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Woman With Fever, Hoarseness, and a Half-Swollen Face


A 55-year-old woman seen because of new lump under right side of her jaw; present for 24 hours. Associated neck discomfort causing dysphagia, and also a raspy turn to the voice; both much worse in last 12 hours. No dyspnea. No sore throat.


A 55-year-old woman seen because of new lump under right side of her jaw; present for 24 hours. Associated neck discomfort causing dysphagia, and also a raspy turn to the voice; both much worse in last 12 hours. No dyspnea. No sore throat.


Temperature of 38.5°C (101.5°F). Patient looks acutely ill but not toxic. Voice hoarse. Dentition, tongue, gums unremarkable. Marked point tenderness just anterior to tragus, posterior to dimple on right cheek. No stridor; lungs show good air exchange and no adventitious sounds.



Something has expanded the parotid space. Pus extruding from the Stensen duct would corroborate parotitis but is uncommon. We have enough evidence without it to diagnose parotitis. The remaining task is to decide whether this is viral mumps, an acute flare of chronic recurrent parotitis, or acute bacterial parotitis.1-4

Even if we did not pick up the parotid swelling, the lack of sore throat moves the differential away from pharyngitis with lymphadenitis; whereas the time course, unswollen lips and tongue, and lack of respiratory embarrassment suggest that this is not anaphylaxis with airway edema. The demographics and the unilaterality place mumps well down the list.


The eyebrows appear to rise normally and symmetrically (though we can't see forehead wrinkling in this view), and the nasolabial fold is not flattened; so the right facial nerve (cranial nerve VII) has been spared despite infection of the parotid gland through which it runs. Facial palsy is not sensitive or specific for parotid disease: bilateral facial palsy, for instance, is seen in neurosarcoidosis and diabetic neuropathy. Unilateral facial palsy, most typically thought of in Bell palsy5 and in malignant neoplasms of the parotid gland,6,7 has been reported, albeit rarely, in candidal8 and tuberculous parotitis.9 Fortunately, peripheral facial palsy in inflammatory conditions often resolves completely.


A formerly common postoperative variant of acute bacterial parotitis known as surgical parotitis, though it also affects patients who are medically critically ill, has become rare.3 It was attributed to dehydration and high oral bacterial counts, with inspissated duct content and poor washout that permitted colonization and then infection. One can wonder whether lack of mucin in the secretion played a role: the parotid is the only purely serous salivary gland. Just to further confuse the issue, most aged patients who don't develop this complication also have dry mouths loaded with oral microbes. Whatever the mechanism, so-called surgical parotitis has become most uncommon.

Increasingly, as with so many other infections, methicillin-resistant Staphylococcus aureus is recovered from cultures in acute bacterial parotitis. Until a few years ago, methicillin-resistant S aureus was regarded as a signpost of frailty and high antibiotic exposure, and a predictor of high early mortality. Now community-acquired strains proliferate widely and infections from them are seen in all segments of the populace.

One small observational study suggests, independent of causative microbe, that acute parotitis in the aged carries a high short-term mortality, and not from the parotitis itself!3 Could susceptibility to this infection have become a newer surrogate marker for host frailty? The study has not been replicated, and the prognostic significance of acute parotitis in the aged must be regarded as unsettled.


Parotid enlargement unless gross or markedly asymmetrical (Figures 1, 2, and 3) is often hard or even impossible to recognize; many persons have fleshy faces that can hide or mimic extra tissue in front of the ear. A family member with longstanding familiarity with the shape of a patient's face can be an ally in deciding whether anything has changed.

The parallel struggle with distinguishing a large front-of-the-neck from a goiter is underscored in our case: from the image alone, one might query thyroid enlargement in this 55-year-old woman. Palpation during deglutition would show whether the area did or did not rise, ie, was or was not thyroid attached to the laryngeal cartilage.

Besides outright misleading contours that make us conclude wrongly about whether a parotid gland is oversized, genuine enlargement can reflect any of a highly diverse range of causes. Abrupt onset makes neoplasia unlikely as the source of the problem, as it does tuberculosis; anorexia and bulimia10,11; alcoholism; HIV disease; intraparotid lymphadenopathy; and obesity.

Besides purely epithelial tumors and mixed lymphoid-epithelial ones, lymphomas can arise in the parotid gland because there are intraparotid lymph nodes. Rapid onset renders any of these most unlikely-despite the faint overtone of Burkitt lymphoma, which can grow wildly nearby in the jaw. While parotid edema could conceivably cause sudden enlargement, I am unfamiliar with any reports of such a condition whether as part of generalized anasarca or from local causes alone, eg, venous obstruction, inflammation, or anaphylaxis.


Viral mumps forms a much greater consideration. Recent epidemics have been seen not in the expected small children, but in teenagers and young adults. These caught much of the medical community off-guard.1,2 Many but not all victims had received only 1 dose of mumps vaccine. Being born before 1957 is still associated with a great likelihood of prior infection with lifetime immunity even if one's initial infection was subclinical.

By doing the arithmetic or asking her birth-year, it can be determined that this woman is old enough that the “pre-1957 protection clause” should apply. Had her finding been bilateral, and if furthermore she had not improved rapidly with antibiotics, one could have considered mumps much more seriously. Since laboratory results play little role in managing conventional mumps, measuring a convalescent titer would not be routine.

Mumps is a curious illness. Today many primary care clinicians recall chiefly that there is an effective vaccine; that small children form (or more accurately used to constitute) the preponderance of cases; that both parotid glands grow large and tender; and that orchitis is a threat to male patients with mumps. The virus also can produce a pancreatitis, a low-grade meningitis and, worse, an encephalitis, accounting for most of the low mortality and underscoring the desirability of universal vaccination for prevention.

The mumps syndrome is sometimes caused by non-mumpvirus agents such as cytomegalovirus. This may be part of the mythology of those who have had it twice. A few other cases could represent unrecognized iodide mumps, which is a subject for another discussion.


Some thoughtful infectious disease specialists and epidemiologists have tried to derive wider, more generalized lessons about vaccination, herd immunity, and evolving infectious diseases from the resurgence of mumps.1,2

Given the intense benefit of all our childhood vaccines, and the senseless and needless tragedy of deaths from preventable diseases, the latest re-arguments about thimerosal preservatives' putatively contributing to autism, after all the scientific scrutiny and reporting, seems like a poignant howl of anguish devoid of sound scientific basis. Consequent avoidance of vaccinations feels to me as though parents are lacking perspective, giving in to a feeling that one is protecting the helpless by defying arbitrary authority because one cares more deeply about the welfare of one's child than does “the medical establishment.”

Any such imputation about our profession of course wounds and insults us profoundly. But the issue is not our psyche; it is the placing of children at needless risk of perilous infections, children who can't decide for themselves, despite clear and compelling objective evidence that the benefits outweigh the (reputed, unproven) risks manyfold.


This patient responded nicely to antibiotics, intravenous fluid repletion, and sialogogues. There was neither protraction of the course, damage to the duct system with later recurrences,4 nor the rare and lethal complication, jugular thrombophlebitis with pulmonary emboli (Lemierre syndrome).12

Schneiderman H. Acute bacterial parotitis and the differential diagnosis of parotid enlargement.
CONSULTANT. 2008;48:630-634.


REFERENCES:1. MacDonald N, Flegel K. Mumps in young adults: the canary in the coal mine. CMAJ. 2007;177:121, 123.
2. Shanley JD. The resurgence of mumps in young adults and adolescents. Cleve Clin J Med. 2007;74:42-44, 47-48.
3. Jibidar H, Souchon S, Miric D, et al. Occurrence of suppurative parotitis in elderly people remains a bad omen. J Am Geriatr Soc. 2008;56:760-761.
4. Baurmash HD. Chronic recurrent parotitis: a closer look at its origin, diagnosis, and management. J Oral Maxillofac Surg. 2004;62:1010-1018.
5. Schneiderman H. Peripheral facial (Bell) palsy and the seventh cranial (facial) nerve. Consultant. 2000;40:1962-1965.
6. Schneiderman H. Parotid enlargement from lymphomatous infiltration and other causes. Consultant. 1994;34:77-78.
7. Schneiderman H. Complete peripheral facial palsy due to parotidectomy for acinic cell cancer of the parotid. Consultant. 2004;44:977-984.
8. Marioni G, Rinaldi R, de Filippis C, et al. Candidal abscess of the parotid gland associated with facial nerve paralysis. Acta Otolaryngol. 2003;123:661-663.
9. Lee IK, Liu JW. Tuberculous parotitis: case report and literature review. Ann Otol Rhinol Laryngol. 2005;114:547-551.
10. Schneiderman H, Eisenberg E. Bulimia: a dangerous variant of anorexia with oral physical signs. Consultant. 1995;35:1695-1700.
11. Schneiderman H. Anorexia nervosa: a scourge often concealed by patients and revealed by physical examination. Consultant. 2005;45:668-674.
12. Hadjihannas E, Kesse KW, d'E Meredith AP. Thrombosis of internal jugular vein associated with acute parotitis. J Laryngol Otol. 2000;114:721-723.

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