[Skip to Content]
Sign In
Individual Sign In
Create an Account
Institutional Sign In
OpenAthens Shibboleth
[Skip to Content Landing]
Views 909
Citations 0
Observation
May 2016

Cutaneous Presentation of Methicillin-Resistant Staphylococcus aureus Sepsis in a Healthy Child

Author Affiliations
  • 1Department of Dermatology, University of Louisville School of Medicine, Louisville, Kentucky
JAMA Dermatol. 2016;152(5):580-582. doi:10.1001/jamadermatol.2015.5367

Septic vasculopathy is a life-threatening condition that can present with cutaneous findings. We present a case of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) sepsis presenting as 2 retiform purpuric patches and diffuse erythematous to violaceous papules.

Report of a Case

A healthy male toddler presented to the emergency department with abdominal pain and distention, fever, and vomiting of 1 day’s duration. He was found to have “bruises” on both flanks (Figure 1A). Workup for child abuse was initiated, and he was treated with enemas for constipation and intramuscular penicillin after positive streptococcal findings. Over the next 2 days, he developed diffuse papules on the trunk and extremities; his condition rapidly deteriorated requiring intubation, vasopressors, and empirical broad-spectrum antibiotics. A dermatology consult was obtained to evaluate his skin eruption.

Figure 1.
Skin Lesions Due to Septic Vasculopathy
Skin Lesions Due to Septic Vasculopathy

A, Purpuric patch on the flank noted at admission, prompting workup for child abuse. B, Erythematous to violaceous papules diffusely scattered on the extremities and trunk.

At the time of consult, he was hyponatremic and neutropenic, and the following laboratory values were recorded: aspartate aminotransferase (AST), 45 U/L; alanine aminotransferase (ALT), 142 U/L; C-reactive protein (CRP), greater than 270 mg/L; erythrocyte sedimentation rate, 43 mm/h; and ferritin, 603 ng/mL. (To convert AST and ALT to microkatals per liter, multiply by 0.0167; CRP to nanomoles per liter, 9.524; and ferritin to picomoles per liter, 2.247.) Urinalysis showed proteinuria and hematuria. Computed tomography of the chest and abdomen demonstrated cavitary lesions in his lungs representing necrotizing pneumonia. Areas of nonenhancement within both kidneys were suspected to represent renal abscesses. On physical examination, purpuric retiform patches were found on each flank (1 of them studded with 2 pustules) with erythematous to violaceous papules diffusely scattered on the extremities and trunk (Figure 1B).

Punch biopsy specimens were taken from an area of purpura for analysis by frozen section, from a pustule for tissue culture, and from a papule for hematoxylin-eosin staining. Within an hour of obtaining the specimens, the pathologist reported frozen section findings of small organisms within the vasculature suggestive of either fungal spores, likely histoplasmosis, or staphylococcal bacteria. Permanent sections revealed a large neutrophilic pustule with inflammation extending throughout the dermis and prominent necrosis with basophilic structures filling necrotic vascular spaces (Figure 2A). Tissue Gram staining confirmed gram-positive cocci in the vessels (Figure 2B). Tissue culture, blood culture, bronchial washings, and fluid from bilateral empyemas all grew CA-MRSA.

Figure 2.
Histopathologic Findings
Histopathologic Findings

A, In this specimen from a papule, a large neutrophilic pustule with inflammation is seen extending throughout the dermis, and prominent necrosis with basophilic structures fills necrotic vascular spaces (original magnification ×40). B, Tissue Gram staining of a papule specimen confirms presence of gram-positive cocci in the vessels (original magnification ×200).

Results from transthoracic echocardiogram and bone scans were negative. Magnetic resonance images of the brain showed multifocal lesions, likely septic emboli. Findings from workup for possible immunodeficiency were negative. The patient was sent to a rehabilitation facility to complete a 6-week course of intravenous vancomycin.

Discussion

The original classifications of CA-MRSA and hospital-acquired MRSA are no longer distinct: CA-MRSA now causes infections in health care settings, and hospital-acquired MRSA spreads in the community.1 In a study on disseminated Staphylococcus in children, MRSA was the causative agent in all cases. Children aged 5 to 12 years were most vulnerable, and trauma was found to be a common precipitating factor.2

Septic vasculitis caused by septicemia from Staphylococci is an immune-complex negative, small-vessel neutrophilic vasculitis.3 Clinical lesions of septic vasculitis are characterized by retiform purpura, petechiae and ecchymoses, vesiculopustules, hemorrhagic bullae, and ulceration.4 In cases of septic emboli without evidence of vasculitis, some prefer the term septic vasculopathy. One study5 compared 32 patients with bacterial sepsis, cutaneous lesions, and biopsy-proven septic vasculopathy. Cutaneous lesions were an early finding of sepsis in most patients (91%; n = 29). Most cases (n = 18) involved the development of lesions simultaneously or within the first 24 hours of sepsis that were disseminated rather than localized. Most lesions presented as purpuric papules and plaques, followed by petechiae, vesicles and bullae, pustules, distal ischemia, and nodules.4 Septic vasculopathy had a mortality rate of 20% in this study,5 making early recognition and treatment essential.

In addition to cutaneous findings, staphylococcal sepsis can involve the lung, heart, kidneys, brain, bone, and joints,6 and it is important to evaluate for these potential sites of involvement. As this case report highlights, consulting dermatologists can play a role in identifying disseminated infections by recognizing the diverse skin manifestations and performing appropriate biopsies for analysis by frozen section, permanent section, and tissue culture.

Back to top
Article Information

Corresponding Author: Cindy Owen, MD, Department of Dermatology, University of Louisville School of Medicine, 3810 Springhurst Blvd, Ste 200, Louisville, KY 40241 (Cindy.owen@louisville.edu).

Published Online: January 27, 2016. doi:10.1001/jamadermatol.2015.5367.

Conflict of Interest Disclosures: None reported.

Additional Information: We acknowledge the Department of Pathology at Norton Kosair Children’s Hospital for their contributions to this article.

References
1.
Thurlow  LR, Joshi  GS, Richardson  AR.  Virulence strategies of the dominant USA300 lineage of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA).  FEMS Immunol Med Microbiol. 2012;65(1):5-22.PubMedGoogle ScholarCrossref
2.
Mandal  K, Roy  A, Sen  S, Bag  T, Kumar  N, Moitra  S.  Disseminated staphylococcal disease in healthy children-experience from two tertiary care hospitals of West Bengal.  Indian J Pediatr. 2014;81(2):133-137.PubMedGoogle ScholarCrossref
3.
Carlson  JA, Chen  KR.  Cutaneous vasculitis update: small vessel neutrophilic vasculitis syndromes.  Am J Dermatopathol. 2006;28(6):486-506.PubMedGoogle ScholarCrossref
4.
Chen  KR, Carlson  JA.  Clinical approach to cutaneous vasculitis.  Am J Clin Dermatol. 2008;9(2):71-92.PubMedGoogle ScholarCrossref
5.
Delgado-Jiménez  Y, Fraga  J, Requena  C,  et al.  Acute bacterial septic vasculopathy.  Int J Dermatol. 2013;52(9):1071-1080.PubMedGoogle ScholarCrossref
6.
Kliegman  R, Stanton  B, St Geme  J, Schor  N, Behrman  R.  Nelson Textbook of Pediatrics. Philadelphia, PA: Elsevier Inc; 2011:19.
×