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Over the past several decades, changes have occurred in the bacterial flora of the oral cavity that directly reflect the identification of organisms in ABP. In part, this change is evident due to the increased incidence of nosocomial and opportunistic infections in patients who are immunocompromised as well as those critically ill patients in hospital intensive care units whose mouths became colonized with microorganisms that were previously only rarely found in the oral cavity (Figure 3.4). Moreover, improved culturing techniques have permitted the identification of anaerobes that were previously difficult to recover in the microbiology laboratory. Finally, the occasionally indiscriminate use of antibiotics has allowed for the occupation of other organisms in the oral cavity such as Gram negative enteric organisms. Bacterial Darwinism has also occurred such that iatrogenically and genetically altered staphylococcal organisms have developed penicillin resistance.

Acute bacterial parotitis has two well‐defined presentations, hospital acquired (Figure 3.4) and community acquired (Figure 3.5) variants. Numerous factors predispose the parotid gland to sialadenitis. Retrograde infection is recognized as the major cause of ABP. Resulting from acute illness, sepsis, trauma, or surgery, depleted intravascular volume may result in diminished salivary flow that in turn diminishes the normal flushing action of saliva as it passes through Stensen duct. Patients with salivary secretions of modest flow rates show bacteria at the duct papillae and in cannulated ducts, while patients with salivary secretions of high rates show bacteria at the duct papillae but not within the duct (Katz et al. 1990). In a healthy state, fibronectin exists in high concentrations within parotid saliva, which promotes the adherence of Streptococcus species and Staphylococcus aureus around the ductal orifice of the Stensen duct (Katz et al. 1990). Low levels of fibronectin such as those occuring in the unhealthy host are known to promote the adherence of Pseudomonas and Escherichia coli. This observation explains the clinical situation whereby colonization resulting from dehydration leads to a Gram positive sialadenitis in ABP compared to the development of Gram negative sialadenitis of the parotid gland in immunocompromised patients (Miloro and Goldberg 2002). Depending on the health of the host, therefore, specific colonized bacteria can infect the parotid gland in a retrograde fashion. Hospital acquired ABP still shows cultures of Staphylococcus aureus in over 50% of cases (Goldberg and Bevilacqua 1995). Methicillin‐resistant Staphylococcus aureus should be ruled out in this population of inpatients. Critically ill and immunocompromised inpatients may also show Pseudomonas, Klebsiella, Escherichia coli, Proteus, Eikenella corrodens, Haemophilus influenzae, Prevotella and Fusobacterium species. Postoperative parotitis has been reported from 1 to 15 weeks following surgery, but most commonly occurs within 2 weeks after surgery (McQuone 1999). The peak incidence of this disease seems to be between postoperative days 5 and 7.

Community acquired ABP is diagnosed five times more commonly than hospital acquired ABP and is diagnosed in emergency departments, offices, and outpatient clinics. This variant of ABP is most commonly associated with staphylococcal and streptococcal species. As community acquired methicillin‐resistant Staphylococcus aureus becomes more common in society, this organism will become more prevalent in community acquired ABP. Etiologic factors in community acquired ABP include medications that decrease salivary flow, trauma to Stensen duct, cheek biting, toothbrush trauma, trumpet blower's syndrome and medical conditions such as diabetes, malnutrition, and dehydration from acute or chronic gastrointestinal disorders with loss of intravascular volume. Sialoliths present in Stensen duct with retrograde infection are less common than in Wharton duct, but this possibility should also be considered in the patient with community acquired ABP.