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Perianal streptococcal infection precipitating pustular psoriasis in an adult
... The terms "anitis" [13,55] and "anusitis" [67] were also used, but only in a few papers. Other authors preferred to name this condition "perianal streptococcal infection" [7,11,16,18,27,33,37,50,60,65,76,77] or "perianal streptococcal disease", as introduced in 1987 by Kokx et al [4,62,64,78] . Mogielnicki et al [5] introduced the term "perineal streptococcal disease", as the infection may extend to genital organs. ...
... Regarding age, PID is particularly encountered in children, especially between the ages of 6 mo and 10 years [2][3][4]8,11,20,22,28] , with a maximum incidence peak between 3 years and 6 years [24] . However, cases have been described in infants less than 6 mo of age [15,23,26,43,57] or older than 10 years [5,10,15,23,26,27,39,48,62] , and even in adults [52,61,[71][72][73][74][75][76][77][78][81][82][83][84] . Boys have been initially described as predominantly affected by PID, representing about or more than 70%-80% of cases [2,4,8,10,15,18,20,21,28] (Table 1). ...
... Although among the included studies, no such immunological complications were found, a urine analysis may be performed to screen for possible PSAGN [7,79] . GAS-associated PID may trigger acute guttate psoriasis (GP) [3,9,19,22,48,53,55,[60][61][62]83] , plaque-psoriasis [56] or pustular psoriasis [77] . Treating PID also resolves the skin disease, as was mostly reported, except for 1 case of GP [3] and 1 of plaque-psoriasis [56] . ...
Abstract: Perianal infectious dermatitis (PID) represents a superficial inflammation of the perianal skin, which is of bacterial origin (classically, group A beta-hemolytic streptococci). This narrative review aims to critically review and summarize the available scientific literature regarding pediatric PID, being the first of its kind, to the best of the author’s knowledge. It also reports the first cases of Romanian children with PID. Multiple databases were subjected to systematic literature search (from 1966 to April 30, 2018) to identify studies and case reports of children with PID. As such, this review provides updated information about essential aspects of PID (epidemiology, etiology, pathogenesis, as well as clinical features, required investigations and therapeutic options) and of diagnostic pitfalls. Although a well-defined entity, PID remains largely underdiagnosed. PID may mimic other common conditions with skin manifestations (like candidiasis, pinworms, eczema, irritant dermatitis, anal fissure, hemorrhoids, Crohn’s disease, psoriasis, seborrheic dermatitis, zinc deficiency dermatosis and even sexual abuse), with consequent unnecessary, sometimes expensive and invasive investigations and futile therapies, which cause patients and families discomfort and distress. Since PID has an unremitting course, early recognition
is imperative, as it allows for prompt and efficacious antibiotic therapy. However, PID represents a stubborn condition and, even if properly treated, its recurrence rate remains high. Further well-designed prospective randomized controlled trials, with adequate follow-up, are required in order to formulate the optimum personalized
antibiotic therapy (oral alone or in association with topical medication), able to prevent recurrences. Awareness of this condition by healthcare professionals should improve patient outcomes.
Key words: Perianal dermatitis; Perianal streptococcal dermatitis; Beta-hemolytic streptococci; Staphylococcus aureus; Perineal streptococcal dermatitis; Perianal swab culture; Differential diagnosis; Antibiotic therapy; Perianal streptococcal disease
... Of these 50 studies, 38 studies evaluated the efficacy of systemic antibiotics, while 12 studies evaluated the efficacy of tonsillectomy, and two studies evaluated both (McMillin and Whyte). The studies consisted of 10 randomized controlled trials (RCTs) [10][11][12][13][14][15][16][17][18][19], 3 openlabel studies [20][21][22], 1 crossover trial [23], 2 single-arm studies [24,25], 1 prospective observational study [26], 1 case-control study [27], 1 retrospective questionnaire analysis [28], 2 cohort studies [29,30], 13 case series [31][32][33][34][35][36][37][38][39][40][41][42][43], and 16 case reports [44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59]. ...
Streptococcal infections may contribute to psoriasis development, and antistreptococcal treatments are considered potential therapies, but their effectiveness remains uncertain due to limited systematic evidence. Our objective was to analyze antistreptococcal therapies' effectiveness in improving psoriasis. We conducted a systematic review following PRISMA guidelines, evaluating antistreptococcal treatment efficacy in psoriasis patients from PubMed, Scopus, and Embase databases until August 14, 2022. Eligible studies included psoriasis patients undergoing antistreptococcal therapy, regardless of demographics or psoriasis type. 50 studies (1778 patients) were analyzed, with penicillins/aminopenicillins as the most studied antibiotics (21 studies), showing mixed outcomes, some reporting significant improvement in guttate psoriasis, while others showed no significant difference. Rifampin demonstrated positive results in most of ten studies, and macrolides showed varying effectiveness in two studies. Tonsillectomy in 14 studies (409 patients) mainly focusing on guttate and chronic plaque psoriasis showed positive outcomes, indicating improved symptoms and quality of life. Limitations include heterogeneous studies, sampling bias, and quality of evidence. This systematic review reveals limited and varied evidence for systemic antibiotic therapy efficacy in psoriasis treatment, while tonsillectomy emerges as a potentially beneficial antistreptococcal option, urging further well-designed, controlled studies with larger sample sizes and standardized protocols for better comparisons.
... 19,20 Many other medications have also been implicated as a trigger, including antibiotics such as amoxicillin, 21 terbinafine, 22 calcipotriol ointment, 23 betamethasone ointment, 23 tumor necrosis factor-alpha (TNF-α) inhibitors, 24,25 ustekinumab, 24,26 and withdrawal of cyclosporine. 27 Infections reported as potential etiological factors in GPP include streptococcal, 28 Trichophyton rubrum, 29 cytomegalovirus, 30,31 Epstein-Barr virus, 32 and varicella-zoster virus. 33 GPP has also been associated with various medical conditions including Turner syndrome, 4 hypoparathyroidism, 34 hypocalcemia, 34 allogeneic stem cell transplantation, 35 rheumatoid arthritis, 36 and cardiomyopathy. ...
Generalized pustular psoriasis (GPP) is a rare and potentially life-threatening variant of psoriasis that is characterized by recurrent, acute onset, widely distributed pustular eruptions on inflamed, erythematous skin. It is important to recognize acute GPP as a subtype of psoriasis associated with high morbidity and mortality so therapy can be initiated without delay. Since GPP was first described in 1910 by Leopold von Zumbusch, it has been inconsistently defined, stratified, and diagnosed in the literature. Multiple definitions and diagnostic criteria have been proposed over the years. Recently, formal consensus guidelines on GPP have been published by international groups. This article reviews the current evidence and understanding in the diagnosis and screening of GPP.
Streptococcal toxic shock syndrome (TSS) is a fulminant disease characterised by rapid progression to multiorgan failure. However, streptococcal TSS manifesting as uterine necrosis (UN) is unusual. Here, we present a case of a woman in her 30s with a constellation of symptoms, including abdominal pain, fatigue and fever. Despite an initially unclear clinical picture, she rapidly developed shock with radiographical evidence of intrabdominal arterial narrowing with spurious multiorgan infarctions and ischaemic colitis. Exploratory laparotomy uncovered unexpected UN requiring hysterectomy. Multiple complications ensued, marked by shock liver, acute renal failure, cutaneous desquamation and distal gangrene. This case highlights a unique presentation of streptococcal TSS as UN and emphasises the rapidly deteriorating nature of the disease.
Generalized pustular psoriasis (GPP) is a severe and life-threatening systemic disease associated with significant morbidity and mortality. Recent progress has been made in understanding the pathogenetic pathways involved in GPP and an intricate interaction between innate and adaptive immune mechanisms has been suggested. Despite formal consensus guidelines on pustular psoriasis currently available in the literature, the definitions and classifications of GPP used across studies were inconsistent. Consequently, there are no unified criteria that can be universally adopted for precise diagnosis, classification and effective treatment of GPP patients with new targeted drugs. The aim of this review was to collect all the main evidence on available diagnostic criteria for GPP and to establish recommendations in order to promote a better stratification and therapeutic management of this severe and heterogeneous disease.
The concept that psoriasis is an autoimmune disease needs to be questioned. The autoimmune label has been based on molecular mimicry between streptococcal and keratin proteins and the existence of homologous peptides between these proteins. However it is only peripheral blood CD8, and not CD4, T lymphocytes that respond to the homologous peptides. This ignores the fact that it is CD4 T cells which are necessary to initiate psoriasis. Recent studies on skin bacterial microbiota have found a variety of bacteria in both normal skin and psoriatic lesions. In biopsy specimens the most common phylum was Firmicutes and the most common genus streptococcus in both psoriasis and normal skin. The innate immune system is activated in psoriasis and recent genetic findings have shown the majority of susceptibility loci are associated with innate immunity. There is a known clinical relationship between both Crohn's disease (CD) and periodontitis, and psoriasis, and psoriasis patients share mutations in some innate immunity genes with individuals with CD. It is now accepted that CD is due to a breakdown of immune tolerance (dysbiosis) to bacteria in the intestine. These findings suggest that psoriasis is initiated by an abnormal response to bacteria in the skin due to genetic factors. This article is protected by copyright. All rights reserved.
Abstract Psoriasis is a chronic skin disorder that affects 1% to 3% of the general population worldwide. Streptococcal infection, especially streptococcal pharyngitis, has been shown to be a significant trigger of psoriasis in some patients, possibly by sensitizing T cells to keratin epitopes in the skin. Due to the role of the palatine tonsils as an immunological organ that may generate autoreactive T cells, tonsillectomy has been investigated as a treatment for psoriasis. Tonsillectomy originally gained acceptance in Japan as a treatment for palmoplantar pustulosis, a condition that shares features with pustular psoriasis. Subsequently, tonsillectomy has been used for the treatment of plaque psoriasis and guttate psoriasis. Recently, the first randomized, controlled clinical trial of tonsillectomy was performed. Here, we review the available evidence for the benefit of tonsillectomy as a treatment for palmoplantar pustulosis and psoriasis. We also discuss molecular studies aimed at understanding the role of tonsils in skin disease.
We evaluated 130 prepubertal girls presenting with a vulvar complaint to determine the spectrum and frequency of conditions seen in this age group. Of the patients, 41 (33%) had atopic or irritant dermatitis, 23 (18%) had lichen sclerosus, 21 (17%) had psoriasis, 15 (12%) had vulvar lesions, most often hemangiomas and nevi, and 13 (10%) had streptococcal vulvovaginitis. Diagnoses less frequently seen were staphylococcal folliculitis (four patients), labial fusion (three patients), genital warts (two patients), molluscum contagiosum of the vulva only (one patient), vulvar bullous pemphigoid (two patients), scabies nodules (one patient), erythema annulare centrifugum (one patient), tinea (two patients), and vitiligo (one patient). We also encountered vulvar presentations of systemic diseases (varicella, staphylococcal scalded skin syndrome, and Henoch–Schönlein purpura, all one patient each). We did not see candidal vulvovaginitis in this age group nor did we encounter bacterial infection with pathogens other than Staphylococcus aureus and S. pyogenes.
A task force of the National Psoriasis Foundation Medical Board was convened to evaluate treatment options for pustular psoriasis. Meetings were held by teleconference. Consensus on treatment of pustular psoriasis was achieved. Pustular psoriasis has been classified into localized and generalized forms. There are a number of treatment modalities, but there is little evidence-based information to guide the management of this type of psoriasis.
The purpose of this article was to present treatment recommendations to aid in the treatment of patients with pustular psoriasis.
A literature review was conducted to examine treatment options for pustular psoriasis and assess the strength of the literature for each option.
Overall the quality of the literature about the treatment of pustular psoriasis is weak. Treatment should be governed by the extent of involvement and severity of disease. Acitretin, cyclosporine, methotrexate, and infliximab are considered to be first-line therapies for those with generalized pustular psoriasis. Adalimumab, etanercept, and psoralen plus ultraviolet A are second-line modalities in this setting. Pustular psoriasis in children, in pregnant women, and in localized forms alter which agents are first-line modalities as concerns such as teratogenicity need to be factored into the decisionmaking for the individual patient.
There are few high-quality studies examining treatment options for pustular psoriasis.
Treatment of patients with pustular psoriasis depends on the severity of presentation and patient's underlying risk factors. The data are extremely limited for this type of psoriasis and we encourage further exploration.
Acute generalized exanthematous pustulosis (AGEP) represents a severe, acute, pustular skin reaction that is most often induced by drugs. AGEP can be difficult to differentiate from generalized pustular psoriasis (GPP) both clinically and histopathologically. We present a systematic description of the histopathological spectrum of AGEP and GPP with a focus on discriminating features.
A retrospective, descriptive, comparative histopathological study was completed utilizing step sections of 43 biopsies of 29 cases with a validated diagnosis of probable or definite AGEP and 24 biopsies of 19 cases with an established diagnosis of GPP.
In AGEP, biopsies from erythema and pustules showed minor differences, whereas histopathology of the acute stage of GPP showed major differences compared to the chronic stage. Comparing AGEP and GPP, the presence of eosinophils, necrotic keratinocytes, a mixed interstitial and mid-dermal perivascular infiltrate and absence of tortuous or dilated blood vessels were in favor of AGEP. Moreover, chronic GPP was characterized by prominent epidermal psoriatic changes. The frequency of a psoriatic background of AGEP patients in our study was higher than that of psoriasis in the general population. However, histopathology of a subgroup of AGEP patients with a personal history of psoriasis revealed no significant differences from the other AGEP patients.
The spectrum of histopathological features of both AGEP and GPP is presented. Despite considerable overlap, subtle consistent histopathological differences and the grade of severity of specific features can help in differentiation. We could neither substantiate earlier reports that follicular pustules exclude AGEP nor did we see vasculitis as a specific feature in AGEP. Our study also supports the concept that AGEP is a separate entity that is distinct from GPP.
Psoriasis is a relatively common disorder in children and can be triggered by an upper respiratory tract infection. The aim of this study was to compare the clinical features of psoriasis in children and adult. In addition, we evaluated the relationship between anti-streptolysin O (ASO) titers and the clinical features of psoriasis. A total of 30 childhood psoriasis patients and 30 adult psoriasis patients were evaluated. Childhood psoriasis had a facial predominance when compared with the adult psoriasis. The childhood psoriasis patients with high ASO titers had guttate psoriasis more frequently than patients with normal ASO titers. In children with plaque-type psoriasis, psoriasis area and severity index score was increased in the high ASO titer group than normal ASO titer group. In conclusion, if the children with psoriasis show increased ASO titer, the physician should pay attention to the worsening of the psoriasis. Furthermore, early treatment of streptococcal infections might be beneficial in childhood psoriasis.
The role of streptococcal infection in the initiation of guttate psoriasis is well-recognized. But the treatment results with oral erythromycin and phenoxymethylpenicillin are conflicting.
Our purpose was to evaluate the effectiveness of these antibiotics in the treatment of streptococcus associated guttate psoriasis comparing with a control group.
A total of 43 male patients with serologic evidence of a recent streptococcal infection were studied. Their mean age was 21 years (ranged between 19 and 23 years). These 43 patients were randomly allocated into three groups (no treatment group n = 15, erythromycin group n = 14, phenoxymethylpenicillin group n = 14). Both the treatment groups were treated for 14 d. All the groups were followed up for additional 4 weeks.
There were no statistically significant improvement in any group and among the groups.
There was no statistically significant improvement in streptococcus associated guttate psoriasis with or without a course of oral penicillin or erythromycin.
Perianal streptococcal dermatitis (PSD) is a recently described cutaneous entity caused by group A beta-hemolytic streptococci. It is characterized by perianal erythema, sometimes associated with functional disturbances. We describe four children (2 boys, 2 girls) who had acute guttate psoriasis and also PSD. One of these patients also had balanoposthitis. A fifth patient experienced an association of PSD and balanoposthitis without psoriasis. To our knowledge, the association between guttate psoriasis and PSD has only been reported in five children, and the one with balanitis has not been previously reported.
A case of allergic contact dermatitis to a shampoo containing zinc pyrithione associated with an eruption of pustular psoriasis is reported. The patient had had stable psoriasis for 5 years, and never any other skin disease. Within 1 week she developed severe generalized pustular psoriasis with many lesions where the shampoo was applied. Treatment with cyclosporin, 200 to 300 mg daily, cleared the eruption within 4 weeks, except for psoriasis of the scalp. Extensive patch testing revealed a relevant sensitization to zinc pyrithione. This case illustrates that a generalized pustular psoriasis can be provoked by a substance present in a hair shampoo. Short-term treatment with cyclosporin is valuable in exacerbations of psoriasis caused by allergic contact dermatitis.
Zinc pyrithione is a shampoo ingredient that has been shown to be safe and effective for dandruff and scalp psoriasis. It is thought to decrease the cell turnover rate in hyperproliferative dermatoses such as psoriasis, and also has fungistatic and antimicrobial activity, although its exact mode of action is unknown. In psoriasis, external factors, such as trauma, infection and drugs, may provoke aggravated manifestations of psoriatic skin lesions. Rarely, irritant or allergic mechanisms are likely causes of psoriatic flare and Kobnerization. A patient had had stable psoriasis for 25 years and no any other skin disease. Within 20 days, she developed an aggravated scaly erythematous patch on the scalp, where a shampoo had been applied, and simultaneously developed pustular psoriasis on both forearms. Patch testing showed a relevant sensitization to zinc pyrithione, and we observed symptomatic aggravation by provocation testing with zinc pyrithione shampoo. We report a rare case of psoriasis aggravated by the induction of allergic contact dermatitis from zinc pyrithione after using antidandruff shampoo.
pyrithione-containing shampoo
pyrithione-containing shampoo. Contact Derm. 2005;52(3):
142-144.
Psoriasis is not an autoimmune disease?
- L. Fry
- B.S. Baker
- A.V. Powels
Psoriasis is not an autoimmune disease?
- L Fry
- B S Baker
- A V Powels
Fry L, Baker BS, Powels AV, et al. Psoriasis is not an
autoimmune disease? Exp Dermatol 2015;24:241-244.