An ulceration on the knee - Clinical Advisor

An ulceration on the knee

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Case #1

A previously healthy 24-year-old man from Honduras presents with a 2-month history of a progressively growing skin lesion on his left knee. He arrived to the United States 1 month earlier and had previously received a 2-week course of unknown antibiotics in Honduras with no improvement. This lesion first appeared after he cut his knee while swimming in a river. It has grown slowly in size and has become increasingly tender over time. He denies any constitutional symptoms. On examination, he has a 7-cm × 6-cm irregularly shaped dark, crusted plaque with central depression and yellowing, and surrounding erythema on his left knee.

Case #2

A 28-year-old woman presents with a draining wound on her right knee. The lesion was the result of a fall that took place 2 days earlier while she was jogging. She has otherwise been healthy. The wound and surrounding area are tender, and she has not applied any treatments to the area. She denies having any constitutional symptoms. On examination, she is afebrile and has a 5-cm × 2.5-cm ulceration with yellow purulent drainage and surrounding erythema on her right knee. There is no fluctuance.

 

Case #1Atypical mycobacteria are mycobacterial species other than Mycobacterium tuberculosis and M leprae. Atypical mycobacterial organisms are ubiquitous in the environment and can be isolated from vegetation, soil, animals, birds, and (especially) water.1 Tap water is the main reservoir for...

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Case #1

Atypical mycobacteria are mycobacterial species other than Mycobacterium tuberculosis and M leprae. Atypical mycobacterial organisms are ubiquitous in the environment and can be isolated from vegetation, soil, animals, birds, and (especially) water.1 Tap water is the main reservoir for most atypical mycobacterial pathogens that affect humans.2 No evidence of person-to-person spread has been reported with atypical mycobacteria.3

Nonmotile acid-fast bacilli (AFB) can be categorized into rapidly growing mycobacteria (RGM) and slowly growing mycobacteria, based on culture characteristics. Runyon4 classified groups based on pigment-forming properties when cultured. Recent technologic advances have also allowed the bacteria to be grouped according to genotypic characteristics.4,5 Clinical syndromes that occur due to atypical mycobacterial infections include pulmonary disease, superficial lymphadenitis, disseminated disease in the severely immunocompromised, and skin and soft tissue infections (SSTIs).

Atypical mycobacterial SSTIs primarily occur after trauma, surgery, or cosmetic procedures as a consequence of direct inoculation by M marinum, M ulcerans, or RGM species, including M fortuitum, M chelonae, and M abscessus.6 Because the organisms are relatively low in virulence, they typically require a break in the skin barrier to cause infection. The prevalence is small, with an estimated rate of 0.9 cases per 100,0007; however, data exist that cutaneous mycobacterial infection may be more prevalent than previously recognized.6,8,9

Skin findings with these infections include abscesses, sporotrichoid nodules, cellulitis, or ulcers; however, morphology can be variable. Two distinctive well-defined species-specific clinical disorders exist: fish-tank granuloma and Buruli ulcer, caused by M marinum and M ulcerans, respectively.10 The majority of cutaneous atypical mycobacterial infections in Europe and the United States are M marinum and the RGM species,2,11 whereas the majority of cases of M ulcerans occur in West and Central Africa.12

Atypical mycobacterial SSTIs are frequently underdiagnosed. Infection by an atypical mycobacterial organism should be considered in all patients with SSTIs resistant to treatment with typical antibacterial medications, particularly those with a history of recent trauma, surgery, or immunosuppression. In immunosuppressed individuals, the infection tends to be more disseminated and may not be associated with trauma.2 Frequently, coinfection with bacteria, including Staphylococcus species, can occur, delaying identification of the atypical mycobacterial infection.13 The differential diagnosis for atypical mycobacterial SSTI includes bacterial infection by S aureus or Streptococcus pyogenes, sporotrichosis, cryptococcosis, blastomycosis, coccidioidomycosis, and cutaneous leishmaniasis.

Typically, skin biopsy with culture is required to establish an accurate diagnosis. Polymerase chain reaction (PCR) can also be used to screen for mycobacterium, with DNA sequencing to identify the exact subtype.9,14 Diagnosis is often delayed due to the lengthy time required for tissue culture. Frequently, acid-fast staining of lesion exudates and skin biopsy are unable to reveal the diagnosis due to small numbers of organisms.2,15 On histopathologic examination, suppurative granulomas are the most characteristic of cutaneous atypical mycobacterial infections, but other patterns have been described and may be more prevalent in immunosuppressed patients.15

The treatment of SSTIs by atypical mycobacterium species has not been well established. Treatment is often guided by recommendations for management of pulmonary infections.8,9 Tetracycline antibiotics, macrolides, quinolones, and antitubercular drugs are the most commonly used drugs, and surgery is a possible adjunct.2,10,16 Combination therapy is often given to minimize development of resistance.16 Susceptibility testing for isolates should be performed16; however, results may be delayed due to the prolonged time culture requires. Length of treatment is not well defined, but it is suggested that antimicrobial therapy be continued for 4 to 8 weeks after the resolution of lesions.2,16 In 10% to 20% of cases, depending on the causative organism, the infection may be self-limiting and resolve over an average period of 8 months.17

For the patient in our case, two 4-mm punch biopsies were performed for hematoxylin and eosin staining and AFB smear and culture, and deep fungal and bacterial cultures. The biopsies showed a suppurative granulomatous dermatitis with neutrophils, lymphocytes, plasma cells, and histiocytes in the dermis. Results of gram, AFB, periodic acid-Schiff, and Giemsa stains were negative for microorganisms. Tissue bacterial cultures showed skin flora. PCR was performed and revealed M marinum. Clarithromycin and rifampin was initiated. At a follow-up visit 6 months later, the lesion had resolved.

Case #2

Methicillin-resistant S aureus (MRSA) infections are common and represent a major cause of nosocomial and community-acquired infections. Healthcare-associated MRSA (HA-MRSA) infections are defined as MRSA infections that occur at least 48 hours following hospitalization, in the presence of an invasive device such as a vascular catheter at time of admission, or that occur with exposure to healthcare risks such as surgery, hospitalization, dialysis or residence in a long-term care facility within 12 months of exposure to healthcare.18 HA-MRSA is typically associated with severe invasive diseases including bloodstream infections, pneumonia, and skin and soft tissue infections (SSTIs).18 Community-acquired MRSA (CA-MRSA) often causes SSTIs in otherwise healthy individuals, particularly in children and young adults.19 In surveillance of CA-MRSA, 77% were categorized as SSTIs, most commonly as abscesses (59%) or cellulitis (42%).20 Over the years, CA-MRSA has been increasing in incidence.21

Transmission of CA-MRSA resulting in skin infection has been reported to occur due to trauma resulting in disruption of skin integrity, including lacerations and microabrasion from shaving and from direct contact in person-to-person spread.22,23 Populations at risk include illicit drug users, prisoners, military trainees, athletes, and children.22-26 Individuals colonized with MRSA, commonly in the nares, can serve as a reservoir for transmission and are also at increased risk for subsequent MRSA infection.27

Purulent material can be obtained from the lesion for gram stain, culture, and susceptibility testing, which is useful in guiding therapy.19 By definition, MRSA organisms are not susceptible to β-lactam antibiotics. Susceptibility of MRSA skin infections to antibiotics can vary depending on location, emphasizing the importance of local antibiotic susceptibility patterns and susceptibility testing.

The differential diagnosis for MRSA skin infections depends on the type of skin infection. The differential for a MRSA cellulitis includes abscess, contact dermatitis, arthropod-reactive dermatitis, panniculitis, and necrotizing fasciitis. The differential for a MRSA abscess includes folliculitis, hidradenitis suppurativa, atypical mycobacterial infection, leishmaniasis, myiasis, and sporotrichosis. The differential for a MRSA folliculitis includes gram-negative folliculitis from Pseudomonas aeruginosa, acne vulgaris, keratosis pilaris, Grover disease, hidradenitis suppurativa, and scabies. In terms of bacterial etiology, methicillin-susceptible S aureus and Group A β-hemolytic streptococcus are also common bacteria that manifest in the same types of skin infections as MRSA.

For very minor skin infections, mupirocin can be used topically.28 For abscesses, surgical drainage is recommended, with addition of antibiotics for severe or extensive disease, systemic illness, comorbidities or immunosuppression, extremes of age, and difficult to drain areas.20,28 Empiric coverage for outpatient CA-MRSA includes clindamycin, trimethoprim-sulfamethoxazole, tetracycline antibiotics, and linezolid.28 Patients with complicated SSTI may require intravenous antibiotics, such as vancomycin, linezolid, daptomycin, or clindamycin.28

For the patient in our case, oral clindamycin was initiated empirically for presumed MRSA cellulitis. A swab of the purulent drainage was sent for gram stain, culture, and susceptibility testing, which came back confirming the diagnosis of MRSA. After completion of 5 days of clindamycin therapy, the patient’s wound resolved.

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Emily Guo, BA, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston.

References

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  3. Falkinham JO. The changing pattern of nontuberculous mycobacterial disease. Can J Infect Dis. 2003;14(5):281-286.
  4. Runyon EH. Anonymous mycobacteria in pulmonary disease. Med Clin North Am. 1959;43(1):273-290.
  5. Brown-Elliott BA, Wallace RJ Jr. Clinical and taxonomic status of pathogenic nonpigmented or late-pigmenting rapidly growing mycobacteria. Clin Microbiol Rev. 2002;15(4):716-746.
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  12. Buruli ulcer (Mycobacterium ulcerans infection). World Health Organization website. http://www.who.int/mediacentre/factsheets/fs199/en/ Updated February 2016. Accessed November 1, 2016.
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  14. Ngan GJ, Ng LM, Jureen R, et al. Development of multiplex PCR assays based on the 16S-23S rRNA internal transcribed spacer for the detection of clinically relevant nontuberculous mycobacteria. Lett Appl Microbiol. 2011;52(5):546-554.
  15. Bartralot R, Pujol RM, García-Patos V, et al. Cutaneous infections due to nontuberculous mycobacteria: histopathological review of 28 cases. Comparative study between lesions observed in immunosuppressed patients and normal hosts. J Cutan Pathol. 2000;27(3):124-129.
  16. Jogi R, Tyring SK. Therapy of nontuberculous mycobacterial infections. Dermatol Ther. 2004;17(6):491-498.
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  18. Klevens RM, Morrison MA, Nadle J, et al; Active Bacterial Core surveillance (ABCs) MRSA Investigators. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007;298(15):1763-1771.
  19. Daum RS. Skin and soft tissue infections caused by methicillin-resistant Staphylococcus aureus. N Engl J Med. 2007;357(4):380-390.
  20. Fridkin SK, Hageman JC, Morrison M, et al; Active Bacterial Core Surveillance Program of the Emerging Infections Program Network. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med. 2005;352(14):1436-1444.
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  22. Begier EM, Frenette K, Barrett NL, et al; Connecticut Bioterrorism Field Epidemiology Response Team. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39(10):1446-1453.
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  24. Gilbert M, MacDonald J, Gregson D, et al. Outbreak in Alberta of community-acquired (USA300) methicillin-resistant Staphylococcus aureus in people with a history of drug use, homelessness, or incarceration. CMAJ. 2006;175(2):149-154.
  25. Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk. JAMA. 1998;279(8):593-598.
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