Thyroiditis is an inflammation of the thyroid gland that can be caused by autoimmune processes, infection, trauma, drug exposure, or neoplastic infiltration in both humans and dogs (1–7). In people, thyroiditis encompasses several distinct entities: Hashimoto’s disease, acute or subacute (de Quervain’s) thyroiditis, and Riedel’s thyroiditis, each defined by clinical features such as painful or painless neck swelling, systemic malaise, and variable thyroid hormone profiles (1–7). Some people experience transient thyrotoxicosis from follicular disruption, whereas others progress directly to hypothyroidism as chronic inflammation or fibrosis destroys functional tissue (3–5, 7).

Given the absence of a well-described canine model for acute, fulminant thyroiditis, human medical literature provides an essential framework for understanding potential pathogenic mechanisms. In people, thyroiditis encompasses several distinct entities. Hashimoto’s disease is characterized by autoantibodies against thyroglobulin and thyroid peroxidase, whereas Riedel’s thyroiditis and the emerging IgG4-related subtype feature invasive fibrosis that can extend into perithyroidal soft tissue, lung, or other organs (5, 7–10). IgG4-related disease in humans involves infiltration of IgG4-positive plasma cells, leading to fibrotic inflammatory lesions in multiple organs, including the thyroid, and is notable for its aggressive tissue invasion and steroid responsiveness (11, 12).

In dogs, the most recognized immune-mediated thyroid disorder is chronic lymphocytic thyroiditis, a slowly progressive analog of human Hashimoto’s disease that culminates in glandular atrophy and overt hypothyroidism without systemic inflammation (13–18). Clinical signs typically include lethargy, weight gain, dermatologic changes, cold intolerance, bradycardia, neuromuscular weakness, reproductive disturbances, behavioral alterations, and occasionally mild anemia. Although toxin-associated acute thyroiditis has been described in connection with Toxoplasma gondii infection (19), an acute, steroid-responsive, immune-mediated form has not been characterized in the veterinary literature. For clarity, we proposed the provisional term steroid-responsive immune-mediated thyroiditis (SRIMT) to describe a case of sudden cervical swelling, profound hypothyroidism, and multi-organ pyogranulomatous inflammation that resolved rapidly with immunomodulatory steroid therapy and recognized a need for further characterization of this process in dogs.

This report documents an SRIMT in a young dog. We detailed its clinical presentation, diagnostic evaluation, and therapeutic response and compared this syndrome with established thyroiditis phenotypes in both human and veterinary medicine. It is important to differentiate this presentation from more common canine diseases causing acute cervical swelling and systemic illness, such as deep cervical abscessation, migrating foreign bodies, sialoceles, or neoplasia (e.g., lymphoma or thyroid carcinoma). This case was unique due to its bilateral thyroidal origin, concurrent systemic pyogranulomatous lesions, and rapid response to immunomodulation rather than antimicrobial or surgical intervention.

A 3-year-old neutered male Posavac Hound (36.4 kg) presented to a referral veterinarian with 3 days of inappetence, drooling, progressive neck swelling, and acute dysphonia. The dog was tachycardic with respiratory stridor. Initial diagnostics revealed a low total thyroxine (TT4: <0.5 μg/dL). Radiographs showed ventral cervical soft tissue swelling, a ~ 5 cm caudal lung mass, and a bronchointerstitial pattern. Cytology of a neck aspirate indicated pyogranulomatous inflammation; bacterial and fungal cultures of neck and lung aspirates were negative. The dog was hospitalized for supportive care and broad-spectrum antibiotics (ampicillin/sulbactam and enrofloxacin), but was referred to a veterinary teaching hospital (VTH) the next day due to concerns regarding neoplasia or an atypical infectious process.

The term steroid-responsive immune-mediated thyroiditis (SRIMT) is proposed to distinguish this abrupt, fulminant presentation from both chronic lymphocytic thyroiditis and infectious thyroid disease in dogs. This dog developed sudden bilateral cervical swelling with stridor and dysphonia, as well as cavitated, hypoattenuating thyroid lobes and putatively sterile pyogranulomatous lesions in the lungs and lymph nodes (Supplementary Figures 1, 2). These features mirror the rapid clinical course of acute or subacute thyroiditis in people (3, 4, 6), yet with more extensive systemic involvement. Endocrine testing confirmed severe primary hypothyroidism, with total and free thyroxine below assay detection and markedly elevated thyroid-stimulating hormone (Table 3). The combination of acute onset, characteristic imaging finding, sterile multi-organ inflammation, and dramatic response to immunomodulatory steroid therapy does not fit any previously recognized canine thyroid disorder, supporting SRIMT as a provisional, distinct phenotype and arguing for further characterization of the pathogenesis and clinical progression of acute SRIMTs in dogs.

In people, subacute (de Quervain’s) thyroiditis typically presents with painful thyroid swelling and a transient thyrotoxic phase without multisystem lesions (6, 21). Hashimoto’s thyroiditis evolves gradually without acute systemic inflammation, and Riedel’s thyroiditis produces dense fibrosis rather than cavitation or rapid clinical progression (6, 22). Chronic lymphocytic thyroiditis in dogs progresses insidiously to atrophy without systemic pyogranulomatous inflammation (17). In contrast, this dog’s increased serum IgG4 fraction, a marker of human IgG4-related disease (23), indicated a potential parallel mechanism for this inflammatory syndrome. While this finding is not diagnostic, it highlights IgG4-driven autoimmunity as a potential pathogenic mechanism in dogs that warrants further investigation. This contrasts sharply with typical canine lymphocytic thyroiditis, which, unlike its human Hashimoto’s counterpart, rarely involves systemic inflammation or the aggressive, fibrotic, or necrotizing features seen in human Riedel’s or de Quervain’s thyroiditis, or in this case (23).

Although a deep cervical infection was initially suspected, extensive microbiologic workup, including cultures, PCR assays, and serology, was uniformly negative. The patient was on broad-spectrum antibiotics for 4 days and experienced no improvement during this time. Contrastingly, the cervical mass began to decrease within 8 h of dexamethasone administration, which occurred before any additional antibiotic dose. Ionized calcium normalized with steroid administration (Table 4), albumin improved by day 31 (Table 1), and thyroglobulin autoantibodies returned to baseline by day 64 (Table 3). Moreover, the lung nodules and splenic foci also regressed on steroid therapy but did not appear antibiotic-responsive.

Alternative diagnoses were systematically excluded. Alternative diagnoses were systematically excluded. Deep cervical infection or abscessation was considered unlikely given the lack of response to 4 days of broad-spectrum antibiotics and the rapid improvement following steroid administration. A migrating foreign body typically causes unilateral tract and focal abscess, but not bilateral thyroid necrosis and systemic pulmonary lesions. Neoplastic processes such as thyroid carcinoma or lymphoma, were considered, but the imaging findings (bilateral, cavitated, and non-invasive) and rapid resolution with steroids are not typical for malignancy. Deep sterile panniculitis normally causes diffuse subcutaneous fat inflammation with a waxing and waning course, unlike the rapid, localized changes seen here. Myxedema coma, a consideration for obtundation and bradycardia in severe hypothyroidism, was unlikely given the rapid rebound in mentation, normothermia, and absence of classic skin changes (non-pitting thickening of skin and subcutaneous tissues). Metastatic carcinoma was ruled out due to the absence of invasive margins on CT, the absence of neoplastic cells on cytology, the response to steroids, and clinical progression. Granulomatous infections, including fungal and mycobacterial diseases, would be expected to progress on immunomodulatory steroid therapy or reappear after antibiotics are stopped; negative cultures and persistent lesion quiescence of antimicrobials argue against these possibilities. Foreign-body reactions are typically unilateral and associated with identifiable material; none of these features were present. Human granulomatous thyroiditis may respond to steroids but lack widespread systemic pyogranulomas and necrotizing lesions. The systemic, multi-organ pyogranulomatous inflammation, rapid steroid response, and absence of characteristic histology effectively rule out classic granulomatous thyroiditis in this case.

The main limitation remains the absence of thyroid histopathology, since cavitation and necrosis precluded follicle sampling. Nevertheless, CT initially showed distorted yet identifiable thyroid lobes with diffuse hypoattenuation indicative of inflammatory thyroiditis, and follow-up imaging showed progressive atrophy consistent with immune-mediated destruction. That pattern implies that some residual functional tissue is present. Documentation of histologic changes in the thyroid gland, quantification of the serum IgG4 concentration, investigation for IgG4-positive plasma cells and other mechanisms of inflammation within the tumoral masses, and additional evaluation for the inciting cause of the response would strengthen the description of this case, but were not possible. Evaluation of these facets in future cases with a similar presentation is recommended to confirm SRIMT as a distinct entity and characterize the involved pathology. Furthermore, as this is a single case report, the true incidence of this condition cannot be determined, and the lack of long-term evaluation means the ultimate clinical course and prognosis are unknown. Conducting multi-center studies to establish relevant databases for a case series would be invaluable for confirming SRIMT as a distinct entity, establishing its prevalence, and fully characterizing the involved pathology. Nonetheless, the abrupt clinical onset, cavitated thyroid lesions, systemic sterile pyogranulomas, marked thyroglobulin autoantibody titers, serum IgG4 elevations, and sustained glucocorticoid response together support an immune-mediated origin. The sustained normalization of thyroid hormones, resolution of cervical swelling, and regression of pulmonary lesions under combined levothyroxine and prednisolone therapy closely parallel the outcomes reported in human acute thyroiditis (4, 21, 24).

This report characterizes acute, steroid-responsive, immune-mediated thyroiditis in a dog that has not been previously described in veterinary medicine. The combination of abrupt, non-painful cervical masses with upper-airway noise, profound hypothyroidism, and sterile pyogranulomatous lesions in the lungs, lymph nodes, and perithyroidal tissues parallels the fulminant presentations seen in human acute or subacute thyroiditis. Diagnosis was established by CT demonstrating cavitated thyroid lobes, comprehensive endocrine testing, and IgG4-enriched serum protein electrophoresis and further supported by rapid, sustained remission with prednisone and levothyroxine. At the 7-month follow-up, all systemic lesions had resolved, and thyroid function remained stable, underscoring the effectiveness of combining immunomodulatory steroid therapy with hormone replacement. Although histologic confirmation was not obtained, the convergence of clinical, imaging, serologic, and therapeutic findings supports an immune-mediated origin. Clinicians should include SRIMT in the differential diagnosis of dogs presenting with acute cervical swelling and multi-organ inflammation. Further evaluation of this mechanism of thyroiditis in dogs is warranted.