The tonsils are lymphoid organs that act as sentinels for the nasopharyngeal region and can be prone to recurrent infection, particularly throughout early childhood. We hypothesise that some cases of tonsillar hyperplasia may be driven by local production of bacterial superantigens (SAg), potent toxins that activate T cells and are best known as the causal agents of toxic shock syndrome and food poisoning. SAgs stimulate non-antigen specific T cell activation through dual specificity for selected TCR Vβ family members and MHC class II. Staphylococcus aureus and Group A Streptococcus (GAS) are common colonisers of the nasopharyngeal region and produce multiple SAgs. Tonsil tissue collected from 81 patients undergoing surgery for recurrent tonsillitis or obstructive sleep apnoea was cultured for aerobic bacteria using standard techniques. S. aureus was cultured from 41/81 (50%) and GAS from 8/81 (10%) of patients. The S. aureus isolates were profiled for SAg genes by multiplex PCR and 22 contained genes for potent Staphylococcal Enterotoxins (SE). Notably, SEC was detected in 11/22 of these isolates. Culture supernatants from isolates containing genes encoding for one or more potent staphylococcal SAg genes were verified as highly mitogenic in a T cell proliferation assay. Tonsil TCR Vβ subsets were profiled by flow cytometry and a skewed distribution of TCR Vβ subsets suggestive of SAg activity detected in 23/81 patients. S. aureus and GAS were confirmed to occupy an invasive location by immuno-histology, either in micro-colonies within the tonsillar tissue, or scattered throughout the tonsil tissue. Collectively these preliminary results suggest potential involvement of bacterial SAgs, particularly staphylococcal SAgs, in tonsillar hyperplasia. A better understanding of the significance of SAgs – and the possibility that S. aureus is a major source of these toxins in tonsil tissues – may lead to improved medical treatments for both recurrent tonsillitis and tonsillar hyperplasia.