Localized Lymphadenitis, Lymphadenopathy, and Lymphangitis

Pathogenesis

Lymph nodes can enlarge as a result of (1) intrinsic proliferation of lymphocytes or reticuloendothelial cells or (2) infiltration by cells from an extrinsic source. Lymphocytes or lymphoblasts proliferate upon recognition of antigenic stimuli, producing lymph node enlargement, which recedes upon antigen clearance. Infectious organisms able to survive intracellularly can represent persistent stimuli and can be associated with chronic lymphatic cellular hyperplasia. Extrinsic invasion of lymph nodes occurs with neutrophils in response to bacteria and bacterial toxins, with histiocytes in histiocytosis and certain storage diseases, and with malignant cells in leukemia, lymphoma, and metastatic solid tumors.

Etiologic Agents

The pyogenic bacteria Staphylococcus aureus and Streptococcus pyogenes account for >80% of acute bacterial lymphadenitis. Lymph node infection usually can be attributed to spread from an adjacent skin infection or inoculation site; occasionally, no clear origin is evident. Acute localized lymphadenitis with or without overlying cellulitis can develop in an infant as a manifestation of late-onset bacteremic group B streptococcal (GBS) disease. ^, Subacute development of localized lymph node enlargement in healthy children occurs with cat-scratch disease ( Bartonella henselae infection) and with nontuberculous mycobacterial infection. Adenitis with fungal pathogens such as Aspergillus or Candida can occur in immunosuppressed patients, such as those with primary immune deficiency (e.g., chronic granulomatous disease) or those who are undergoing chemotherapy for an oncologic diagnosis. Unusual pathogens can produce lymphadenitis in otherwise healthy people after specific environmental exposures (e.g., Francisella tularensis after tick bite/animal skinning or Corynebacterium pseudotuberculosis in sheep handlers).

History and Clinical Findings

Certain clinical features may be useful in guiding the evaluation of localized lymph node infections ( Table 20.1 ). Small inguinal, cervical, or axillary lymph nodes can be palpated in about a third of healthy infants. Subsequent antigenic stimulation leads to steady enlargement of lymphoid tissue from infancy through puberty. As a result, the vast majority of healthy children have palpable cervical, inguinal, and axillary nodes. In contrast, other peripheral node groups (e.g., posterior auricular, supraclavicular, epitrochlear, iliac, and popliteal) are always considered abnormal if they can be palpated on examination.

A careful history must be obtained regarding the time of onset and rate of lymph node enlargement ( Box 20.1 ). The skin and soft-tissue areas drained by the enlarged nodes should be examined for signs of infection and disruption. History of exposure to animals should be detailed. Occurrence of bites (including tick bites) or traumatic scratches or other papular or ulcerative skin lesions should also be elicited. Weight loss, protracted fever, rash, generalized lymphadenopathy, or hepatosplenomegaly suggests a systemic disease. Lymph nodes associated with viral infection tend to be small, bilateral, freely mobile, and variably tender. The presence of erythema, warmth, and tenderness overlying a node typically indicates a pyogenic acute inflammatory response related to a bacterial pathogen. Fluctuance of the lymph node is suggestive of acute pyogenic bacterial adenitis but also can be seen with more indolent pathogens, including nontuberculous mycobacteria (NTM); and presence of overlying violaceous hue raises suspicion of the latter ( Fig. 20.1 ). Most acutely infected lymph nodes in children are rubbery or firm in consistency and freely mobile. Fixation of the node to underlying tissue raises concern for a neoplastic process.

Differential Diagnosis

Knowledge of lymphatic drainage patterns is essential to identification of the primary focus of infection and the most likely etiologic agents in the child with localized lymphadenopathy. The regions drained by specific lymph node groups are listed in Table 20.1 , along with the associated infections encountered in each case.