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A 5-year-old boy with fever, swelling in his left arm
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A previously healthy 5 ½-year-old male presented to his primary’s office with a 1-day history of fever to 102.1·F, chills, headache and decreased appetite. His examination documented the fever, chills, mild tachypnea, tachycardia with good color, a capillary refill of 2 seconds and a moderately ill-appearing child who was easily consoled. His left forearm had diffuse swelling and what appeared to be a few pustular lesions on an erythematous base, initially thought to be related to insect bites (Figure 1). Additionally, the left shoulder was swollen with pain on range of motion testing.
He was referred to the hospital for further evaluation and admission. Lab tests on admission showed a CBC with a WBC count of 19,200 cells/mcL with 86% neutrophils. The erythrocyte sedimentation rate and C-reactive protein level were mildly elevated and blood culture is pending. The pustular lesion on his forearm was drained (Figure 2) and sent for stains (all negative) and culture (pending). An MRI of the left arm revealed extensive lymphadenopathy and soft tissue inflammation and swelling that extended to the shoulder, but no bone or joint involvement. Orthopedic surgery took the patient to the OR for surgical exploration, but no further purulence was found.
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Figure 1: The patient’s left forearm had
diffuse swelling and what appeared to be a few pustular lesions on an
erythematous base, initially thought to be related to insect bites. |
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Figure 2: The pustular lesion on his forearm
was drained (Figure 2). |
He was empirically treated with IV cefazolin and clindamycin with slow defervescence. After 6 days, he was discharged home on amoxicillin-clavulanate (Augmentin, GlaxoSmithKline). You are notified 1 week later that the culture of the arm lesion was growing a weakly Gram-positive, acid-fast filamentous organism (Figure 3).
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Figure 3: The culture of the arm lesion was
growing a weak Gram-positive, acid-fast filamentous organism. |
What’s Your Diagnosis?
A. Mycobacterium marinum
B. Sporothrix schenckii
C. Staphylococcus aureus
D. Nocardia brasiliensis
The culture turned out to grow
N. brasiliensis (D), the most common cause of lymphocutaneous nocardiosis. The hints really leave no other choice. This organism is a fairly ubiquitous, weakly Gram-positive, acid-fast filamentous organism and can be found in the soil, including the sand in a child’s sandbox (Figure 4, the first child I saw with cutaneous nocardiosis acquired from the baby’s sandbox). The skin lesion typically begins with inoculation due to a minor injury that develops one or more pustules that grows into an abscess with surrounding pyoderma that may develop into an ulcer.
According to Chadwick and Thomson’s excellent review in Chapter 136 of Principles and Practice of Pediatric Infectious Diseases, Third Edition, these lesions can be indistinguishable from cutaneous sporotrichosis (Figure 5), which of course is caused by the fungus S. schenckii. This choice was ruled out by the stains of the organism that grew.
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Figure 4: The first child I saw with
cutaneous nocardiosis acquired from the baby’s sandbox. |
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Figure 5: The lesions can be indistinguishable from cutaneous sporotrichosis, which of course is caused by the fungus S. schenckii |
Severe nocardiosis usually occurs in the immunocompromised, including those on chemotherapy or steroids, and usually involves the respiratory tract. But certainly, soft-tissue infections can occur in compromised patients, and if severe, as in the patient presented, it is strongly recommended that the patient have an immune system evaluation.
In this patient, his immune workup was normal. The treatment is surgical drainage and a long course of appropriate antimicrobial therapy. The drug of choice for uncomplicated lymphocutaneous nocardiosis is a sulfonamide. In this country, we usually use trimethoprim-sulfamethoxazole. The duration of therapy ranges from 6 to 12 weeks. For complicated cases, especially in immunocompromised patients, one should consult with an infectious disease expert for guidance.
M. marinum is an acid-fast organism that causes an infection that also requires an injury to the skin and, furthermore, must be in contaminated, non-chlorinated water, allowing the entry of the organism. This results in a chronic sore that may also resemble sporotrichosis and nocardiosis (Figure 6). Spread beyond the inoculation site is unlikely. It is usually self-limited in immunocompetent patients but can be treated with clarithromycin, doxycycline, TMP-SMX or rifampin plus ethambutol for 4 to 6 weeks.
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Figure 6: This results in a chronic sore
that may also resemble sporotrichosis and nocardiosis. |
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Figure 7: S. aureus, the most common cause of soft-tissue infections,
typically is acute in onset and produces cellulitis with abscess formation with
copious, yellow pus. |
S. aureus, the most common cause of soft-tissue infections, typically is acute in onset and produces cellulitis with abscess formation with copious, yellow pus (Figure 7). Diagnosis is made relatively quickly with culture. Of course, the Gram’s stain would show cocci rather than filamentous organisms.
Columnist Comments
I would like to thank Michael W. Cater, MD, for contributing this very interesting case of lymphocutaneous nocardiosis. Dr. Cater has a general pediatric practice in Tustin, Calif., and has contributed several excellent cases over the years for the readers of this column. I hope he continues to share his patients’ cases for our educational benefit.
Lastly, it is with great sadness that we learned of the recent death of Heinz Eichenwald, MD, who died Sept. 8 at 85 years of age. The first time I heard Heinz Eichenwald lecture was as an attendee at The Variety Children’s Hospital (now Miami Children’s Hospital) Pediatric Review Course in Miami in 1981. Dr. Eichenwald spoke on otitis media. As I recall, about a month later, he was moderating at the inaugural National Pediatric Infectious Diseases Seminar (NPIDS), where I saw him again (I was cramming for the boards). Almost every year thereafter, I saw Dr. Eichenwald at the NPIDS, where he was usually a moderator. Over the years, my wife, Ellen, and I became good friends with Heinz and his wife, Linda (shown on Heinz’s left in Figure 8 with Ellen at one of the NPIDS in New Orleans).
He was always a soft-spoken and patient gentleman whose quiet demeanor concealed a brilliant and accomplished mind. During his years as chairman of pediatrics at The University of Texas Southwestern Medical School, he built the department into one of the premier pediatric programs in the country. He also was involved in promoting pediatric education in South Vietnam while the war was still under way.
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Figure 8: From the left, Heinz
Eichenwald’s wife, Linda Eichenwald, Eichewald and Ellen Brien. |
His lifelong dedication to pediatric education leaves a legacy that will continue to reach far into the future through the hands of pediatric providers he influenced over the years, benefiting patients yet to be born.
For more information:
- Long SS. Principles and Practice of Pediatric Infectious Diseases, 3rd ed. Philadelphia, Pa.; Elsevier/Churchill Livingstone; 2009.
James H. Brien, DO, is Vice Chair for Education at The Children’s Hospital at Scott and White and is the Associate Professor of Pediatrics at Texas A&M University, College of Medicine, Temple, Texas. email: jhbrien@aol.com. Disclosure: Dr. Brien reports no relevant financial disclosures.
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