Correspondence
Pseudomonas Hot-Foot Syndrome
N Engl J Med 2001; 345:1643-1644November 29, 2001
- Article
To the Editor:
We are surprised by the certainty with which Fiorillo et al. (Aug. 2 issue)1 conclude that the so-called pseudomonas hot-foot syndrome accounts for the unprecedented cluster of cases they describe. All 40 cases occurred 10 to 40 hours after the children had been in a wading pool, but Pseudomonas aeruginosa was found in only one child. Water samples from the pool yielded the same microorganism. Invariably, the lesions resolved with the treatment of symptoms. Effective disinfection of the water did not end the outbreak. It ceased only after the floor of the pool had been sanded, although cultures of swabs from the inlets and floor still yielded P. aeruginosa.
These findings do not prove that there was a causal relation between P. aeruginosa and the skin lesions. Since the presence of P. aeruginosa is common in warm and humid environments,2 its detection in a single patient suggests an incidental infection.
The entity that the authors describe is consistent with idiopathic palmoplantar hidradenitis.3,4 Despite the authors' claim, the inflammatory infiltrate in this disorder is not “confined to the eccrine apparatus” but may extend to the subcutaneous fat and perivascular space and may even cause abscess formation.4,5 Friction and a damp environment appear to contribute to the pathogenesis of idiopathic palmoplantar hidradenitis.3 The report by Fiorillo et al. supports this notion, suggests an experimental model for the disorder, and may lead to an understanding of its pathogenesis.
5 ReferencesAlex Zvulunov, M.D.
Joseftal Hospital, Eilat 88000, Israel
azvulun@bgumail.bgu. ac. il Akiva Trattner, M.D.
Rabin Medical Center, Petah Tiqva 49100, IsraelSody Naimer, M.D.
Ben Gurion University, Beer Sheva 84101, Israel1
Fiorillo L ,Zucker M ,Sawyer D ,Lin AN . The pseudomonas hot-foot syndrome. N Engl J Med 2001;345:335-338
Full Text | Web of Science | Medline2
Ratnam S ,Hogan K ,March SB ,Butler RW . Whirlpool-associated folliculitis caused by Pseudomonas aeruginosa: report of an outbreak and review. J Clin Microbiol 1986;23:655-659
Web of Science | Medline3
Naimer SA ,Zvulunov A ,Ben-Amitai D ,Landau M . Plantar hidradenitis in children induced by exposure to wet footwear. Pediatr Emerg Care 2000;16:182-183
CrossRef | Web of Science | Medline4
Rabinowitz LG ,Cintra ML ,Hood AF ,Esterly NB . Recurrent palmoplantar hidradenitis in children. Arch Dermatol 1995;131:817-820
CrossRef | Web of Science | Medline5
Landau M ,Metzker A ,Gat A ,Ben-Amitai D ,Brenner S . Palmoplantar eccrine hidradenitis: three new cases and review. Pediatr Dermatol 1998;15:97-102
CrossRef | Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: Of the 40 children we described, only 1 child (and the child's family) consented to the incision of a pustule for culture. As we reported, the culture yielded a strain of P. aeruginosa with a DNA pattern (identified by pulsed-field gel electrophoresis) that was identical to that of the P. aeruginosa isolated from the pool water, a finding strongly suggesting that P. aeruginosa in the water was the cause of the lesions. Because all 40 children had virtually identical lesions within 40 hours after using the same pool, and all the lesions had a similar clinical course, it is most likely that this disorder was caused by the same agent. The statement by Zvulunov et al. that the outbreak “ceased only after the floor of the pool had been sanded” is incorrect. New cases occurred even after the floor had been sanded, as we reported. In fact, we noted the persistence of P. aeruginosa in the inlets, floor, and drain after the floor had been sanded. The outbreak ended only after these areas were further disinfected with a quaternium ammonium compound and ozone treatment.
As we pointed out, the clinical findings in our patients were similar to those in patients with idiopathic palmoplantar hidradenitis. In a series of 22 patients with idiopathic palmoplantar hidradenitis, the inflammatory infiltrate was “very similar” in all the patients and was “localized to the eccrine apparatus, particularly to the coils.”1 In two other patients, the infiltrate showed “slight extension to the neighboring periglandular connective tissue and subcutis,”2 but this observation is uncommonly reported. It is possible that the biopsies in both our patients were performed at the height of the inflammatory response, accounting for the marked inflammation in the subcutis. Our data suggest that P. aeruginosa may be the cause in a subgroup of patients with idiopathic palmoplantar hidradenitis, especially those with deep extension of the inflammatory infiltrate and those in whom the condition occurs as part of an outbreak. We believe the data in our report support the role of P. aeruginosa as the etiologic agent in the lesions in our patients.
2 ReferencesLoretta Fiorillo, M.D.
Douglas Sawyer, M.D.
Andrew N. Lin, M.D.
University of Alberta, Edmonton, AB T6G 2G3, Canada1
Simon M Jr ,Cremer H ,von den Driesch P . Idiopathic recurrent palmoplantar hidradenitis in children: report of 22 cases. Arch Dermatol 1998;134:76-79
CrossRef | Web of Science | Medline2
Rabinowitz LG ,Cintra ML ,Hood AF ,Esterly NB . Recurrent palmoplantar hidradenitis in children. Arch Dermatol 1995;131:817-820
CrossRef | Web of Science | Medline
