Article Type
Article
Changed
Fri, 09/06/2024 - 09:52
Display Headline
Multiple Draining Sinus Tracts on the Thigh
Author(s)
Toan S. Bui, BS
Dirk M. Elston, MD

The Diagnosis: Mycobacterial Infection

An injury sustained in a wet environment that results in chronic indolent abscesses, nodules, or draining sinus tracts suggests a mycobacterial infection. In our patient, a culture revealed MycobacteriuM fortuitum, which is classified in the rapid grower nontuberculous mycobacteria (NTM) group, along with Mycobacterium chelonae and Mycobacterium abscessus.1 The patient’s history of skin injury while cutting wet grass and the common presence of M fortuitum in the environment suggested that the organism entered the wound. The patient healed completely following surgical excision and a 2-month course of clarithromycin 1 g daily and rifampin 600 mg daily.

MycobacteriuM fortuitum was first isolated from an amphibian source in 1905 and later identified in a human with cutaneous infection in 1938. It commonly is found in soil and water.2 Skin and soft-tissue infections with M fortuitum usually are acquired from direct entry of the organism through a damaged skin barrier from trauma, medical injection, surgery, or tattoo placement.2,3

Skin lesions caused by NTM often are nonspecific and can mimic a variety of other dermatologic conditions, making clinical diagnosis challenging. As such, cutaneous manifestations of M fortuitum infection can include recurrent cutaneous abscesses, nodular lesions, chronic discharging sinuses, cellulitis, and surgical site infections.4 Although cutaneous infection with M fortuitum classically manifests with a single subcutaneous nodule at the site of trauma or surgery,5 it also can manifest as multiple draining sinus tracts, as seen in our patient. Hence, the diagnosis and treatment of cutaneous NTM infection is challenging, especially when M fortuitum skin manifestations can take up to 4 to 6 weeks to develop after inoculation. Diagnosis often requires a detailed patient history, tissue cultures, and histopathology.5

In recent years, rapid detection with polymerase chain reaction (PCR) techniques has been employed more widely. Notably, a molecular system based on multiplex real-time PCR with high-resolution melting was shown to have a sensitivity of up to 54% for distinguishing M fortuitum from other NTM.6 More recently, a 2-step real-time PCR method has demonstrated diagnostic sensitivity and specificity for differentiating NTM from Mycobacterium tuberculosis infections and identifying the causative NTM agent.7

Compared to immunocompetent individuals, those who are immunocompromised are more susceptible to less pathogenic strains of NTM, which can cause dissemination and lead to tenosynovitis, myositis, osteomyelitis, and septic arthritis.8-12 Nonetheless, cases of infections with NTM—including M fortuitum—are becoming harder to treat. Several single nucleotide polymorphisms and point mutations have been demonstrated in the ribosomal RNA methylase gene erm(39) related to clarithromycin resistance and in the rrl gene related to linezolid resistance.13 Due to increasing inducible resistance to common classes of antibiotics, such as macrolides and linezolid, treatment of M fortuitum requires multidrug regimens.13,14 Drug susceptibility testing also may be required, as M fortuitum has shown low resistance to tigecycline, tetracycline, cefmetazole, imipenem, and aminoglycosides (eg, amikacin, tobramycin, neomycin, gentamycin). Surgery is an important adjunctive tool in treating M fortuitum infections; patients with a single lesion are more likely to undergo surgical treatment alone or in combination with antibiotic therapy.15 More recently, antimicrobial photodynamic therapy has been explored as an alternative to eliminate NTM, including M fortuitum.16

The differential diagnosis for skin lesions manifesting with draining fistulae and sinus tracts includes conditions with infectious (cellulitis and chromomycosis) and inflammatory (pyoderma gangrenosum [PG] and hidradenitis suppurativa [HS]) causes.

Cellulitis is a common infection of the skin and subcutaneous tissue that predominantly is caused by gram-positive organisms such as β-hemolytic streptococci.17 Clinical manifestations include acute skin erythema, swelling, tenderness, and warmth. The legs are the most common sites of infection, but any area of the skin can be involved.17 Cellulitis comprises 10% of all infectious disease hospitalizations and up to 11% of all dermatologic admissions.18,19 It frequently is misdiagnosed, perhaps due to the lack of a reliable confirmatory laboratory test or imaging study, in addition to the plethora of diseases that mimic cellulitis, such as stasis dermatitis, lipodermatosclerosis, contact dermatitis, lymphedema, eosinophilic cellulitis, and papular urticaria.20,21 The consequences of misdiagnosis include but are not limited to unnecessary hospitalizations, inappropriate antibiotic use, and delayed management of the disease; thus, there is an urgent need for a reliable standard test to confirm the diagnosis, especially among nonspecialist physicians. 20 Most patients with uncomplicated cellulitis can be treated with empiric oral antibiotics that target β-hemolytic streptococci (ie, penicillin V potassium, amoxicillin).17 Methicillin-resistant Staphylococcus aureus coverage generally is unnecessary for nonpurulent cellulitis, but clinicians can consider adding amoxicillin-clavulanate, dicloxacillin, and cephalexin to the regimen. For purulent cellulitis, incision and drainage should be performed. In severe cases that manifest with sepsis, altered mental status, or hemodynamic instability, inpatient management is required.17

Chromomycosis (also known as chromoblastomycosis) is a chronic, indolent, granulomatous, suppurative mycosis of the skin and subcutaneous tissue22 that is caused by traumatic inoculation of various fungi of the order Chaetothyriales and family Herpotrichiellaceae, which are present in soil, plants, and decomposing wood. Chromomycosis is prevalent in tropical and subtropical regions.23,24 Clinically, it manifests as oligosymptomatic or asymptomatic lesions around an infection site that can manifest as papules with centrifugal growth evolving into nodular, verrucous, plaque, tumoral, or atrophic forms.22 Diagnosis is made with direct microscopy using potassium hydroxide, which reveals muriform bodies. Fungal culture in Sabouraud agar also can be used to isolate the causative pathogen.22 Unfortunately, chromomycosis is difficult to treat, with low cure rates and high relapse rates. Antifungal agents combined with surgery, cryotherapy, or thermotherapy often are used, with cure rates ranging from 15% to 80%.22,25

Pyoderma gangrenosum is a reactive noninfectious inflammatory dermatosis associated with inflammatory bowel disease and rheumatoid arthritis. The exact etiology is not clearly understood, but it generally is considered an autoinflammatory disorder.26 The most common form—classical PG—occurs in approximately 85% of cases and manifests as a painful erythematous lesion that progresses to a blistered or necrotic ulcer. It primarily affects the lower legs but can occur in other body sites.27 The diagnosis is based on clinical symptoms after excluding other similar conditions; histopathology of biopsied wound tissues often are required for confirmation. Treatment of PG starts with fast-acting immunosuppressive drugs (corticosteroids and/or cyclosporine) followed by slowacting immunosuppressive drugs (biologics).26

Hidradenitis suppurativa is a chronic recurrent disease of the hair follicle unit that develops after puberty.28 Clinically, HS manifests with painful nodules, abscesses, chronically draining fistulas, and scarring in areas of the body rich in apocrine glands.29,30 Treatment of HS is challenging due to its diverse clinical manifestations and unclear etiology. Topical therapy, systemic treatments, biologic agents, surgery, and light therapy have shown variable results.28,31

References
  1. Franco-Paredes C, Marcos LA, Henao-Martínez AF, et al. Cutaneous mycobacterial infections. Clin Microbiol Rev. 2018;32: E00069-18. doi:10.1128/CMR.00069-18
  2. Brown TH. The rapidly growing mycobacteria—MycobacteriuM fortuitum and Mycobacterium chelonae. Infect Control. 1985;6:283-238. doi:10.1017/s0195941700061762
  3. Hooper J; Beltrami EJ; Santoro F; et al. Remember the fite: a case of cutaneous MycobacteriuM fortuitum infection. Am J Dermatopathol. 2023;45:214-215. doi:10.1097/DAD.0000000000002336
  4. Franco-Paredes C, Chastain DB, Allen L, et al. Overview of cutaneous mycobacterial infections. Curr Trop Med Rep. 2018;5:228-232. doi:10.1007/s40475-018-0161-7
  5. Gonzalez-Santiago TM, Drage LA. Nontuberculous mycobacteria: skin and soft tissue infections. Dermatol Clin. 2015;33:563-77. doi:10.1016/j.det.2015.03.017
  6. Peixoto ADS, Montenegro LML, Lima AS, et al. Identification of nontuberculous mycobacteria species by multiplex real-time PCR with high-resolution melting. Rev Soc Bras Med Trop. 2020;53:E20200211. doi:10.1590/0037-8682-0211-2020
  7. Park J, Kwak N, Chae JC, et al. A two-step real-time PCR method to identify Mycobacterium tuberculosis infections and six dominant nontuberculous mycobacterial infections from clinical specimens. Microbiol Spectr. 2023:E0160623. doi:10.1128/spectrum.01606-23
  8. Fowler J, Mahlen SD. Localized cutaneous infections in immunocompetent individuals due to rapidly growing mycobacteria. Arch Pathol Lab Med. 2014;138:1106-1109. doi:10.5858/arpa.2012-0203-RS
  9. Gardini G, Gregori N, Matteelli A, et al. Mycobacterial skin infection. Curr Opin Infect Dis. 2022;35:79-87. doi:10.1097/QCO.0000000000000820
  10. Wang SH, Pancholi P. Mycobacterial skin and soft tissue infection. Curr Infect Dis Rep. 2014;16:438. doi:10.1007/s11908-014-0438-5
  11. Griffith DE, Aksamit T, Brown-Elliott BA, et al; ATS Mycobacterial Diseases Subcommittee; American Thoracic Society; Infectious Disease Society of America. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175:367-416. doi:10.1164/rccm.200604-571ST
  12. Mougari F, Guglielmetti L, Raskine L, et al. Infections caused by Mycobacterium abscessus: epidemiology, diagnostic tools and treatment. Expert Rev Anti Infect Ther. 2016;14:1139-1154. doi:10.1080/14787210.201 6.1238304
  13. Tu HZ, Lee HS, Chen YS, et al. High rates of antimicrobial resistance in rapidly growing mycobacterial infections in Taiwan. Pathogens. 2022;11:969. doi:10.3390/pathogens11090969
  14. Hashemzadeh M, Zadegan Dezfuli AA, Khosravi AD, et al. F requency of mutations in erm(39) related to clarithromycin resistance and in rrl related to linezolid resistance in clinical isolates of MycobacteriuM fortuitum in Iran. Acta Microbiol Immunol Hung. 2023;70:167-176. doi:10.1556/030.2023.02020
  15. Uslan DZ, Kowalski TJ, Wengenack NL, et al. Skin and soft tissue infections due to rapidly growing mycobacteria: comparison of clinical features, treatment, and susceptibility. Arch Dermatol. 2006;142:1287-1292. doi:10.1001/archderm.142.10.1287
  16. Miretti M, Juri L, Peralta A, et al. Photoinactivation of non-tuberculous mycobacteria using Zn-phthalocyanine loaded into liposomes. Tuberculosis (Edinb). 2022;136:102247. doi:10.1016/j.tube.2022.102247
  17. Bystritsky RJ. Cellulitis. Infect Dis Clin North Am. 2021;35:49-60. doi:10.1016/j.idc.2020.10.002
  18. Christensen K, Holman R, Steiner C, et al. Infectious disease hospitalizations in the United States. Clin Infect Dis. 2009;49:1025-1035. doi:10.1086/605562
  19. Yang JJ, Maloney NJ, Bach DQ, et al. Dermatology in the emergency department: prescriptions, rates of inpatient admission, and predictors of high utilization in the United States from 1996 to 2012. J Am Acad Dermatol. 2021;84:1480-1483. doi:10.1016/J.JAAD.2020.07.055
  20. Cutler TS, Jannat-Khah DP, Kam B, et al. Prevalence of misdiagnosis of cellulitis: a systematic review and meta-analysis. J Hosp Med. 2023;18:254-261. doi:10.1002/jhm.12977
  21. Keller EC, Tomecki KJ, Alraies MC. Distinguishing cellulitis from its mimics. Cleve Clin J Med. 2012;79:547-52. doi:10.3949/ccjm.79a.11121
  22. Brito AC, Bittencourt MJS. Chromoblastomycosis: an etiological, epidemiological, clinical, diagnostic, and treatment update. An Bras Dermatol. 2018;93:495-506. doi:10.1590/abd1806-4841.20187321
  23. McGinnis MR. Chromoblastomycosis and phaeohyphomycosis: new concepts, diagnosis, and mycology. J Am Acad Dermatol. 1983;8:1-16.
  24. Rubin HA, Bruce S, Rosen T, et al. Evidence for percutaneous inoculation as the mode of transmission for chromoblastomycosis. J Am Acad Dermatol. 1991;25:951-954.
  25. Bonifaz A, Paredes-Solís V, Saúl A. Treating chromoblastomycosis with systemic antifungals. Expert Opin Pharmacother. 2004;5:247-254.
  26. Maverakis E, Marzano AV, Le ST, et al. Pyoderma gangrenosum. Nat Rev Dis Primers. 2020;6:81. doi:10.1038/s41572-020-0213-x
  27. George C, Deroide F, Rustin M. Pyoderma gangrenosum—a guide to diagnosis and management. Clin Med (Lond). 2019;19:224-228. doi:10.7861/clinmedicine.19-3-224
  28. Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res. 2020;9:F1000 Faculty Rev-1049. doi:10.12688/f1000research.26083.1
  29. Garg A, Lavian J, Lin G, et al. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77:118-122. doi:10.1016/j.jaad.2017.02.005
  30. Daxhelet M, Suppa M, White J, et al. Proposed definitions of typical lesions in hidradenitis suppurativa. Dermatology. 2020;236:431-438. doi:10.1159/000507348
  31. Amat-Samaranch V, Agut-Busquet E, Vilarrasa E, et al. New perspectives on the treatment of hidradenitis suppurativa. Ther Adv Chronic Dis. 2021;12:20406223211055920. doi:10.1177/20406223211055920
Article PDF
ct114003071.pdf
Author and Disclosure Information

Toan S. Bui is from the University of Maryland School of Medicine, Baltimore. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Toan S. Bui, BS, 655 W Baltimore St S, Baltimore, MD 21201 ([email protected]).

Cutis. 2024 September;114(3):71, 77-78. doi:10.12788/cutis.1084

Issue
Cutis - 114(3)
Publications
MDedge Dermatology
Cutis
Topics
Infectious Diseases
Page Number
71,77-78
Sections
Photo Challenge
Author(s)
Toan S. Bui, BS
Dirk M. Elston, MD
Author(s)
Toan S. Bui, BS
Dirk M. Elston, MD
Author and Disclosure Information

Toan S. Bui is from the University of Maryland School of Medicine, Baltimore. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Toan S. Bui, BS, 655 W Baltimore St S, Baltimore, MD 21201 ([email protected]).

Cutis. 2024 September;114(3):71, 77-78. doi:10.12788/cutis.1084

Author and Disclosure Information

Toan S. Bui is from the University of Maryland School of Medicine, Baltimore. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Toan S. Bui, BS, 655 W Baltimore St S, Baltimore, MD 21201 ([email protected]).

Cutis. 2024 September;114(3):71, 77-78. doi:10.12788/cutis.1084

Article PDF
ct114003071.pdf
Article PDF
ct114003071.pdf
Related Articles
Necrotic Papules in a Pediatric Patient
Scarring Head Wound

The Diagnosis: Mycobacterial Infection

An injury sustained in a wet environment that results in chronic indolent abscesses, nodules, or draining sinus tracts suggests a mycobacterial infection. In our patient, a culture revealed MycobacteriuM fortuitum, which is classified in the rapid grower nontuberculous mycobacteria (NTM) group, along with Mycobacterium chelonae and Mycobacterium abscessus.1 The patient’s history of skin injury while cutting wet grass and the common presence of M fortuitum in the environment suggested that the organism entered the wound. The patient healed completely following surgical excision and a 2-month course of clarithromycin 1 g daily and rifampin 600 mg daily.

MycobacteriuM fortuitum was first isolated from an amphibian source in 1905 and later identified in a human with cutaneous infection in 1938. It commonly is found in soil and water.2 Skin and soft-tissue infections with M fortuitum usually are acquired from direct entry of the organism through a damaged skin barrier from trauma, medical injection, surgery, or tattoo placement.2,3

Skin lesions caused by NTM often are nonspecific and can mimic a variety of other dermatologic conditions, making clinical diagnosis challenging. As such, cutaneous manifestations of M fortuitum infection can include recurrent cutaneous abscesses, nodular lesions, chronic discharging sinuses, cellulitis, and surgical site infections.4 Although cutaneous infection with M fortuitum classically manifests with a single subcutaneous nodule at the site of trauma or surgery,5 it also can manifest as multiple draining sinus tracts, as seen in our patient. Hence, the diagnosis and treatment of cutaneous NTM infection is challenging, especially when M fortuitum skin manifestations can take up to 4 to 6 weeks to develop after inoculation. Diagnosis often requires a detailed patient history, tissue cultures, and histopathology.5

In recent years, rapid detection with polymerase chain reaction (PCR) techniques has been employed more widely. Notably, a molecular system based on multiplex real-time PCR with high-resolution melting was shown to have a sensitivity of up to 54% for distinguishing M fortuitum from other NTM.6 More recently, a 2-step real-time PCR method has demonstrated diagnostic sensitivity and specificity for differentiating NTM from Mycobacterium tuberculosis infections and identifying the causative NTM agent.7

Compared to immunocompetent individuals, those who are immunocompromised are more susceptible to less pathogenic strains of NTM, which can cause dissemination and lead to tenosynovitis, myositis, osteomyelitis, and septic arthritis.8-12 Nonetheless, cases of infections with NTM—including M fortuitum—are becoming harder to treat. Several single nucleotide polymorphisms and point mutations have been demonstrated in the ribosomal RNA methylase gene erm(39) related to clarithromycin resistance and in the rrl gene related to linezolid resistance.13 Due to increasing inducible resistance to common classes of antibiotics, such as macrolides and linezolid, treatment of M fortuitum requires multidrug regimens.13,14 Drug susceptibility testing also may be required, as M fortuitum has shown low resistance to tigecycline, tetracycline, cefmetazole, imipenem, and aminoglycosides (eg, amikacin, tobramycin, neomycin, gentamycin). Surgery is an important adjunctive tool in treating M fortuitum infections; patients with a single lesion are more likely to undergo surgical treatment alone or in combination with antibiotic therapy.15 More recently, antimicrobial photodynamic therapy has been explored as an alternative to eliminate NTM, including M fortuitum.16

The differential diagnosis for skin lesions manifesting with draining fistulae and sinus tracts includes conditions with infectious (cellulitis and chromomycosis) and inflammatory (pyoderma gangrenosum [PG] and hidradenitis suppurativa [HS]) causes.

Cellulitis is a common infection of the skin and subcutaneous tissue that predominantly is caused by gram-positive organisms such as β-hemolytic streptococci.17 Clinical manifestations include acute skin erythema, swelling, tenderness, and warmth. The legs are the most common sites of infection, but any area of the skin can be involved.17 Cellulitis comprises 10% of all infectious disease hospitalizations and up to 11% of all dermatologic admissions.18,19 It frequently is misdiagnosed, perhaps due to the lack of a reliable confirmatory laboratory test or imaging study, in addition to the plethora of diseases that mimic cellulitis, such as stasis dermatitis, lipodermatosclerosis, contact dermatitis, lymphedema, eosinophilic cellulitis, and papular urticaria.20,21 The consequences of misdiagnosis include but are not limited to unnecessary hospitalizations, inappropriate antibiotic use, and delayed management of the disease; thus, there is an urgent need for a reliable standard test to confirm the diagnosis, especially among nonspecialist physicians. 20 Most patients with uncomplicated cellulitis can be treated with empiric oral antibiotics that target β-hemolytic streptococci (ie, penicillin V potassium, amoxicillin).17 Methicillin-resistant Staphylococcus aureus coverage generally is unnecessary for nonpurulent cellulitis, but clinicians can consider adding amoxicillin-clavulanate, dicloxacillin, and cephalexin to the regimen. For purulent cellulitis, incision and drainage should be performed. In severe cases that manifest with sepsis, altered mental status, or hemodynamic instability, inpatient management is required.17

Chromomycosis (also known as chromoblastomycosis) is a chronic, indolent, granulomatous, suppurative mycosis of the skin and subcutaneous tissue22 that is caused by traumatic inoculation of various fungi of the order Chaetothyriales and family Herpotrichiellaceae, which are present in soil, plants, and decomposing wood. Chromomycosis is prevalent in tropical and subtropical regions.23,24 Clinically, it manifests as oligosymptomatic or asymptomatic lesions around an infection site that can manifest as papules with centrifugal growth evolving into nodular, verrucous, plaque, tumoral, or atrophic forms.22 Diagnosis is made with direct microscopy using potassium hydroxide, which reveals muriform bodies. Fungal culture in Sabouraud agar also can be used to isolate the causative pathogen.22 Unfortunately, chromomycosis is difficult to treat, with low cure rates and high relapse rates. Antifungal agents combined with surgery, cryotherapy, or thermotherapy often are used, with cure rates ranging from 15% to 80%.22,25

Pyoderma gangrenosum is a reactive noninfectious inflammatory dermatosis associated with inflammatory bowel disease and rheumatoid arthritis. The exact etiology is not clearly understood, but it generally is considered an autoinflammatory disorder.26 The most common form—classical PG—occurs in approximately 85% of cases and manifests as a painful erythematous lesion that progresses to a blistered or necrotic ulcer. It primarily affects the lower legs but can occur in other body sites.27 The diagnosis is based on clinical symptoms after excluding other similar conditions; histopathology of biopsied wound tissues often are required for confirmation. Treatment of PG starts with fast-acting immunosuppressive drugs (corticosteroids and/or cyclosporine) followed by slowacting immunosuppressive drugs (biologics).26

Hidradenitis suppurativa is a chronic recurrent disease of the hair follicle unit that develops after puberty.28 Clinically, HS manifests with painful nodules, abscesses, chronically draining fistulas, and scarring in areas of the body rich in apocrine glands.29,30 Treatment of HS is challenging due to its diverse clinical manifestations and unclear etiology. Topical therapy, systemic treatments, biologic agents, surgery, and light therapy have shown variable results.28,31

The Diagnosis: Mycobacterial Infection

An injury sustained in a wet environment that results in chronic indolent abscesses, nodules, or draining sinus tracts suggests a mycobacterial infection. In our patient, a culture revealed MycobacteriuM fortuitum, which is classified in the rapid grower nontuberculous mycobacteria (NTM) group, along with Mycobacterium chelonae and Mycobacterium abscessus.1 The patient’s history of skin injury while cutting wet grass and the common presence of M fortuitum in the environment suggested that the organism entered the wound. The patient healed completely following surgical excision and a 2-month course of clarithromycin 1 g daily and rifampin 600 mg daily.

MycobacteriuM fortuitum was first isolated from an amphibian source in 1905 and later identified in a human with cutaneous infection in 1938. It commonly is found in soil and water.2 Skin and soft-tissue infections with M fortuitum usually are acquired from direct entry of the organism through a damaged skin barrier from trauma, medical injection, surgery, or tattoo placement.2,3

Skin lesions caused by NTM often are nonspecific and can mimic a variety of other dermatologic conditions, making clinical diagnosis challenging. As such, cutaneous manifestations of M fortuitum infection can include recurrent cutaneous abscesses, nodular lesions, chronic discharging sinuses, cellulitis, and surgical site infections.4 Although cutaneous infection with M fortuitum classically manifests with a single subcutaneous nodule at the site of trauma or surgery,5 it also can manifest as multiple draining sinus tracts, as seen in our patient. Hence, the diagnosis and treatment of cutaneous NTM infection is challenging, especially when M fortuitum skin manifestations can take up to 4 to 6 weeks to develop after inoculation. Diagnosis often requires a detailed patient history, tissue cultures, and histopathology.5

In recent years, rapid detection with polymerase chain reaction (PCR) techniques has been employed more widely. Notably, a molecular system based on multiplex real-time PCR with high-resolution melting was shown to have a sensitivity of up to 54% for distinguishing M fortuitum from other NTM.6 More recently, a 2-step real-time PCR method has demonstrated diagnostic sensitivity and specificity for differentiating NTM from Mycobacterium tuberculosis infections and identifying the causative NTM agent.7

Compared to immunocompetent individuals, those who are immunocompromised are more susceptible to less pathogenic strains of NTM, which can cause dissemination and lead to tenosynovitis, myositis, osteomyelitis, and septic arthritis.8-12 Nonetheless, cases of infections with NTM—including M fortuitum—are becoming harder to treat. Several single nucleotide polymorphisms and point mutations have been demonstrated in the ribosomal RNA methylase gene erm(39) related to clarithromycin resistance and in the rrl gene related to linezolid resistance.13 Due to increasing inducible resistance to common classes of antibiotics, such as macrolides and linezolid, treatment of M fortuitum requires multidrug regimens.13,14 Drug susceptibility testing also may be required, as M fortuitum has shown low resistance to tigecycline, tetracycline, cefmetazole, imipenem, and aminoglycosides (eg, amikacin, tobramycin, neomycin, gentamycin). Surgery is an important adjunctive tool in treating M fortuitum infections; patients with a single lesion are more likely to undergo surgical treatment alone or in combination with antibiotic therapy.15 More recently, antimicrobial photodynamic therapy has been explored as an alternative to eliminate NTM, including M fortuitum.16

The differential diagnosis for skin lesions manifesting with draining fistulae and sinus tracts includes conditions with infectious (cellulitis and chromomycosis) and inflammatory (pyoderma gangrenosum [PG] and hidradenitis suppurativa [HS]) causes.

Cellulitis is a common infection of the skin and subcutaneous tissue that predominantly is caused by gram-positive organisms such as β-hemolytic streptococci.17 Clinical manifestations include acute skin erythema, swelling, tenderness, and warmth. The legs are the most common sites of infection, but any area of the skin can be involved.17 Cellulitis comprises 10% of all infectious disease hospitalizations and up to 11% of all dermatologic admissions.18,19 It frequently is misdiagnosed, perhaps due to the lack of a reliable confirmatory laboratory test or imaging study, in addition to the plethora of diseases that mimic cellulitis, such as stasis dermatitis, lipodermatosclerosis, contact dermatitis, lymphedema, eosinophilic cellulitis, and papular urticaria.20,21 The consequences of misdiagnosis include but are not limited to unnecessary hospitalizations, inappropriate antibiotic use, and delayed management of the disease; thus, there is an urgent need for a reliable standard test to confirm the diagnosis, especially among nonspecialist physicians. 20 Most patients with uncomplicated cellulitis can be treated with empiric oral antibiotics that target β-hemolytic streptococci (ie, penicillin V potassium, amoxicillin).17 Methicillin-resistant Staphylococcus aureus coverage generally is unnecessary for nonpurulent cellulitis, but clinicians can consider adding amoxicillin-clavulanate, dicloxacillin, and cephalexin to the regimen. For purulent cellulitis, incision and drainage should be performed. In severe cases that manifest with sepsis, altered mental status, or hemodynamic instability, inpatient management is required.17

Chromomycosis (also known as chromoblastomycosis) is a chronic, indolent, granulomatous, suppurative mycosis of the skin and subcutaneous tissue22 that is caused by traumatic inoculation of various fungi of the order Chaetothyriales and family Herpotrichiellaceae, which are present in soil, plants, and decomposing wood. Chromomycosis is prevalent in tropical and subtropical regions.23,24 Clinically, it manifests as oligosymptomatic or asymptomatic lesions around an infection site that can manifest as papules with centrifugal growth evolving into nodular, verrucous, plaque, tumoral, or atrophic forms.22 Diagnosis is made with direct microscopy using potassium hydroxide, which reveals muriform bodies. Fungal culture in Sabouraud agar also can be used to isolate the causative pathogen.22 Unfortunately, chromomycosis is difficult to treat, with low cure rates and high relapse rates. Antifungal agents combined with surgery, cryotherapy, or thermotherapy often are used, with cure rates ranging from 15% to 80%.22,25

Pyoderma gangrenosum is a reactive noninfectious inflammatory dermatosis associated with inflammatory bowel disease and rheumatoid arthritis. The exact etiology is not clearly understood, but it generally is considered an autoinflammatory disorder.26 The most common form—classical PG—occurs in approximately 85% of cases and manifests as a painful erythematous lesion that progresses to a blistered or necrotic ulcer. It primarily affects the lower legs but can occur in other body sites.27 The diagnosis is based on clinical symptoms after excluding other similar conditions; histopathology of biopsied wound tissues often are required for confirmation. Treatment of PG starts with fast-acting immunosuppressive drugs (corticosteroids and/or cyclosporine) followed by slowacting immunosuppressive drugs (biologics).26

Hidradenitis suppurativa is a chronic recurrent disease of the hair follicle unit that develops after puberty.28 Clinically, HS manifests with painful nodules, abscesses, chronically draining fistulas, and scarring in areas of the body rich in apocrine glands.29,30 Treatment of HS is challenging due to its diverse clinical manifestations and unclear etiology. Topical therapy, systemic treatments, biologic agents, surgery, and light therapy have shown variable results.28,31

References
  1. Franco-Paredes C, Marcos LA, Henao-Martínez AF, et al. Cutaneous mycobacterial infections. Clin Microbiol Rev. 2018;32: E00069-18. doi:10.1128/CMR.00069-18
  2. Brown TH. The rapidly growing mycobacteria—MycobacteriuM fortuitum and Mycobacterium chelonae. Infect Control. 1985;6:283-238. doi:10.1017/s0195941700061762
  3. Hooper J; Beltrami EJ; Santoro F; et al. Remember the fite: a case of cutaneous MycobacteriuM fortuitum infection. Am J Dermatopathol. 2023;45:214-215. doi:10.1097/DAD.0000000000002336
  4. Franco-Paredes C, Chastain DB, Allen L, et al. Overview of cutaneous mycobacterial infections. Curr Trop Med Rep. 2018;5:228-232. doi:10.1007/s40475-018-0161-7
  5. Gonzalez-Santiago TM, Drage LA. Nontuberculous mycobacteria: skin and soft tissue infections. Dermatol Clin. 2015;33:563-77. doi:10.1016/j.det.2015.03.017
  6. Peixoto ADS, Montenegro LML, Lima AS, et al. Identification of nontuberculous mycobacteria species by multiplex real-time PCR with high-resolution melting. Rev Soc Bras Med Trop. 2020;53:E20200211. doi:10.1590/0037-8682-0211-2020
  7. Park J, Kwak N, Chae JC, et al. A two-step real-time PCR method to identify Mycobacterium tuberculosis infections and six dominant nontuberculous mycobacterial infections from clinical specimens. Microbiol Spectr. 2023:E0160623. doi:10.1128/spectrum.01606-23
  8. Fowler J, Mahlen SD. Localized cutaneous infections in immunocompetent individuals due to rapidly growing mycobacteria. Arch Pathol Lab Med. 2014;138:1106-1109. doi:10.5858/arpa.2012-0203-RS
  9. Gardini G, Gregori N, Matteelli A, et al. Mycobacterial skin infection. Curr Opin Infect Dis. 2022;35:79-87. doi:10.1097/QCO.0000000000000820
  10. Wang SH, Pancholi P. Mycobacterial skin and soft tissue infection. Curr Infect Dis Rep. 2014;16:438. doi:10.1007/s11908-014-0438-5
  11. Griffith DE, Aksamit T, Brown-Elliott BA, et al; ATS Mycobacterial Diseases Subcommittee; American Thoracic Society; Infectious Disease Society of America. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175:367-416. doi:10.1164/rccm.200604-571ST
  12. Mougari F, Guglielmetti L, Raskine L, et al. Infections caused by Mycobacterium abscessus: epidemiology, diagnostic tools and treatment. Expert Rev Anti Infect Ther. 2016;14:1139-1154. doi:10.1080/14787210.201 6.1238304
  13. Tu HZ, Lee HS, Chen YS, et al. High rates of antimicrobial resistance in rapidly growing mycobacterial infections in Taiwan. Pathogens. 2022;11:969. doi:10.3390/pathogens11090969
  14. Hashemzadeh M, Zadegan Dezfuli AA, Khosravi AD, et al. F requency of mutations in erm(39) related to clarithromycin resistance and in rrl related to linezolid resistance in clinical isolates of MycobacteriuM fortuitum in Iran. Acta Microbiol Immunol Hung. 2023;70:167-176. doi:10.1556/030.2023.02020
  15. Uslan DZ, Kowalski TJ, Wengenack NL, et al. Skin and soft tissue infections due to rapidly growing mycobacteria: comparison of clinical features, treatment, and susceptibility. Arch Dermatol. 2006;142:1287-1292. doi:10.1001/archderm.142.10.1287
  16. Miretti M, Juri L, Peralta A, et al. Photoinactivation of non-tuberculous mycobacteria using Zn-phthalocyanine loaded into liposomes. Tuberculosis (Edinb). 2022;136:102247. doi:10.1016/j.tube.2022.102247
  17. Bystritsky RJ. Cellulitis. Infect Dis Clin North Am. 2021;35:49-60. doi:10.1016/j.idc.2020.10.002
  18. Christensen K, Holman R, Steiner C, et al. Infectious disease hospitalizations in the United States. Clin Infect Dis. 2009;49:1025-1035. doi:10.1086/605562
  19. Yang JJ, Maloney NJ, Bach DQ, et al. Dermatology in the emergency department: prescriptions, rates of inpatient admission, and predictors of high utilization in the United States from 1996 to 2012. J Am Acad Dermatol. 2021;84:1480-1483. doi:10.1016/J.JAAD.2020.07.055
  20. Cutler TS, Jannat-Khah DP, Kam B, et al. Prevalence of misdiagnosis of cellulitis: a systematic review and meta-analysis. J Hosp Med. 2023;18:254-261. doi:10.1002/jhm.12977
  21. Keller EC, Tomecki KJ, Alraies MC. Distinguishing cellulitis from its mimics. Cleve Clin J Med. 2012;79:547-52. doi:10.3949/ccjm.79a.11121
  22. Brito AC, Bittencourt MJS. Chromoblastomycosis: an etiological, epidemiological, clinical, diagnostic, and treatment update. An Bras Dermatol. 2018;93:495-506. doi:10.1590/abd1806-4841.20187321
  23. McGinnis MR. Chromoblastomycosis and phaeohyphomycosis: new concepts, diagnosis, and mycology. J Am Acad Dermatol. 1983;8:1-16.
  24. Rubin HA, Bruce S, Rosen T, et al. Evidence for percutaneous inoculation as the mode of transmission for chromoblastomycosis. J Am Acad Dermatol. 1991;25:951-954.
  25. Bonifaz A, Paredes-Solís V, Saúl A. Treating chromoblastomycosis with systemic antifungals. Expert Opin Pharmacother. 2004;5:247-254.
  26. Maverakis E, Marzano AV, Le ST, et al. Pyoderma gangrenosum. Nat Rev Dis Primers. 2020;6:81. doi:10.1038/s41572-020-0213-x
  27. George C, Deroide F, Rustin M. Pyoderma gangrenosum—a guide to diagnosis and management. Clin Med (Lond). 2019;19:224-228. doi:10.7861/clinmedicine.19-3-224
  28. Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res. 2020;9:F1000 Faculty Rev-1049. doi:10.12688/f1000research.26083.1
  29. Garg A, Lavian J, Lin G, et al. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77:118-122. doi:10.1016/j.jaad.2017.02.005
  30. Daxhelet M, Suppa M, White J, et al. Proposed definitions of typical lesions in hidradenitis suppurativa. Dermatology. 2020;236:431-438. doi:10.1159/000507348
  31. Amat-Samaranch V, Agut-Busquet E, Vilarrasa E, et al. New perspectives on the treatment of hidradenitis suppurativa. Ther Adv Chronic Dis. 2021;12:20406223211055920. doi:10.1177/20406223211055920
References
  1. Franco-Paredes C, Marcos LA, Henao-Martínez AF, et al. Cutaneous mycobacterial infections. Clin Microbiol Rev. 2018;32: E00069-18. doi:10.1128/CMR.00069-18
  2. Brown TH. The rapidly growing mycobacteria—MycobacteriuM fortuitum and Mycobacterium chelonae. Infect Control. 1985;6:283-238. doi:10.1017/s0195941700061762
  3. Hooper J; Beltrami EJ; Santoro F; et al. Remember the fite: a case of cutaneous MycobacteriuM fortuitum infection. Am J Dermatopathol. 2023;45:214-215. doi:10.1097/DAD.0000000000002336
  4. Franco-Paredes C, Chastain DB, Allen L, et al. Overview of cutaneous mycobacterial infections. Curr Trop Med Rep. 2018;5:228-232. doi:10.1007/s40475-018-0161-7
  5. Gonzalez-Santiago TM, Drage LA. Nontuberculous mycobacteria: skin and soft tissue infections. Dermatol Clin. 2015;33:563-77. doi:10.1016/j.det.2015.03.017
  6. Peixoto ADS, Montenegro LML, Lima AS, et al. Identification of nontuberculous mycobacteria species by multiplex real-time PCR with high-resolution melting. Rev Soc Bras Med Trop. 2020;53:E20200211. doi:10.1590/0037-8682-0211-2020
  7. Park J, Kwak N, Chae JC, et al. A two-step real-time PCR method to identify Mycobacterium tuberculosis infections and six dominant nontuberculous mycobacterial infections from clinical specimens. Microbiol Spectr. 2023:E0160623. doi:10.1128/spectrum.01606-23
  8. Fowler J, Mahlen SD. Localized cutaneous infections in immunocompetent individuals due to rapidly growing mycobacteria. Arch Pathol Lab Med. 2014;138:1106-1109. doi:10.5858/arpa.2012-0203-RS
  9. Gardini G, Gregori N, Matteelli A, et al. Mycobacterial skin infection. Curr Opin Infect Dis. 2022;35:79-87. doi:10.1097/QCO.0000000000000820
  10. Wang SH, Pancholi P. Mycobacterial skin and soft tissue infection. Curr Infect Dis Rep. 2014;16:438. doi:10.1007/s11908-014-0438-5
  11. Griffith DE, Aksamit T, Brown-Elliott BA, et al; ATS Mycobacterial Diseases Subcommittee; American Thoracic Society; Infectious Disease Society of America. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175:367-416. doi:10.1164/rccm.200604-571ST
  12. Mougari F, Guglielmetti L, Raskine L, et al. Infections caused by Mycobacterium abscessus: epidemiology, diagnostic tools and treatment. Expert Rev Anti Infect Ther. 2016;14:1139-1154. doi:10.1080/14787210.201 6.1238304
  13. Tu HZ, Lee HS, Chen YS, et al. High rates of antimicrobial resistance in rapidly growing mycobacterial infections in Taiwan. Pathogens. 2022;11:969. doi:10.3390/pathogens11090969
  14. Hashemzadeh M, Zadegan Dezfuli AA, Khosravi AD, et al. F requency of mutations in erm(39) related to clarithromycin resistance and in rrl related to linezolid resistance in clinical isolates of MycobacteriuM fortuitum in Iran. Acta Microbiol Immunol Hung. 2023;70:167-176. doi:10.1556/030.2023.02020
  15. Uslan DZ, Kowalski TJ, Wengenack NL, et al. Skin and soft tissue infections due to rapidly growing mycobacteria: comparison of clinical features, treatment, and susceptibility. Arch Dermatol. 2006;142:1287-1292. doi:10.1001/archderm.142.10.1287
  16. Miretti M, Juri L, Peralta A, et al. Photoinactivation of non-tuberculous mycobacteria using Zn-phthalocyanine loaded into liposomes. Tuberculosis (Edinb). 2022;136:102247. doi:10.1016/j.tube.2022.102247
  17. Bystritsky RJ. Cellulitis. Infect Dis Clin North Am. 2021;35:49-60. doi:10.1016/j.idc.2020.10.002
  18. Christensen K, Holman R, Steiner C, et al. Infectious disease hospitalizations in the United States. Clin Infect Dis. 2009;49:1025-1035. doi:10.1086/605562
  19. Yang JJ, Maloney NJ, Bach DQ, et al. Dermatology in the emergency department: prescriptions, rates of inpatient admission, and predictors of high utilization in the United States from 1996 to 2012. J Am Acad Dermatol. 2021;84:1480-1483. doi:10.1016/J.JAAD.2020.07.055
  20. Cutler TS, Jannat-Khah DP, Kam B, et al. Prevalence of misdiagnosis of cellulitis: a systematic review and meta-analysis. J Hosp Med. 2023;18:254-261. doi:10.1002/jhm.12977
  21. Keller EC, Tomecki KJ, Alraies MC. Distinguishing cellulitis from its mimics. Cleve Clin J Med. 2012;79:547-52. doi:10.3949/ccjm.79a.11121
  22. Brito AC, Bittencourt MJS. Chromoblastomycosis: an etiological, epidemiological, clinical, diagnostic, and treatment update. An Bras Dermatol. 2018;93:495-506. doi:10.1590/abd1806-4841.20187321
  23. McGinnis MR. Chromoblastomycosis and phaeohyphomycosis: new concepts, diagnosis, and mycology. J Am Acad Dermatol. 1983;8:1-16.
  24. Rubin HA, Bruce S, Rosen T, et al. Evidence for percutaneous inoculation as the mode of transmission for chromoblastomycosis. J Am Acad Dermatol. 1991;25:951-954.
  25. Bonifaz A, Paredes-Solís V, Saúl A. Treating chromoblastomycosis with systemic antifungals. Expert Opin Pharmacother. 2004;5:247-254.
  26. Maverakis E, Marzano AV, Le ST, et al. Pyoderma gangrenosum. Nat Rev Dis Primers. 2020;6:81. doi:10.1038/s41572-020-0213-x
  27. George C, Deroide F, Rustin M. Pyoderma gangrenosum—a guide to diagnosis and management. Clin Med (Lond). 2019;19:224-228. doi:10.7861/clinmedicine.19-3-224
  28. Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res. 2020;9:F1000 Faculty Rev-1049. doi:10.12688/f1000research.26083.1
  29. Garg A, Lavian J, Lin G, et al. Incidence of hidradenitis suppurativa in the United States: a sex- and age-adjusted population analysis. J Am Acad Dermatol. 2017;77:118-122. doi:10.1016/j.jaad.2017.02.005
  30. Daxhelet M, Suppa M, White J, et al. Proposed definitions of typical lesions in hidradenitis suppurativa. Dermatology. 2020;236:431-438. doi:10.1159/000507348
  31. Amat-Samaranch V, Agut-Busquet E, Vilarrasa E, et al. New perspectives on the treatment of hidradenitis suppurativa. Ther Adv Chronic Dis. 2021;12:20406223211055920. doi:10.1177/20406223211055920
Issue
Cutis - 114(3)
Issue
Cutis - 114(3)
Page Number
71,77-78
Page Number
71,77-78
Publications
MDedge Dermatology
Cutis
Publications
MDedge Dermatology
Cutis
Topics
Infectious Diseases
Article Type
Article
Display Headline
Multiple Draining Sinus Tracts on the Thigh
Display Headline
Multiple Draining Sinus Tracts on the Thigh
Sections
Photo Challenge
Questionnaire Body

A 40-year-old woman presented with multiple draining sinus tracts on the right thigh following an injury sustained weeks earlier while mowing wet grass.

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Gate On Date
Wed, 09/04/2024 - 11:00
Un-Gate On Date
Wed, 09/04/2024 - 11:00
Use ProPublica
CFC Schedule Remove Status
Wed, 09/04/2024 - 11:00
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article
Teaser Media
Article PDF Media