Peritonsillar abscess may not always be a complication of acute tonsillitis: A prospective cohort study.

The present study aimed to specify diagnostics for peritonsillar abscesses (PTAs) and to clarify the role of minor salivary glands. This prospective cohort study included 112 patients with acute tonsillitis (AT) and PTA recruited at a tertiary hospital emergency department between February and October 2017. All patients completed a questionnaire concerning their current disease. Serum amylase (S-Amyl) and C-reactive protein (S-CRP) levels, tonsillar findings, and pus aspirate samples and throat cultures were analyzed. Eight of 58 PTA patients (13.8%) had no signs of tonsillar infection. The absence of tonsillar erythema and exudate was associated with low S-CRP (p<0.001) and older age (p<0.001). We also observed an inverse correlation between S-Amyl and S-CRP levels (AT, r = -0.519; PTA, r = -0.353). Therefore, we observed a group of PTA patients without signs of tonsillar infection who had significantly lower S-CRP levels than other PTA patients. These findings support that PTA may be caused by an etiology other than AT. Variations in the S-Amyl levels and a negative correlation between S-Amyl and S-CRP levels may indicate that minor salivary glands are involved in PTA development.

Peritonsillar Abscess: Complication of Acute Tonsillitis or Weber's Glands Infection?

OBJECTIVE: To review the literature concerning the 2 primary hypotheses put forth to explain the pathogenesis of peritonsillar abscess: "the acute tonsillitis hypothesis" (peritonsillar abscess is a complication of acute tonsillitis) and "the Weber gland hypothesis" (peritonsillar abscess is an infection of Weber's glands). DATA SOURCES: PubMed, EMBASE. REVIEW METHODS: Data supporting or negating one hypothesis or the other were elicited from the literature. CONCLUSIONS: Several findings support the acute tonsillitis hypothesis. First, the 2 main pathogens in peritonsillar abscess have been recovered from pus aspirates and bilateral tonsillar tissues with high concordance rates, suggesting that both tonsils are infected in patients with peritonsillar abscess. Second, studies report signs of acute tonsillitis in the days prior to and at the time of peritonsillar abscess. Third, antibiotic treatment reduces the risk of abscess development in patients with acute tonsillitis. However, some findings suggest involvement of the Weber's glands in peritonsillar abscess pathogenesis. First, high amylase levels have been found in peritonsillar pus. Second, the majority of peritonsillar abscesses are located at the superior tonsillar pole in proximity of the Weber's glands. We propose a unified hypothesis whereby bacteria initially infect the tonsillar mucosa and spread via the salivary duct system to the peritonsillar space, where an abscess is formed. IMPLICATIONS FOR PRACTICE: Our findings support the rationale for antibiotic treatment of patients with severe acute tonsillitis to reduce the risk of abscess development. Improved understanding of peritonsillar abscess pathogenesis is important for the development of efficient prevention strategies.

Multiple suppurative cystic lesions of the lips and buccal mucosa: a case of suppurative stomatitis glandularis.

Cheilitis glandularis (CG) is a rare inflammatory salivary gland disease that usually affects the lips. Although the etiology of CG is still unknown, it is believed to be a hereditary disease with an autosomal dominant pattern of inheritance. Three clinical presentations of CG are described in the literature: simple, superficial suppurative, and deep suppurative. A case of deep suppurative CG that extended to the buccal mucosa has been previously reported as suppurative stomatitis glandularis (SSG). Here we report a case of SSG in a 64-year-old white female with a history of bilateral renal transplants for adult polycystic kidney disease, who presented with painful swollen lips and bilateral buccal mucosal lesions. The diagnosis and management of the case is discussed. To the best of our knowledge, this is the second report of SSG, a rare condition affecting the minor salivary glands in the oral cavity.

[Investigation of the infectious route of peritonsillar abscess].

One hundred and thirty-one cases of peritonsillar abscess were studied to investigate the pathogenesis and the infectious route. The involved tonsils were resected in 83 patients. The surface of the resected tonsils was smooth and intact, neither ulceration nor pustular sinus was found on the surface of the upper part of these tonsils. There were some inflammatory and/or fibrotic minor salivary glands (Weber's glands) on the top of the quinsy tonsils. The glands adjacent to the tonsils of non-quinsy patients had normal appearance. It suggests that the origin of peritonsillar infection might be the Weber's glands rather than extension from acutely inflamed tonsil.

[Interrelationship between Epstein-Barr virus and Sjögren's syndrome].

We designed a specific primer of EB virus Bam W fragment and EBV DNA sequence by using the polymerase chain reaction (PCR) to amplify the EBV DNA sequences and then performing the hybridization analysis (dot blot and Southern transfer) with a gamma 32P end-labelled internal oligonucleotide probe. There was a significantly higher positive rate of 24% (7/29) for the labial glands of Sjögren's syndrome patients than 68% (20/29) for gamma 32P Bam W probe. In situ DNA hybridization, with (alpha 35S) DCTP labelled EBV DNA probe, the EBV genomes were demonstrated in the labial glands of the Sjögren's syndrome patients (16/28). Moreover, the elevated content of EBV DNA was identified in those with more severe destruction of labial glands. We conclude that EBV has a normal site of latency at salivary glands in a nonpathogenic state, and may be reactivated in Sjögren's syndrome patients and play a role in the pathogenesis of this disease. The great sensitivity of PCR and the ability to analyze very small tissue biopsies (fresh or paraffin-embedded) make this technique applicable to clinical diagnosis.

Persistence of Epstein-Barr virus in salivary gland biopsies from healthy individuals and patients with Sjögren's syndrome.

Salivary gland biopsies from 12 patients with primary Sjögren's syndrome and 10 controls were examined for Epstein-Barr virus (EBV) DNA by in-situ hybridization and for EBV proteins by immunofluorescence and peroxidase techniques. Viral DNA was found in biopsies from two out of 12 patients with primary Sjögren's syndrome and six out of the 10 controls. The DNA and early antigen were in epithelial cells lining the ducts and acini, early antigen expression being limited to the luminal side of the epithelium. In eight biopsies studied with other antibodies, membrane antigen was identified in both acini and ducts but viral capsid antigen and Epstein-Barr nuclear antigen were not detected. EBV was found in biopsies from five of the controls without inflammation or Class II expression. This suggests that, in health, persistence and replication occur without inducing an immune response, possibly due to the restricted expression of early antigen on the luminal of the epithelium, away from immune surveillance. The inflammation in Sjögren's syndrome could be due to a breakdown of this unusual mechanism for viral persistence leading to a vigorous immune response to the virus. However our study provides no evidence to suggest that EBV infection load is increased in this disease.