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Year : 2021  |  Volume : 22  |  Issue : 4  |  Page : 339-341

Atypical manifestations of cutaneous staphylococcal infection in infants – Generalized bullous impetigo and asymmetrical peripheral gangrene

Department of Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission06-Apr-2020
Date of Decision26-Apr-2020
Date of Acceptance30-Mar-2021
Date of Web Publication01-Oct-2021

Correspondence Address:
Rahul Mahajan
Department of Dermatology, Venereology and Leprology, Post Graduate Institute of Medical Education and Research, Sector 12, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpd.IJPD_54_20

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Introduction: Impetigo is the bacterial infection of the skin most commonly seen in infants and children. Bullous and nonbullous are the two forms of impetigo. It usually presents with vesicles, bullae, crusted erosions, or ulcers. Case report: We report two cases in which the first case showed crusted erosions all over the body and the second one had bullous lesions over the extremities, which eventually lead to gangrene of fingers and toes. These were due to the bacterial infections of the skin. Discussion: Superficial bacterial infection should be one of the differential diagnoses, whenever there is diffuse exfoliation of the skin or peripheral gangrene.

Keywords: Impetigo, meningocele, staphylococcus aureus, gangrene, staphylococcal scalded skin syndrome

How to cite this article:
Bishnoi A, Raj D, Mahajan R. Atypical manifestations of cutaneous staphylococcal infection in infants – Generalized bullous impetigo and asymmetrical peripheral gangrene. Indian J Paediatr Dermatol 2021;22:339-41

How to cite this URL:
Bishnoi A, Raj D, Mahajan R. Atypical manifestations of cutaneous staphylococcal infection in infants – Generalized bullous impetigo and asymmetrical peripheral gangrene. Indian J Paediatr Dermatol [serial online] 2021 [cited 2021 Dec 6];22:339-41. Available from: https://www.ijpd.in/text.asp?2021/22/4/339/327453

  Introduction Top

Bacterial infection of the skin is a common condition in children and adolescents. Bullous impetigo (BI) is one of the common diseases in this category. It is usually caused by Staphylococcus aureus Scientific Name Search  and Streptococcus pyogenes. Clinically, impetigo shows multiple grouped vesicles and bullae that contain yellowish fluid, usually on the face which rupture leading to erosions and crust formation.[1] Herein, we report two cases with atypical presentation of BI.

  Case Report Top

An eight-month-old infant presented to us with fever and crusted erosions all over the body for a duration of one week. The baby also had a lumbar meningocele from birth. On examination, there were numerous vesicopustules on an erythematous base and few, large flaccid bullae filled with purulent material that had gravitated down reminiscing hypopyon sign [Figure 1]. There was generalized involvement of the integument with lesions present on the scalp, face, trunk, and limbs. At multiple sites, the bullae had ruptured to form annular to circumscribed, superficial, raw erythematous erosions with mild crusting and scaling, which were discrete at places and were coalescing to form large crusted plaques on the shoulders and anterior trunk.
Figure 1: An 8-month-old infant with lumbar meningocele has generalized distribution of pustules and large pus-filled bulla with gravitational percolation of pus presenting as hypopyon sign. Also visible are numerous raw erythematous erosions with superficial crusting that are discrete as well as coalescing to form large crusted plaques on the shoulder and anterior trunk

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A thorough history and examination did not reveal any underlying focus of infection. There was history neither of any drug intake in the mother nor of bullous skin lesions in the family. Palms, soles, nails, and mucosae were normal. Although febrile, the infant showed no signs of systemic toxicity. Investigations were done to rule out syphilis. Antinuclear antibody titers were not raised in both the infant and the mother. A Tzanck smear done from the base of the bulla revealed rare acantholytic cells but no giant cells. A Gram stain from the lesion demonstrated numerous Gram-positive cocci arranged in the clusters. The culture from the pus grew coagulase-positive S. aureus. Patient's complete blood count was as follows: Hb - 7 g/dL, Total leukocyte count (TLC) - 13,970/mm3, platelets - 3.44 L, P/L/M/E - 58/34/8/0, and primary immunodeficiency was ruled out. Histopathological and direct immunofluorescence examination of the skin biopsy was noncontributory. A diagnosis of extensive BI was made, and the infant recovered completely after institution of intravenous clindamycin (20 mg/kg divided 8-hourly) as per the sensitivity patterns.

The second patient was a one year-old boy, admitted with complaints of bullous lesions on both hands and feet of 30 days' duration. The patient was admitted in a private hospital before coming to us and was treated with systemic antibiotics for sepsis. He had gangrene of fingers of the right hand for which amputation of the fingers at proximal interphalangeal joint was done. On examination, both lower legs and both hands revealed greenish-yellow fluid-filled bullae, which broke down eventually to form raw areas and dry gangrene over both lower legs and both hands [Figure 2]a and [Figure 2]b. There was no underlying focus of infection in the infant. Systemic examination revealed no abnormality. The child's complete blood count was as follows: Hb - 7.2 g/dL, TLC - 18480, platelets - 6.2 L, P/L/M/E - 36/51/13/0 and coagulation profile was as follows: PT - 13.2, PTI - 86%, INR - 1.16, APTT - 26.9, D-dimer - 2.28, and fibrinogen - 74. As in the child discussed above, biochemical and immunologic investigations were normal. Genetic tests such as factor V Leiden mutation, protein C, and protein S were normal. Doppler sonography of all limbs revealed normal flow. A Tzanck smear done from the base of the bulla revealed no acantholytic cells and no giant cells. A Gram stain from the lesion demonstrated numerous Gram-positive cocci arranged in the clusters. The culture from the pus grew coagulase-positive S. aureus. A diagnosis of atypical BI with asymmetrical peripheral gangrene was made, and the infant recovered completely with injection ceftriaxone (100 mg/kg/day) and injection clindamycin (30 mg/kg/day) according to culture sensitivity.
Figure 2: (a) A single bullae containing greenish-yellow fluid over the right lower leg with few surrounding bullae with erythematous background. (b) Gangrenous change over the toes of the left leg

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The clinical differential diagnoses for vesicles, pustules, and erosions in an infant are numerous.[2] Both BI and staphylococcal scalded skin syndrome (SSSS) are mediated by epidermolytic toxins released from S. aureus, which are glutamate-specific serine proteases and have been equated with molecular scissors that cause cleavage of skin adhesion molecule desmoglein 1.[3],[4] It is important to delineate SSSS that presents with potato-chip desquamation of the skin, which usually initiates at the perioral area and spreads to the major flexures and trunk, leaving bright red glistening raw surface beneath. SSSS requires a nidus of staphylococcal infection (e.g. omphalitis, pyoderma) from which the epidermolytic/exfoliative toxin B is released in the bloodstream. Individuals having decreased renal clearance of the toxin (adults with renal failure/infants with immature renal excretion) develop the epidermolytic effects of the toxin, which results in generalized skin tenderness, erythema, and peeling that is more pronounced on perioral, periocular, and flexural sites.[2] Mild shearing force on normal-appearing skin shall result in peeling off of the integument (positive Nikolsky's sign). The patient may remain stable (unless there is superinfection of the eroded skin, sepsis, or hemodynamic imbalance, resulting from the potential skin failure), and the cultures of the skin samples are usually sterile.[2] Occurrence of necrosis and gangrene of the skin as seen in the second patient is very rare.

BI, on the other hand, is a bullous pyoderma caused by S. aureus and represents a localized effect of epidermolytic toxin A that causes blistering of the skin, resulting in pus-filled bullae. The generalized erythema and tenderness as seen in SSSS are not observed in BI, and Nikolsky's sign is negative (as seen in our patient). The process may become generalized rarely, as in the first patient, and can lead to septicemia. The fragile pustules on an erythematous base are the primary lesions that expand rapidly to form pus-filled bullae and rupture to form erythematous erosions having thin crusting.[1] The treatment of both conditions is institution of antistaphylococcal antibiotics. Varicella, eczema herpeticum, and candidiasis are other infectious conditions that can simulate BI,[1],[2] but subtle clinical and laboratory features (vesicle as the primary lesion in varicella/monomorphic small punched out crusted erosions and polycyclic erosions in eczema herpeticum with giant cells on Tzanck smear/satellite pustules in candidiasis with evidence of budding yeasts on potassium hydroxide mount) can help differentiate the same. Symmetrical peripheral gangrene is the gangrenous change of extremities in the absence of major vascular occlusive disease. In symmetrical peripheral gangrene, the exact pathomechanism of vascular occlusion is uncertain. It is described as the cutaneous marker of disseminated intravascular coagulation. The other proposed mechanisms include Shwartzman reaction, bacterial endotoxin release, low flow states, and spastic process of vessels. It is associated with infections, drugs, connective tissue disorders, myeloproliferative disorders, and hyperviscosity syndromes.[5]

  Conclusion Top

The atypical presentation of BI with gangrenous change and extensive involvement by BI was striking and responded to antibiotics. Since pediatricians encounter such cases more frequently, there should be a low threshold for referral to dermatologists.

Declaration of consent

The authors certify that they have obtained all appropriate consent forms, duly signed by the parent(s) of the patient. In the form the parent(s) has/have given his/her/their consent for the images and other clinical information of their child to be reported in the journal. The parents understand that the names and initials of their child will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Wick MR. Bullous, pseudobullous, & pustular dermatoses. Semin Diagn Pathol 2017;34:250-60.  Back to cited text no. 1
Sandhu K, Kanwar AJ. Generalized bullous impetigo in a neonate. Pediatr Dermatol 2004;21:667-9.  Back to cited text no. 2
Nishifuji K, Sugai M, Amagai M. Staphylococcal exfoliative toxins: “Molecular scissors” of bacteria that attack the cutaneous defense barrier in mammals. J Dermatol Sci 2008;49:21-31.  Back to cited text no. 3
Hanakawa Y, Schechter NM, Lin C, Garza L, Li H, Yamaguchi T, et al. Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome. J Clin Invest 2002;110:53-60.  Back to cited text no. 4
Ghosh SD, Bandyopadhyay D. Symmetrical peripheral gangrene. Indian J Dermatol Venereol Leprol 2011;77:244-8.  Back to cited text no. 5
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