A 4-year-old with foot laceration

Issue: March 2009

A previously healthy 4-year-old girl presented to our clinic to be evaluated for a possible infection after injuring herself at the beach.

Five weeks prior to the visit, the young girl was with her family at the Chesapeake Bay. She lacerated her foot on a wet piece of wood near the medial aspect of the proximal first toe. Her family washed the wound out, removed some small wood splinters from the wound and placed a bandage over it. During the course of the next four weeks, she had continued redness, development of scaly bumps around the wound site and increasing tenderness. There was no lymphangitis noted and no fever, although her father reported that there was some purulent drainage from the wound two weeks prior to presentation. The family used soap and water without any antibiotic ointment to clean and dress the wound.


The patient lacerated her foot on a wet piece of wood near the medial aspect of the proximal first toe. The wound was mildly tender and erythematous. There was no evidence of warmth or purulence.

The child’s past medical history was unremarkable without any history of chronic or recurrent infections and no prior episodes of delayed wound healing. She did not have any allergies and was not receiving any medications. Her vaccinations were up to date to include a current tetanus vaccine.

Vital signs on presentation were normal. Her physical exam was unremarkable except for the lesion on her toe. The wound was mildly tender and erythematous. There was no evidence of warmth or purulence. There was no hepatosplenomegaly and no lymphadenopathy noted.

What is your differential?

Concern was for a chronic/smoldering infection. Possible retained foreign body was also considered. The history of exposure to brackish water as well as wood is unique to a number of infectious organisms. Consideration however must be given to common causes of soft tissue infection including Staphylococcus aureus. Wound infections with this organism usually present within a few days of the trauma with local signs of inflammation and possibly fever, chills or other constitutional signs. Purulent discharge will often be present. As for other organisms, Vibrio vulnificus can cause wound infections after exposure to warm seawater, especially in the Gulf of Mexico. It is typically associated with fever, cellulitis, swelling and intense pain at the wound site. Edwardsiella tarda is associated with infection/cellulitis, usually occurring after local trauma ranging from superficial abrasion to deep penetrating wounds. It is commonly found combined with Aeromonas hydrophilain aquatic injuries. Cellulitis typically develops eight to 48 hours after trauma. Other clinical findings include localized skin nodules, soft tissue abscess, furuncles and cellulitis with bullous formation.

The nontuberculous mycobacterium (NTM) are also responsible for post-traumatic skin infections. Most of these are caused by Mycobacterium marinum, M. ulcerans, M. fortuitum, M. chelonae and M. goodii . M. marinum usually follows aquatic injury and presents as nontender superficial papules at the site of injury.

M. ulcerans is found in Australia and Central Africa and presents as a single large, painless ulcer. The other NTMs (M. fortuitum, M. chelonae and M. goodii) are rapidly growing mycobacteria. Infection usually presents after penetrating injury and manifests as cellulitis, draining abscesses or a single minimally tender nodule.

Sporotrichosis due to the fungus Sporothrix schenckii is another syndrome to consider due to the contact with plant matter. Cutaneous infection usually occurs after traumatic inoculation of the organism, usually via wood splinters. The initial lesion appears one to four weeks after exposure and consists of a small, firm painless papule or vesicle. The papule slowly enlarges during several weeks, becoming indurated and red. Within two weeks skin necrosis can occur with resultant ulceration.

So with this differential, the next question was what to do about this wound. Ultrasound of the area was recommended to evaluate for any potential retained wood splinters. It was decided that cultures would be required to evaluate for NTM and fungi. A punch biopsy at the site of the wound was obtained and stains and cultures for bacteria, fungi and acid-fast bacilli were completed. The first result to return was the bacterial culture, which grew out a coagulase-negative Staphylococcus (speciation not completed). The fungal smear was negative, as was the culture. The tissue specimen was placed in formalin. Pathology showed a necrotizing granulomatous dermatitis. Special staining including periodic acid-Schiff and Giemsa were performed for fungal organisms and were negative. Brown-Hopps and Twort tissue gram stain to differentiate and demonstrate gram-positive and gram-negative bacteria in tissue were also completed. Ziehl-Neelsen and Fite stains were completed, which yielded acid-fast bacilli. The acid-fast bacilli culture was positive and was eventually identified as M. marinum.

Case Discussion

The answer is Mycobacterium marinum.

As mentioned in the differential, M. marinum is a slow-growing aerobic mycobacterium that causes disease in humans via contamination through an altered skin barrier. It was first isolated in 1926 from saltwater fish in a Philadelphia aquarium. The first reported human infection was described in the 1950s after the patient developed granulomatous lesions after swimming in a local pool.

The organism is found in fresh, brackish and salt water environments. Exposure after trauma is the mechanism most often associated with disease, with home fish tanks often being implicated as a source of infection. M. marinum infections, most notably septic arthritis, have also been associated with the use of Antitumor necrosis factor (TNF)-α therapy in patients with psoriasis, rheumatoid arthritis and Crohn’s disease.

M. marinum is difficult to grow and requires two to five weeks on special medium. It is also temperature sensitive and will not grow at 37°C but rather requires incubation at temperatures from 30° to 32°C.

Clinical presentation

Lesions usually occur at the site of inoculum and are most often found in areas prone to skin injury. The name “fish tank finger” has been given to these infections when located on this extremity. Other common sites of infection are the backs of hands in fish handlers and the feet of swimmers. Lesions have been categorized based on the extent of involvement, usually after they have been present for a period of two to eight weeks. Type I lesions are superficial in nature, resolve spontaneously and consist of a solitary mildly tender erythematous papule. They may further develop into a scaling, violaceous plaque or nodule, which may ultimately ulcerate. Type II lesions consist of single or multiple tender granulomas with or without ulceration. They may be edematous and may drain. Type III involve the deep layers, with dissemination to underlying tendons, bones and joints and along pathways of lymphatic drainage. These lesions are more commonly associated with immunocompromised patients, especially those receiving chronic steroid therapy or in individuals with AIDS. Unfortunately, patients may develop recurrent infections with M. marinum, as immunity to the organism does not seem to develop.

Diagnosis

The diagnosis is often made on the basis of suspicion, although definitive diagnosis requires isolation of the organism. Since M. marinum is commonly found in the environment, contamination of the culture or transient colonization can occur. Repeated isolation of numerous colonies on the culture, or an acid-fast bacilli smear-positive sample are likely to represent true disease. On histopathology, there will usually be evidence of nonspecific inflammation but may also have a granulomatous infiltrate, similar to that seen in tuberculosis. Ziehl-Neelsen, and Fite stains will help to elicit acid-fast bacilli. There is also a polymerase chain reaction-enzyme-linked immunosorbent assay available for species identification.

Treatment

Treatment of M. marinum can often be challenging. Many of these infections will resolve spontaneously after two to three years. There are not any specific criteria for treatment, but many different therapies have been reported as effective. Some have advocated cryotherapy or surgical debridement, which is best used to manage serious localized disease. Antibiotics are frequently used, but unfortunately are not always effective. M. marinum is relatively resistant to some anti-TB drugs such as isoniazid and streptomycin (Myambutol, Stat-Trade), but is fairly sensitive to ethambutol and rifabutin (Mycobutin, Pharmacia & Upjohn). Therapeutic success has been seen with tetracyclines, trimethroprim, and macrolides. Clarithromycin (Biatin, Abbott) and at least one other drug, such as ethambutol or rifampin, are usually the treatments of choice to minimize the risk for resistance. Monotherapy with either trimethoprim-sulfamethoxazole, clarithromycin or doxycycline has also been reported to be successful with resolution by three months. Treatment should occur for four to six weeks after resolution of lesions, with total therapy usually ranging from three to six months.

Nicole Thomas, MD, is a Lieutenant Colonel in the U.S. Air Force. She is currently a Pediatric Infectious Disease Fellow at the F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences in Bethesda, Md.

Michael Rajnik, MD, is a Lieutenant Colonel in the U.S. Air Force. He is currently the Pediatric Infectious Disease Fellowship Director and Assistant Professor of Pediatrics at the F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences in Bethesda, Md.

Disclaimer: The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Defense.

For more information:

AAP. Diseases caused by nontuberculous mycobacteria (atypical mycobacteria, mycobacteria other than Mycobacterium tuberculosis. In: Pickering LK, Baker CJ, Long SS, McMillan JA. Red Book: 2006 Report of the Committee on Infectious Diseases 27th Ed. Elk Grove Village, IL: American Academy of Pediatrics; 2006: 698-704.

Dermatol Online J. 2008; 14:7.

Dermatol Clin. 2009; 27: 63-73.

Wallace RJ. Mycobacterium species, non-tuberculosis. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practices of Pediatric infectious Diseases, 3rd ed. New York: Churchill, Livingstone; 2008: 788-792.

Edited by Michael Rajnik, MD

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