Management of lymphadenopathy and lymphadenitis depends on patient age, associated findings, node size and location, and severity of the acute systemic symptoms. In children most cases of cervical lymphadenopathy, without other signs of acute inflammation, require no specific therapy and usually regress within 2 to 3 weeks. Progression to lymphadenitis or development of generalized lymphadenopathy requires further evaluation.
The specific treatment of cervical lymphadenitis dependson the underlying etiology. Empirical treatment targeting
S. aureus and group A streptococcus includes a penicillinase-resistant penicillin (e.g., oxacillin) or first-generationcephalosporin (e.g., cefazolin). For patients with hypersensitivity to β-lactam antibiotics, or if community-acquired methicillin-resistant S. aureus is suspected, clindamycin is appropriate.Response to empirical antibiotic therapy for suppurative cervical lymphadenitis obviates the need for further evaluation.Absence of a clinical response within 48 to 72 hours is an indication for further laboratory evaluation and possible excisionalbiopsy and culture.
There is no specific treatment for infectious mononucleosis. Cat-scratch disease usually does not require treatment because the lymphadenopathy resolves in 2 to 4 months without sequelae. Azithromycin may hasten resolution and reduces node size at 30 days but no benefit is evident at 90 days. Aspiration is indicated for suppurative nodes. The recommended treatment of cervical lymphadenitis caused by nontuberculous mycobacteria is complete surgical excision. Antimycobacterial drugs are necessary only if there is recurrence or inability to excise infected nodes completely, or if M. tuberculosis is identified, which requires 6 months of antituberculous chemotherapy (see Chapter 124).
Most acute infections caused by S. aureus and group A streptococcus respond to treatment and have an excellent prognosis. Complications such as abscess formation, cellulitis, andbacteremia may occur. Abscess formation is treated with incision and drainage in conjunction with appropriate antibiotictherapy.
Infectious mononucleosis usually resolves in 2 to 4 weeks,but fatigue and malaise may wax and wane for several weeks tomonths. EBV also is associated with numerous complicationsduring the acute illness. Neurologic complications includeseizures, aseptic meningitis syndrome, Bell palsy, transversemyelitis, encephalitis, and Guillain-Barre syndrome. Hematologic complications include Coombs-positive hemolytic anemia, antibody-mediated thrombocytopenia, hemophagocyticsyndrome, and, rarely, aplastic anemia. Corticosteroids havebeen used for respiratory compromise resulting from tonsillar hypertrophy, which responds rapidly, and for thrombocytopenia, hemolytic anemia, and neurologic complications.Splenic rupture is very rare. X-linked lymphoproliferative disease, which results from a mutation of the SH2D1A gene located in the Xq25 region, manifests as fulminant infectiousmononucleosis with primary EBV infection and progresses tomalignant lymphoproliferative disease or dysgammaglobulinemia.
EBV infection, as with other herpesviruses, persists for life, but no symptoms are attributed to intermittent reactivation in immunocompetent hosts. EBV is causally associated with nasopharyngeal carcinoma; Burkitt lymphoma; Hodgkin disease; leiomyosarcoma in immunocompromised persons; and EBV lymphoproliferative disease, especially in posttransplant patients and in those with acquired immunodeficiency syndrome (AIDS).