Guttate Psoriasis Triggered by Streptococcal Pharyngitis in Older Patients: A Case Report.

Introduction
Guttate psoriasis is a subtype of psoriasis characterized by the sudden onset of small, round, scaly plaques, often triggered by infections, most notably group A Streptococcus (GAS) [1,2]. The keratinocyte proliferation seen in guttate psoriasis plaques is thought to result from dysregulation of the T-helper 17 (Th17) axis, which activates pro-inflammatory cytokines, such as interleukin (IL)-17, IL-22, IL-23, and tumor necrosis factor (TNF)-α [3].
In the case of guttate psoriasis triggered by GAS, molecular mimicry is also believed to play a role. After targeting Streptococcus bacteria, the immune system is thought to mistakenly target keratinocytes in the skin because of similar surface components [4,5]. This immune response results in the characteristic small, red, scaly papules and plaques seen in guttate psoriasis [6].
Although the association between streptococcal infection and guttate psoriasis is well documented [2,6,7], guttate psoriasis is rarely reported in older adults, whose immune responses to infections tend to be less robust [8,9]. This rarity can make diagnosis challenging and delay appropriate treatment in the older population. The present case underscores the importance of including guttate psoriasis in the differential diagnosis of older patients presenting with recent upper respiratory infections and acute skin lesions, particularly those patients with multiple comorbidities.

Case Report
A 66-year-old woman with a relevant medical history of type 2 diabetes mellitus, vitamin D deficiency, endometriosis, and colon cancer treated with surgical resection presented to the emergency department on December 18, 2024, with a 1-week history of sore throat and body aches. Physical examination revealed erythematous tympanic membranes and a moist oropharynx with mucus. Polymerase chain reaction testing confirmed GAS infection, leading to the diagnosis of acute streptococcal pharyngitis. The patient was started on azithromycin 500 mg, followed by 250 mg for 4 days.
On December 22, the patient developed vomiting and diarrhea, which was diagnosed as norovirus gastroenteritis, leading her to prematurely stop her antibiotic course. By December 28, her gastrointestinal symptoms had resolved. However, she reported the appearance of a new skin rash that had initially started on her abdomen as a small, red, non-pruritic, scaly macule. Over the next 5 days, the rash progressed rapidly, spreading centrifugally to the chest and upper back.
This rash initially appeared as numerous well-marginated, scaly, oval-to-round macules distributed across the trunk. The appearance of the rash, the absence of pruritic lesions, and a positive yellow fluorescence on Wood lamp testing led to an initial diagnosis of Tinea versicolor. The patient was therefore prescribed oral fluconazole and topical ketoconazole cream.
By January 3, 2025, despite the antifungal treatment, the rash continued to progress, with new lesions appearing on the neck, arm, and lower legs as oval-to-round macules (0.5–1 cm), accompanied by scaling and joint pain in the fingers. The patient denied fever or pruritus. A laboratory evaluation conducted during the visit revealed the following: HbA1c, 10% (increased); glucose, 168 mg/dL (increased); vitamin D, 16 ng/mL (decreased); C-reactive protein (CRP), 16.4 mg/L (elevated); and erythrocyte sedimentation rate (ESR), 30 mm/h (elevated).
Given her recent streptococcal infection, lack of response to antifungal therapy, elevated inflammatory markers, and the morphological evolution of the rash, the diagnosis of guttate psoriasis became the leading clinical suspicion. She was referred to the dermatology department for further confirmation of her diagnosis.
At her dermatology follow-up on January 20, 2025, the rash was clinically confirmed with skin biopsy as guttate psoriasis. Treatment was initiated with topical clobetasol propionate 0.05% cream applied twice daily to the affected area.
By March 2025 (8 weeks after therapy initiation), the patient had significant regression of the lesion, with marked reduction in erythema and scaling (Figures 1, 2). No new lesions had developed, and her joint pain had resolved. At her last follow-up, she remained clinically stable without any recurrence.
Refer to Table 1 for an overview of the patient’s clinical course and timeline.
Written informed consent for publication was obtained from the patient.

Discussion

Immune Dysregulation and Guttate Psoriasis
The development of guttate psoriasis is believed to be a result of an exaggerated immune response to streptococcal antigens. Streptococcal M proteins share epitopes with keratin; therefore, due to molecular mimicry, T-cell cross-reactivity occurs, leading to skin-targeted inflammation [10,11]. Specifically, dysregulation of the Th17 helper axis activates Th17-derived cytokines, such as IL-17, IL-22, IL-23, and TNF-α. These cytokines then play a central role in keratinocyte hyperproliferation, vascular activation, and T-cell infiltration, resulting in the characteristic lesion of psoriasis [3,8]. Comparisons between guttate psoriasis and other forms of psoriasis have also shown increased Th17 cells in the former, further supporting the crucial role of T cells in plaque formation, specifically in guttate psoriasis [3].
In our patient, the development of a widespread scaly rash along with elevated ESR and CRP several days after a streptococcal pharyngitis infection suggests a systemic inflammatory response consistent with Th17 axis activation. The presence of joint pain further indicates systemic involvement of the cytokine-mediated inflammation characteristic of guttate psoriasis.
While the aforementioned immune mechanisms are well documented in younger cohorts, age-related immune alterations can reduce these responses in older patients, contributing to the rarity of guttate psoriasis in this population [6,12]. However, comorbidities, such as our patient’s vitamin D deficiency, may override this age-related decline and play a role in disease development. Vitamin D has been shown to play a key role in the balance of the immune system, and its deficiency can lead to dysregulation of immune responses, including the T-cell reactivity observed in guttate psoriasis [4,13]. This case emphasizes that although age can play a role in the development of guttate psoriasis, existing comorbidities can contribute to the development of this condition in populations in which it is not typically expected.
While the role of the immune system helps explain disease pathogenesis, it also provides insight into treatment strategies. In the present case, clobetasol propionate, a topical corticosteroid, was used for treatment. This medication works by inhibiting cytokine-mediated inflammation, including pathways involving IL-17, IL-22, IL-23, and TNF-α [6]. The resolution of skin lesions seen in this patient following treatment supports the presence of an inflammatory process in guttate psoriasis, as corticosteroids primarily act by reducing inflammation.

Post-Streptococcal Sequelae
Acute rheumatic fever (ARF) is recognized as a classic post-streptococcal complication, primarily affecting the heart, joints, and skin. The cardiac damage, especially to the mitral valve, is severe and results from antigen-antibody reactions triggered by GAS [14,15]. This process illustrates how a strong adaptive immune response in ARF can lead to significant tissue destruction [10]. However, ARF has now become increasingly rare in developed regions, due to widespread use of antibiotics, such as penicillin, and long-term prophylaxis in diagnosed cases of streptococcal pharyngitis.
In contrast, guttate psoriasis is an acute inflammatory skin condition that follows infection with GAS but manifests differently than ARF. It typically presents as small, drop-like scaly lesions on the skin within weeks of the infection and is often associated with elevated anti-streptococcal antibodies, such as ASO titers [4,5,9]. Unlike plaque psoriasis, which involves persistent, difficult-to-detect GAS due to internalization into epithelial cells or formation of biofilms, guttate psoriasis has a clearer link to recent GAS exposure [4,5]. Unlike ARF, which causes destructive inflammation in numerous areas of the body, guttate psoriasis remains largely limited to the skin and is usually self-limiting. However, both conditions demonstrate how the immune response to GAS can extend beyond the throat and lead to significant, sometimes systemic, consequences [10,14].
Along with guttate psoriasis, other rare immune-mediated complications can occur after a GAS infection, such as streptococcal pharyngitis–associated myocarditis. This form of myocarditis develops shortly after streptococcal infection, due to immune cross-reactivity with cardiac tissue, a mechanism similar to that demonstrated in post-streptococcal skin complications [14,15]. This further supports the concept that GAS infections can trigger multiple autoimmune responses, resulting in diverse clinical manifestations.
Additionally, the Streptococcus genus is associated with a broad spectrum of immune-related clinical complications. Streptococcus gordonii, although not a group A species, has been implicated in rare infections, such as prosthetic joint infections [16]. While the pathogenesis of the cases differs, such cases underscore the importance of recognizing atypical streptococcal outcomes.
Although ARF remains a classic sequela of streptococcal pharyngitis, this case of guttate psoriasis in a 66-year-old woman, along with other atypical sequelae, underscores the need for clinicians to monitor for a broad spectrum of immune-mediated and infectious complications [14–16]. Recognizing these atypical sequelae and immune-mediated complications is particularly important in older adults, in whom presentations can be less expected or more subtle [9].

Comorbidities and Disease Progression
Our patient had multiple comorbidities that may have contributed to the increased likelihood of both the susceptibility to guttate psoriasis and the disease course. These comorbidities include poorly controlled type 2 diabetes mellitus (HbA1c of 10%), vitamin D deficiency (16 ng/mL), and a history of colon cancer.
Diabetes mellitus is associated with chronic systemic inflammation, impaired neutrophil function, and delayed wound healing. These factors can lead to impaired skin barrier function, which can aggravate or prolong psoriatic eruptions and increase the risk of misdiagnosis in dermatological conditions [9]. In the present case, the widespread rash, slow recovery, and need for topical corticosteroids suggest impaired skin barrier integrity.
Beyond these structural and functional skin impairments, immune system dysregulation can also play a critical role in guttate psoriasis. Vitamin D, for instance, plays a key immunomodulatory role by regulating the Th17 response. Due to this role, a deficiency in this vitamin may have contributed to a dysregulation of the immune system in our patient, thereby contributing to the development and progression of guttate psoriasis [4,13]. Along with this, vitamin D deficiency has been associated with increased psoriasis severity and reduced therapeutic response [3,5].
Additionally, the patient’s medical history of colon cancer and endometriosis presents a broader picture of a patient with underlying immune dysregulation. This background may have increased her risk for developing post-infectious immune-mediated conditions, such as guttate psoriasis [8,9].
These factors together highlight the importance of a holistic approach to disease management, especially in older patients with multiple comorbidities. Therefore, understanding how these underlying conditions can affect disease development and treatment response is essential to providing comprehensive care [4,6,9].

Treatment Strategy and Clinical Insights
This case emphasizes the importance of considering guttate psoriasis in the differential diagnosis of patients presenting with a new-onset rash following a streptococcal infection, especially in older patients with a history of autoimmune or inflammatory conditions [2,8,9]. While guttate psoriasis is typically reported in younger populations, this patient demonstrates that it can also be seen in older adults with complex medical backgrounds, which highlights the need for close monitoring [8,9].
Management of guttate psoriasis remains largely supportive, as treatment recommendations are based on limited evidence [6]. The first step in management typically involves treatment of the initiating trigger, often GAS, with the appropriate antibiotics. In this case, the patient received azithromycin for streptococcal pharyngitis, which was confirmed to be caused by GAS. Although the antibiotic course was interrupted due to gastrointestinal illness, symptomatic resolution of the pharyngitis was seen.
Currently, topical corticosteroids and calcipotriol are considered the first-line treatment for localized lesions in guttate psoriasis, due to the ease of use and efficacy [6]. Our patient was prescribed clobetasol propionate cream, which led to a noticeable regression in lesion size and scaling over the course of 2 months, consistent with reports of clinical improvement in similar cases [1,6].
Clinical data have also supported the use of phototherapy for widespread or refractory cases. Ultraviolet B and psoralen plus ultraviolet A therapy have shown improvements in psoriasis, with UVB therapy leading to diminished T-cell reactivity [11]. Although it was not required for our patient, phototherapy remains a viable option, particularly in patients with suboptimal response to topical agents.
Systemic treatments, such as methotrexate or cyclosporine, are mostly used in extensive or resistant disease but are not well documented in the case of the guttate subtype [6,11]. Biologics, including inhibitors of IL-17, IL-23, and IL-12/23, have been shown to help in chronic plaque psoriasis and are sometimes used off-label for severe guttate psoriasis [11]. One study on the use of risankizumab monotherapy demonstrated no recurrence of disease for up to 24 months after 3 doses of the medication and withdrawal of therapy. However, more evidence is required to support the effects of this therapy.
In our patient, clobetasol propionate 0.05% was selected as the first-line treatment due to the localized nature of her guttate psoriasis and her overall stable condition. Given her advanced age, history of colon cancer, and poorly controlled diabetes mellitus, all factors that increase the risk of immunosuppression, systemic treatments were avoided [9]. Elevated inflammatory markers, such as CRP and ESR, indicated ongoing systemic inflammation and thus required careful monitoring. Additionally, her vitamin D deficiency likely contributed to the development and progression of lesions [4], highlighting the importance of managing comorbidities alongside dermatologic therapy. This case ultimately demonstrates the value of a personalized treatment plan in older patients with multiple comorbidities to optimize outcomes while minimizing risks [6,9].

Novel Clinical Implications and Significance
This case highlights an unusual presentation of guttate psoriasis in an older adult patient, a condition more commonly seen in children and young adults. The presence of multiple comorbidities, such as poorly controlled diabetes, vitamin D deficiency, and a history of colon cancer, may have influenced both the onset and the prolonged course of the disease. These factors likely contributed to a dysregulated immune system and the development of guttate psoriasis. While guttate psoriasis is generally self-limiting, this case shows how it can present more severely in older adults with complex medical backgrounds. It adds to the limited literature on post-streptococcal immune responses in older populations and highlights the need to consider guttate psoriasis as a differential diagnosis for rashes following upper respiratory infections in older patients. Further studies are needed to better understand how age and comorbidities affect the disease course and treatment outcomes in such cases.

Conclusions
This case highlights a rare presentation of guttate psoriasis triggered by group A streptococcal pharyngitis in a 66-year-old woman. This case also demonstrates that, while the exact mechanisms of development remain unclear, this condition should be considered by clinicians in all patients with recent upper respiratory infections, regardless of age. Unlike more familiar post-streptococcal complications, guttate psoriasis presents with distinct clinical features, thereby aiding in its recognition. This report adds to the understanding of atypical outcomes following streptococcal infections, particularly in older populations with multiple comorbidities.