Infectious thyroiditis is also known as acute thyroiditis, suppurative thyroiditis, bacterial thyroiditis, and pyogenic thyroiditis (Table 1). Bacterial infections of the thyroid are rare, with only 224 cases having been reported in the literature from 1900 to 1980 and only 60 cases reported in the paediatric literature. Bacterial infections are the aetiology of most cases of infectious thyroiditis and the infections are generally suppurative and acute. Infectious thyroiditis caused by fungal and parasitic infections are more frequently chronic and indolent. In this section, emphasis will be placed on bacterial infections.
Table1. Comparison between the syndromes of thyroiditis
Aetiology and Pathogenesis
The thyroid gland’s high iodine content, significant vascularity, lymphatic drainage, as well as its protective capsule provide the thyroid gland with notable resistance to infection. The most common predisposing factor to infections of the thyroid appears to be pre- existing thyroid disease. Simple goitre, nodular goitre, Hashimoto’s thyroiditis, or thyroid carcinoma has been observed in up to two- thirds of women and one- half of men with infectious thyroiditis. Patients with HIV infection are a population particularly at risk for bacterial thyroiditis. As with other opportunistic infections in patients with HIV infection, infections of the thyroid gland are often chronic and insidious in onset.
In the adult, Staphylococcus aureus and Streptococcus pyogenes are the offending pathogens in about 40% of patients (Table 2). In children, α - and β - haemolytic streptococcus and a variety of anaerobes account for about 70% of cases, while mixed pathogens are identified in over 50% of cases. In comparison to an earlier review examining all reported cases of suppurative thyroiditis up until 1983, the most recent review reports that fungal infections are exceedingly rare and syphilitic infections have not been recently reported. Cases of thyroidal infections with methicillin- resistant Staphylococcus aureus (MRSA) have been reported. Other thyroidal bacterial pathogens that have been shown to cause infectious thyroiditis include Salmonella Actinomyces, Actinobacillus actinomycetemcomitans, Brucella melitensis, Clostridium septicum, Eikenella corrodens, Enterobacter, Escherichia coli, Haemophilus influenzae, Klebsiella, Pseudomonas aeruginosa, Serratia marcescens, and Acinetobacter baumannii.
Infection and suppuration may result from direct spread from a nearby infection, or via the bloodstream or lymphatics. The seminal observation regarding the pathogenesis of bacterial thyroiditis was made in 1979 when Takai et al. reported seven cases of infectious thyroiditis due to a fistula originating from the left pyriform sinus. Subsequently, multiple case series of patients with infectious thyroiditis have described pyriform sinus fistulae, primarily left- sided, especially in those with recurrent episodes. Additional reports identified infected embryonic cysts from the third and fourth brachial pouches and thyroglossal duct cysts as routes of thyroidal infection. On pathological examination, characteristic changes of acute bacterial inflammation, including necrosis and abscess formation, are frequently seen.
Clinical Manifestations
Bacterial thyroiditis is often preceded by an upper respiratory tract infection, which may induce inflammation of the fistula and pro mote the transmission of pathogens to the thyroid. Consistent with these observations, bacterial thyroiditis is more common in the late autumn and late spring. Over 90% of patients will present with thyroidal pain, tenderness, fever, and local compression resulting in dysphagia and dysphonia; the pain is often referred diffusely to adjacent structures. Systemic symptoms such as fever, chills, tachycardia, and malaise may be present.
Laboratory and Radiologic Findings
Thyroid function tests are usually normal; however, cases of hypothyroidism and thyrotoxicosis have been reported and thyroid function should be assessed. A nuclear medicine thyroid scan may show the suppurative region as a ‘cold’ area, whereas an ultrasound examination may demonstrate a hypoechoic lesion . The poly morphonuclear leucocyte count and the sedimentation rate are usually elevated. The organism frequently can be identified by Gram’s stain and culture.
Diagnosis
The diagnosis is made with a fine- needle aspiration, Gram’s stain, and culture. Symptomatically, infectious thyroiditis may be difficult to differentiate from subacute thyroiditis in the early phases, although the characteristic thyroid function changes in the latter disease should be helpful in discriminating between the two. Leucocytosis and an elevated ESR are not discriminatory tests as they are commonly observed in both subacute thyroiditis and infectious thyroiditis. In general, patients with bacterial thyroiditis have a greater febrile response than those with subacute thyroiditis. Once abscess formation has occurred, the local redness, lymphadenopathy, hyperpyrexia, and leucocytosis should lead to the correct diagnosis. Malignant neoplasms and haemorrhages into cysts may sometimes present with manifestations that mimic this disorder.
Course and Management
The prognosis of bacterial thyroiditis is often dependent on the prompt recognition and treatment of this disorder, as mortality may approach 100% if the diagnosis is delayed and appropriate anti microbial therapy is not instituted. Much depends upon the identification of the microorganism either from needle aspirate, incision, and drainage, or occasionally from blood culture. If no organisms are seen on the Gram’s stain, nafcillin and gentamicin or a third- generation cephalosporin is appropriate initial therapy in adults while clindamycin or a penicillin with a β- lactamase inhibitor is reasonable in children. If an abscess develops and prompt response to antibiotics does not occur, incision and drainage is necessary. Sometimes partial lobectomy must be performed, especially if the disease is recurrent. Usually the lesions heal with reasonable speed after initiation of the correct antimicrobial agent, and recurrences are uncommon. Mortality from acute bacterial thyroiditis has markedly improved from the 20– 25% reported in the early 1900s, with an extensive review by Berger estimating an overall mortality of 8.6%. A ten- year review involving over 100 patients failed to list mortality as a complication of acute bacterial thyroiditis.
