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Acute infection can involve any salivary gland, although the major salivary glands (parotid, submandibular, and sublingual glands) are affected far more often than the minor salivary glands. This article will review the pathogenesis of bacterial and viral infections of the salivary glands, as well as the epidemiology and predisposing conditions associated with these disease processes. The clinical features, diagnostic evaluation, treatment, complications and prognosis of bacterial and viral infections of the salivary glands will be discussed. Additional causes of acute salivary inflammation, such as granulomatous disease, autoimmune conditions, and neoplasms, are reviewed elsewhere, as are chronic infectious processes. Because the parotid gland is subject to acute infection more commonly than any other salivary tissue, this article also will review factors accounting for the parotid gland's predilection for infection.
ACUTE BACTERIAL INFECTION OF THE SALIVARY GLANDS
Introduction
The earliest report of acute bacterial sialadenitis dates back to 1828, describing a 71-year-old gentleman with a parotid infection that progressed to gangrene.
Awareness of acute salivary infection was increased in 1881, when President Garfield died from acute parotitis following abdominal surgery and associated systemic dehydration.
With the advent of antibiotic therapy, mortality rates decreased, but acute bacterial parotitis remains a formidable infection. Present day mortality rates are cited at 20% to 50%.
Acute bacterial infections of the salivary glands result from two important physiologic mechanisms. First, retrograde contamination of the salivary ducts and parenchymal tissues by bacteria inhabiting the oral cavity provides a bacterial source of infection.
Second, stasis of salivary flow through the ducts and parenchyma promotes acute suppurative infection. This process can affect any of the major salivary glands, but most commonly involves the parotid gland.
The parotid gland's predilection for infection is attributed to several physiologic and anatomic factors. The composition of parotid secretions differs from those derived from the submandibular and sublingual glands. Saliva produced from the parotid gland is primarily serous, whereas that originating from the submandibular and sublingual glands has a greater proportion of mucinous material. Mucoid saliva contains many elements that protect against bacterial infection, including lysosomes and IgA antibodies, which serve an antimicrobial function. Mucins also contain sialic acid, which agglutinates bacteria, preventing its adherence to host tissues. Finally, specific glycoproteins found in mucins bind epithelial cells, competitively inhibiting bacterial attachment to these cells.
In addition to salivary composition, anatomic factors may play a minor role in the predilection of bacterial infections for the parotid gland. Stensen's duct lies adjacent to the upper mandibular molars, whereas Wharton's duct rests on the floor of the mouth near the tongue. Tongue mobility may prevent salivary stasis in the area of Wharton's ducts, reducing the rate of infections involving the submandibular gland.
Sialolithiasis can produce mechanical obstruction of the duct, resulting in salivary stasis and subsequent bacterial infection. Calculus formation is associated frequently with acute bacterial infections of the submandibular gland because Wharton's duct is far more likely to harbor a calculus than Stensen's duct. Eighty-five percent to 90% of salivary calculi are located in the submandibular duct.
Submandibular secretions are more mucinous than parotid secretions, and therefore more viscid. They also are more alkaline, containing a higher percentage of calcium phosphates. These characteristics contribute to the formation of submandibular calculi.
Despite the submandibular gland's predisposition for calculus formation, the parotid gland remains the most common site of acute suppurative salivary infection.
Epidemiology/Risk Factors
Numerous factors are associated with salivary stasis and increased risk for acute suppurative infection of a salivary gland. Systemic dehydration is a classic cause of salivary stasis in postoperative patients.
Many surgical procedures are associated with uncompensated losses of blood and body fluids. The majority of both upper and lower aerodigestive tract procedures require patients to be routinely maintained without oral intake postoperatively. Consequently, these patients are without regular salivary stimulation. Acute bacterial parotitis in this population is well-documented,
Suppurative parotitis has been linked so closely to prior surgical procedures that it is known also as surgical parotitis or postoperative parotitis. Patients undergoing major abdominal surgery and repair of fractured hips also were noted to be particularly susceptible to postoperative dehydration.
Postoperative parotitis has been reported from 1 to 15 weeks following surgery, but most commonly appears within 2 weeks after the procedure. The peak incidence of this disease occurs between postoperative days 5 and 7.
Several cases of postoperative parotitis, however, have been reported to occur in the immediate postoperative period, and were observed in the recovery room. These cases were associated with spinal anesthesia, which causes a peripheral vasodilatation that can lead to hypovolemia and dehydration.
In addition to postoperative dehydration, patients with chronic, debilitating medical conditions and those with compromised immune function demonstrate increased risk for the development of acute parotitis. An increased incidence of acute salivary gland infections also has been noted in the human immunodeficiency virus (HIV) population.
The medical illnesses predisposing to acute salivary infection are:
Hepatic failure
Renal failure
Diabetes mellitus
Hypothyroidism
Malnutrition
HIV
Sjögren's syndrome
Depression
Anorexia/bulimia
Hyperuricemia
Hyperlipoproteinemia
Cystic fibrosis
Lead intoxication
Cushing's disease
Many commonly prescribed medications, including antihypertensives, antihistamines, and antidepressants, have been associated also with acute bacterial sialadenitis. These medications contribute to oral or systemic dehydration by a variety of mechanisms, including anticholinergic and diuretic effects. The medications predisposing to acute salivary infection are:
Antihistamines
Diuretics
Tricyclic antidepressants
Phenothiazines
Beta blockers
Barbiturates
Anticholinergics
Several psychiatric conditions have been linked to acute salivary infections, posing additional risk independent of that associated with many psychoactive medications. The anorexia and adipsia commonly seen in depressed patients can result in dehydration.
Mechanical obstruction of salivary outflow also predisposes to acute infection. Salivary calculi commonly arise from Wharton's ducts, as discussed, and can contribute to the development of acute infection of the submandibular gland. Sialolithiasis, however, generally is associated with chronic, recurrent salivary gland infections rather than acute suppurative processes.
Mucous plugs obstructing the salivary ducts may be allergy-mediated. Systemic eosinophilia and eosinophil-rich mucous plugs have been associated with acute bacterial parotitis in children,
Stenosis or stricture of the salivary ducts because of previous infection or trauma can cause mechanical ductal obstruction, as can a foreign body. Feathers, food particles, and grass seeds have been reported to obstruct the salivary ducts, resulting in acute bacterial infection.
Sialectasis, or salivary ductal dilation, increases the risk for retrograde contamination. Sialectasis is associated with a number of conditions ranging from cystic fibrosis to pneumoparotitis. Pneumoparotitis is a rare condition generally related to activities generating high intraoral pressure, such as trumpet playing and glass blowing, and has been linked to acute sialadenitis.
Although bacterial parotitis can affect individuals of any age, several age groups are at increased risk for this condition. Neonatal suppurative parotitis is a well-known entity, generally occurring in the first 2 weeks of life.
who demonstrate a greater propensity for dehydration than term infants. Unlike parotitis in the adult population, neonatal parotitis is often bilateral.
and nutritional status is often poor in this age group. Patients in the sixth and seventh decades often suffer chronic debilitating medical illnesses and require treatment with medications predisposing to salivary gland infections. Recovery from surgical procedures generally is more tenuous in this group, where comorbidities such as congestive heart failure and renal insufficiency often limit fluid resuscitation. The risk factors for acute bacterial infection of the salivary glands are:
Dehydration
Recent surgery
Recent anesthesia
Advanced age
Prematurity (infants)
Prior radiation therapy
Immune compromise
Medical illness
Medications
Sialolithiasis
Sialectasia
Septic focus in oral cavity
Oral cavity neoplasm
Tracheostomy
Pneumoparotitis
Ductal foreign body
Bacteriology
Staphylococcus aureus is the most common bacterial cause of acute suppurative parotitis and has been cultured in 50% to 90% of cases.
Streptococcal species, including Streptococcus pneumoniae and Streptococcus pyogenes (beta-hemolytic streptococcus), as well as Haemophilus influenzae, have been recognized as common causes of acute pyogenic sialadenitis.
Less frequently, gram-negative organisms, including Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa, have been cultured from salivary gland infections.
In Southeast Asia, Pseudomonas pseudomallei, an organism found in soil and surface water, is a common cause of acute parotitis, especially in children.
More recently, the importance of anaerobic organisms in acute bacterial infections within the salivary glands has been recognized. Bacteroides, peptostreptococcal, and fusobacterial species have been cultured from as many as 43%.
The apparent increase in incidence of strictly anaerobic organisms is likely secondary to improved culture techniques rather than a change in microbiology.
Others postulate that this increase in anaerobic and gram-negative organisms reflects nosocomial disease, because this infection demonstrates a predisposition for debilitated and postsurgical patients likely to be hospitalized.
Cases of unusual pathogens generally are identified in infections of the parotid gland, because 92% of acute submandibular infections are community acquired, resulting from the more common staphylococcal and streptococcal species.
have been reported as extremely rare etiologic agents in acute parotitis, but tuberculosis and syphilis usually are associated with a painless, chronic salivary gland infection that can be confused with neoplasm.
Clinical Presentation
Patients with acute salivary infection complain of localized symptoms, including sudden onset of pain and swelling overlying the affected gland. Although primarily a unilateral disease, acute salivary gland infection is bilateral in 10% to 25% of cases.
Symptoms may be exacerbated by meals. A review of the patient's medical history may reveal one or more of the risk factors for acute salivary infection. Knowledge of the patient's intake and output can help confirm dehydration, one of the most significant risk factors for this infection.
Physical examination reveals induration, erythema, edema, and extreme tenderness over the cheek and angle of the mandible in parotid infections (Fig. 1), and over the submandibular triangle in infections of the submandibular gland. Intraorally, Stensen's or Wharton's ducts may appear erythematous or inflamed, and massage of the affected salivary gland may express pus from the respective ductal orifice. In cases of early infection or ductal obstruction, however, purulence will not be visualized. Fluctuance is rarely palpable externally, especially in parotid infections. The dense fibrous nature of the enveloping fascia restricts the disease to diffuse parenchymal involvement rather than discrete abscess formation. In submandibular infections, a calculus may be palpable along the course of Wharton's duct.
Figure 1Patient with acute suppurative infection of the left parotid gland, demonstrating significant swelling of the gland.
Signs of local or systemic dehydration may be present as well. The mucous membranes of the oral cavity may appear dry or crusted, indicating reduced salivary flow, and skin turgor may be reduced.
Association with systemic sepsis is far more common to infections of parotid gland, compared to those of the submandibular gland. The tendency for more severe infection to arise from the parotid gland reflects both the greater overall incidence of infection in this gland, and the propensity for parotitis to occur in a more debilitated population, as described previously. Patients with acute suppurative parotitis may appear toxic and display high fever, profound dehydration, and even delirium. Patients may ultimately develop signs of multiorgan system failure.
Diagnostic Evaluation
Acute salivary gland infection is primarily a clinical diagnosis, and additional testing is rarely contributory. In critically ill patients, or in those failing to respond to conventional therapy, further diagnostic evaluation is indicated.
Laboratory evaluation in patients with acute sialadenitis will reveal an elevated white blood cell count with a predominance of neutrophils. Serum amylase is generally within normal limits.
If an abscess collection is suspected based on physical findings or lack of response to treatment, needle aspiration can be employed diagnostically. Cultures should be obtained on all aspirated material.
Imaging studies are not recommended initially, but failure to improve after 48 hours of aggressive medical therapy is an indication for obtaining a CT, MR imaging, or ultrasound to exclude abscess formation. Sialography is contraindicated in the setting of acute infection of the salivary gland, and has been reported to trigger episodes of sialadenitis.
Because progression to abscess formation is rare, imaging studies typically reveal diffuse inflammation of the affected gland (Fig. 2), or may identify a calculus within the gland (Fig. 3). The majority of submandibular calculi are radiopaque, whereas parotid calculi are generally radiolucent.
In patients not responding to standard therapy, the diagnostic evaluation is expanded to exclude disease processes that mimic acute bacterial sialadenitis. Lymphoma,
have been confused with acute bacterial sialadenitis. To identify these nonbacterial causes of acute salivary inflammation, additional laboratory testing (ANA, SS-A and SS-B antibodies, RF, and ANCA) and imaging may be useful (Fig. 4). Fine needle aspiration biopsy or, in some cases, removal of the affected gland, may be necessary to obtain a tissue diagnosis. The evaluation of viral infections is discussed separately.
Figure 4Axial CT image of a patient with a right intraparotid lymph node (arrow) secondary to cat-scratch disease. The patient was initially diagnosed with acute suppurative parotitis.
Treatment of acute sialadenitis is directed at reversal of the underlying medical conditions responsible for the infection and initiation of appropriate antimicrobial therapy. Antisialogogic medications are discontinued whenever possible. Attempts must be made to reverse salivary stasis and stimulate salivary flow by application of warm compresses, maximization of oral hygiene and mouth irrigations, and administration of sialagogues, such as lemon drops or orange juice. External or bimanual massage of the gland both intraorally and externally should be employed if the patient can tolerate these measures. When neither saliva nor pus can be expressed from Stensen's duct, cannulation and serial dilation of the duct with lacrimal probes can establish ductal patency.
Antimicrobial therapy initially is directed toward the gram-positive and anaerobic organisms identified as common causes of acute bacterial sialadenitis. Over 70% of organisms cultured produce beta-lactamase or penicillinase.
Augmented penicillins (Augmentin and Unasyn) contain beta-lactamase inhibitors (clavulanate and sulbactam), whereas antistaphylococcal penicillins (oxacillin, dicloxacillin, and methicillin) and second generation cephalosporins are penicillinase resistant. Any one of these antibiotics can be used for the treatment of acute sialadenitis. Some authors have suggested combining these agents with metronidazole,
or, alternatively, using clindamycin to broaden coverage against anaerobic organisms.
Treatment is administered orally in the absence of systemic illness, but failure to respond within 48 hours is an indication for administration of an intravenous antibiotic. If cultures were obtained from Stensen's or Wharton's duct or from needle aspiration of the gland, results are used to further direct specific antibiotic therapy. In recalcitrant infections, a third generation cephalosporin may be added to enhance gram-negative coverage. Some even advocate the addition of an aminoglycoside in critically ill patients.
The preponderance of methicillin-resistant S aureus (MRSA), particularly in nosocomial and nursing home environments, has prompted the recommendation of vancomycin for patients in these groups.
The role of surgery in the treatment of acute bacterial sialadenitis is limited. When a discrete abscess is identified (Fig. 5), surgical drainage is undertaken. A small population of patients without discrete abscess who are refractory to nonoperative interventions may be candidates for surgical exploration, if their medical condition permits. The gland is approached with a standard, anteriorly based facial flap, and multiple, superficial, radial incisions are created in the parotid fascia parallel to the facial nerve branches. The wound is loosely approximated over a drain. The central aspect of the wound is often allowed to heal by secondary intention. Surgery occasionally is indicated for tissue diagnosis in a select group of patients not responding to standard therapy to identify one of the conditions mimicking acute sialadenitis.
Figure 5Axial CT image of a left parotid abscess (arrow).
Complications of acute bacterial salivary infections can result from direct extension of infection into surrounding tissues or from hematogenous spread of infection. Local infection can coalesce into abscess formation, and abscess ruptures into the facial tissues, external auditory canal, and temporomandibular joint (TMJ) have been reported.
The submandibular space and the parotid space both communicate directly with the deep neck spaces through the parapharyngeal space. Further, the fascial capsule surrounding the parotid gland displays anatomic weakness on the deep surface of the gland adjacent to the loose areolar tissues of the lateral pharyngeal wall.
Extension of an abscess into the parapharyngeal space may result in any of the complications associated with deep space neck abscesses, including airway obstruction, mediastinitis, internal jugular vein thrombosis, and carotid artery erosion. Pneumonia may result from aspiration of an abscess rupturing into the airway. Diffuse, necrotizing mediastinitis has been reported also.
Dysfunction of one or more branches of the facial nerve is a rare complication of acute parotitis. Secondary to perineuritis or direct neural compression,
Gradual onset of facial weakness in the setting of acute parotitis may herald the presence of an abscess, and a lower threshold for surgical exploration is warranted in such patients.
In addition, these patients must be followed until complete resolution of facial weakness is documented, because this symptom more commonly is associated with neoplasm.
Because of the underlying debilitation of most patients afflicted with bacterial parotitis, the most ominous consequences of this infection are systemic. Acute parotitis can lead rapidly to systemic sepsis. Further progression to septic shock or multisystem organ failure is nearly universally fatal in these patients.
Prognosis
The prognosis of acute bacterial sialadenitis is variable, and primarily related to the medical condition of the afflicted patient. In patients with significant identifiable risk factors, this infection is a predictor of poor prognosis, associated with a 20% to 50% mortality.
In healthy patients, early recognition and timely initiation of therapeutic interventions generally lead to complete resolution of infection without adverse sequelae. A small number of patients suffer from chronic recurrent parotitis, likely secondary to ductal stenosis sustained during the initial infection. These cases will require formal parotidectomy, ideally performed at a time when inflammation and infection are minimal.
ACUTE VIRAL INFECTION OF THE SALIVARY GLANDS
Introduction
The term “mumps” classically designates a viral parotitis caused by the paramyxovirus, but a broad range of viral pathogens have been identified as causes of acute viral infection of the salivary glands. Derived from the Danish mompen, meaning mumbling, the name was given to describe the characteristic muffled speech that patients demonstrate because of glandular inflammation and trismus. The pathogenesis, clinical presentation, and diagnostic evaluation of acute viral infections of the salivary glands will be discussed in this section, and contrasted to those of acute bacterial salivary infections.
Pathogenesis
As opposed to bacterial sialadenitis, viral infections of the salivary gland are systemic from the onset. The virus is endemic in the community, spread by air-borne droplets, and enters the body through the upper respiratory tract. Patients experience a 2 to 3 week incubation period after exposure, during which the virus multiplies in the upper respiratory tract or parotid gland, followed by a 3 to 5 day period of viremia. The virus then localizes to biologically active tissue, such as the salivary glands, germinal tissues, and the central nervous system.
Although the viruses causing the mumps syndrome demonstrate a strong predilection for parotid tissue, the infection can involve the submandibular or sublingual glands.
Adults rarely are infected because of immunity conferred by childhood exposure or measles-mumps-rubella vaccine. Prior to the widespread use of the live attenuated Jeryl Lynn vaccine, cases were clustered in epidemic fashion. Sporadic cases and smaller outbreaks are observed today, likely resulting from nonparamyxoviral infection, failure of immunity, or lack of vaccination.
Classic mumps syndrome is caused by paramyxovirus, an RNA virus related to the influenza and parainfluenza viruses. A variety of other viruses, however, have been cultured from the blood or salivary fluid in cases of acute viral parotitis. These include influenza and parainfluenza (types 1 and 3) viruses, Coxsackie viruses A and B, ECHO virus, and lymphocytic choriomeningitic virus.
also have been reported as causes of acute parotitis in patients with HIV disease. HIV involvement of the parotid glands is a rare cause of acute viral parotitis, and is associated more commonly with chronic, cystic parotid enlargement.
Approximately one third of patients experience prodromal symptoms prior to the development of parotitis consisting of headache, myalgias, arthralgias, anorexia, and malaise. The onset of salivary involvement is heralded by earache, followed by pain localized to the gland, trismus, and dysphagia. Pain often is exacerbated by stimulation of salivary flow during eating or chewing.
Physical examination reveals swelling of the involved salivary gland, which can become tense and firm, but not erythematous or warm. Swelling typically lasts 1 to 5 days, and can displace the ipsilateral pinna. In 75% of cases, swelling involves both parotid glands.
Systemically, the patient also may demonstrate low grade fever, especially during the prodromal period. A broad range of additional signs and symptoms result from viral involvement of the central nervous system or other glandular tissues.
Diagnostic Evaluation
In contrast to patients with acute bacterial sialadenitis, laboratory evaluation in patients with acute viral infection of the salivary glands reveals leukocytopenia with relative lymphocytosis, and an increased serum amylase.
Viral serology is essential to confirming a diagnosis of viral parotitis. Complement-fixing antibodies appear following exposure to the paramyxovirus. “S,” or soluble, antibodies directed against the nucleoprotein core of the virus, appear within the first week of infection, and peak within 2 weeks. S antibodies disappear within 8 to 9 months, and therefore are associated with active infection or recent vaccination. “V,” or viral, antibodies directed against the outer surface hemagglutinin, appear several weeks after the S antibodies, and persist at low levels for approximately 5 years following exposure. V antibodies, therefore, are associated with past infection, prior vaccination, and the late stages of active infection.
If initial serology is noncontributory, a nonparamyxovirus may be responsible for acute viral salivary infection. Antibody titers against such viral antigens as influenza, parainfluenza, Coxsackie viruses, ECHO viruses, and lymphocytic choriomeningitis (LCM) viruses can be obtained. A fourfold rise in antibody titer is diagnostic of acute infection. Rarely, the virus can be cultured from blood, saliva, breast milk, or cerebrospinal fluid (CSF). Blood tests for the HIV virus also should be obtained in these cases, because this disease has been a reported cause of acute parotid inflammation.
Of note, the mumps skin test is not useful in the diagnosis of acute infection, because dermal hypersensitivity does not develop until 3 or 4 weeks following viral exposure.
Imaging studies are not obtained routinely in cases of suspected viral salivary gland infection. CT or MR imaging is undertaken only when symptoms are protracted, or the presentation is atypical, as in cases of unilateral glandular involvement. Imaging studies in cases of viral salivary gland infection typically reveal diffuse glandular inflammation.
Treatment
Treatment of viral salivary gland infection is primarily supportive, including rest and adequate hydration, because the disease is self-limited. Antipyretics and anti-inflammatory medications are of benefit.
The most significant advancement in the treatment of mumps parotitis is prevention by vaccination. The live attenuated Jeryl Lynn vaccine became available in 1967.
Commonly combined with the measles and rubella vaccines, the mumps vaccine is administered in a single, subcutaneous dose after 12 months of age. It produces measurable antibody titers in 90% of recipients. No deaths and very few side effects have been associated with the vaccine.
Cases of mumps parotitis have been reported in immunized patients, and likely represent salivary infection with a nonparamyxovirus or, rarely, failed vaccination.
Complications of acute viral parotitis are not true complications of salivary infection, but rather relate to the systemic nature of the disease. As noted previously, the virus disseminates hematogenously, and can localize in a number of biologically active tissues. The following discussion pertains to classic paramyxoviral mumps syndrome. The other viruses responsible for acute parotitis are less common, and understanding of their associated complications is more limited.
Orchitis is the most common condition complicating paramyxoviral parotitis, occurring in 20% to 30% of males.
Involvement of germinal tissues does not appear to result in sterility. Mastitis affects 30% of females over the age of 15, and has been reported in association with decreased lactation.
This complication remains rare, however, because only 15% of cases occur in patients over 15. Aseptic meningitis occurs in 10% of patients affected with mumps, and asymptomatic meningeal inflammation is probably far more common. Five percent of patients experience pancreatitis.
of patients with mumps syndrome. The onset of deafness is rapid, and develops toward the end of the parotitis. Tinnitus, aural fullness, and vertigo often accompany the hearing loss, but these symptoms resolve over a period of several weeks. In contrast, the hearing loss is usually permanent, and is often profound. In 80% of cases, hearing loss is unilateral. There is no treatment currently available for mumps deafness, but for the 20% of patients with bilateral, profound, sensorineural hearing loss, cochlear implantation has been employed.
Additional complications of the mumps syndrome have been reported and include myocarditis, polyarthritis, hemolytic anemia, plasmacytosis, lymphocytic leukemoid reactions, and thrombocytopenia.
These associated conditions usually are self-limited, and resolve with or without steroid therapy.
Prognosis
Although the complications associated with viral salivary infection are generally self-limited, a very small number of patients experience permanent hearing loss, and isolated reports of fatalities secondary to mumps-associated complications have been made. The vast majority of patients experiencing an episode of acute viral infection of the salivary glands recover without specific treatment or adverse sequelae.
SUMMARY
Acute bacterial and viral infections of the salivary glands present with a broad spectrum of severity. The morbidity of bacterial infection depends largely on the medical condition of the patient. In high risk patients, this disease is associated with significant complications and mortality, whereas bacterial sialadenitis in an otherwise healthy patient generally responds to outpatient therapy. The majority of viral infections are caused by the paramyxovirus, and are associated with the mumps syndrome. Recognition of additional potential viral causes, as well as common sequelae of viral parotitis, is important for the clinician. Both bacterial and viral infections predominantly affect the parotid glands.
References
Ah-see K.W.
McLaren K.
Maran A.G.D.
et al.
Wegener's granulomatosis presenting as major salivary gland enlargement.
Address reprint requests to Shelly J. McQuone, MD, Department of Otorhinolaryngology–Head and Neck Surgery, University of Pennsylvania Health System, Pennsylvania Hospital, 800 Spruce Street, Philadelphia, PA 19107, e-mail: shmcqu@pahosp.com
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