you have available and your own personal preferences. At the start of the treatment, it will be wise to do frequent dressing changes and gradually decrease the frequency as the wound improves. In most situations in rural areas, you cannot expect the patient to return for a new visit the next day, and we advise you to use the time to inform the patient/caretakers thoroughly and teach them how to do the dressing changes themselves. To summarize the treatment options, we have listed them here:
2% vinegar, Super-oxidized water or 3% hydrogen peroxide
Gentiana violet 1-2% solution applied to the entire wound bed at least during the first two dressing changes ( at least during the first treatment at your clinic)
Primary Wound dressings if resources are limited:
Honey ( applied daily until necrosis has cleared, then longer intervals)
White granulated sugar ( applied daily until necrosis has cleared, then longer intervals)
Activated carbon powder: fill the entire wound cavity with this powder. If the wound is drier, it can also be mixed with honey at a 50:50 ratio.
Cotton gauze dressings. If the wound has much exudate, place the cotton gauze in dry. If the ulcer is drier, pre-moisten the gauze slightly with saline or, for example, 2% vinegar. You can use a 50:50 mixture of zinc paste and petrolatum jelly as a barrier layer over the entire wound surface to prevent the gauze from sticking to the wound bed. We recommend frequent dressing changes when using the gauze method.
Secondary wound dressings if resources are limited:
ladies hygiene pads
Primary wound dressings, if all resources are available
Silver coated polyurethane dressings
Iodine containing polyurethane dressings
Other treatment modalities (advanced):
Negative pressure wound therapy (NPWT) once the wound is clean and shows early granulation. Note: we do not recommend the start of NPWT before four weeks of antibiotic treatment have been given. We do not have any documentation about how M ulcerans thrive under the partially anaerobic environment of the NPWT treated wound. NPWT with irrigation is preferred here, in our opinion.
Platelet-rich plasma (PRP) may be useful if there is exposed bone or tendon.
Partial-thickness skin transplant, ultra-thin transfer of epidermal cells ( blister technique) or pinch/punch grafting. Again, wait at least 4 weeks into the antibiotic treatment before attempting a skin graft.
Figure 10 We are impressed with the logistics of this wound care center on the Ivory Coast, where multiple patients at the same time can be treated with irrigation of their leg ulcers. The design of the washbasins is well carried out and may be an inspiration for others starting a wound clinic in Africa. Image copyrightWikipediaia commons: Yotsu RR "Integrated Management of Skin NTDs—Lessons Learned from Existing Practice and Field Research." Tropical Medicine and Infectious Disease DOI:10.3390/tropicalmed3040120. PMID 30441754. ISSN 2414-6366.
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