The epidemiology of infectious cervical adenitis is that of its etiologic agents. Although often it is a manifestation of focal viral infection involving the upper respiratory tract, it also may be part of a generalized reticuloendothelial response to systemic infection. Viruses commonly associated with prominent cervical lymph node enlargement include Epstein-Barr virus (EBV), cytomegalovirus (CMV), and the human immunodeficiency virus (HIV). Age, geographic location, and socioeconomic status affect the incidence and clinical features of cervical adenitis. As a general principle, younger urban dwellers of lower socioeconomic status have a higher incidence of infection. Geographic location also may be important in some children—for example, those residing in the southwestern United States, where Yersinia pestis has become endemic.

Although patients at any age may be affected, most children with cervical adenitis are 1 to 4 years old. This age restriction and the peak in incidence reflect the prevalence of infections caused by viral agents, Staphylococcus aureus, group A streptococci, and atypical mycobacteria. The increasing incidence of nosocomial and community-acquired methicillin-resistant S. aureus (MRSA) infections noted in the United States and elsewhere, especially in children, requires that this organism be strongly considered as a possible cause. The genders are affected equally by cervical adenitis, with two exceptions. Some studies indicate a female predominance for granulomatous lymphadenitis caused by atypical mycobacteria, and young infants with the cellulitis-adenitis syndrome caused by group B streptococci are predominantly male. Droplet-borne and direct contact transmission are the routes of acquisition for most viral causes of cervical adenitis and for bacterial disease caused by group A streptococci and Mycobacterium tuberculosis. The remaining bacterial agents are normal inhabitants of the mouth, oropharynx, and nose or are bacteria inoculated by trauma to the skin with secondary spread to regional nodes. No ethnic predilection avails for acute bacterial cervical adenitis (Table 256.1). In contrast, adenitis caused by atypical mycobacteria occurs commonly in whites, whereas that caused by M. tuberculosis tends to have a greater incidence in African American and Hispanic populations. For children living in temperate climates, an increase in incidence occurs during the winter and spring months. A history of dog or cat contact, bite, or scratch may be a helpful clue in suggesting specific causative agents, such as Pasteurella multocida, Bartonella henselae, or Toxoplasma gondii. Similarly, a history of a minor inoculation wound of the skin proximal to affected cervical lymph nodes should suggest the possibility of such soil organisms as Nocardia brasiliensis, atypical mycobacteria, or gram-negative enteric organisms. Finally, HIV should be added to the list of agents causing cervical adenopathy, and, because most HIV-infected children are infected perinatally, the epidemiology reflects that of the mothers.

The pathogenesis of cervical adenitis is elucidated poorly. Apparently, a microorganism first must infect asymptomatically the upper respiratory tract, anterior nares, mouth, or skin of the head or neck before spreading to the cervical lymph nodes. Overt infection of the skin, teeth, or oropharynx may occur in association with cervical adenitis, but clinically evident infection proximal to the affected nodes is not a requisite. For example, asymptomatic colonization of the anterior nares routinely precedes the development of cervical adenitis resulting from S. aureus. The common occurrence of group A streptococcal adenitis in children younger than 2 years old, in contrast to the infrequency with which streptococcal pharyngitis is observed in infants, suggests that adenitis may result when host defense mechanisms are insufficient to limit this organism to mucous membrane sites in the pharynx. Some investigators consider group A streptococci to be responsible for invasion of the nodes, with S. aureus playing a secondary role in patients from whose infected cervical lymph nodes both agents have been isolated. Dental caries or abscesses may predispose to the development of anaerobic cervical adenitis. However, when proper culture techniques are used, mixed aerobic-anaerobic infections frequently are diagnosed. This outcome suggests that elaboration of extracellular enzymes by mixed mouth flora may have a role in the pathogenesis of these infections. Certain infections are characterized by direct inoculation of skin proximal to regional lymph nodes (e.g., group A streptococci, Nocardia, B. henselae). Finally, viral cervical adenitis may reflect either a local response to a virus invading the oropharynx or respiratory tract (e.g., adenovirus) or a more generalized reticuloendothelial response to systemic viral infection (e.g., EBV). Some have stated that in considering the pathogenesis of cervical adenitis in children, physicians should consider the three Ts: tonsils, teeth, and areas of skin trauma.

The increased size of lymph nodes (greater than 1.0 cm) in response to infection is the result of an increase in the number of cells. While the lymph node is filtering pyogenic microorganisms, chemoattraction of neutrophils to the lymph node may result in the formation of microabscesses and small areas of necrosis or in frank suppuration. Rapid, extensive reactions almost always are caused by pyogenic organisms, notably S. aureus or group A streptococci. Granuloma formation with a delayed cellular immune response leading over a period of weeks or months to a “cold” abscess is characteristic of infection caused by mycobacteria, fungi, or B. henselae (Fig. 256.1). Tuberculous cervical lymphadenopathy occurs through pulmonary infection and involvement of the regional and more distant lymph nodes. Nontuberculous mycobacteria are ubiquitous in the environment; oropharyngeal acquisition followed by local infection leads to lymph node involvement. With both M. tuberculosis and atypical mycobacteria, biopsy material usually reveals extensive replacement of normal architecture by caseating granulomas surrounded by epithelioid cells and giant cells, and acid-fast organisms are demonstrable in sections that are appropriately stained in approximately 50% of cases. Epithelioid granulomas infiltrated with neutrophils, forming large pus-filled sinuses, are characteristic of the lymph nodes excised from children with cat-scratch adenitis. Once infection has resolved, destruction of nodal tissue sometimes leads to healing with fibrous tissue proliferation, most often in the submandibular group, and this may persist indefinitely.

Cervical adenitis may be classified according to its mode of presentation as acute, in which symptoms are of less than 2 weeks’ duration, or as subacute to chronic (Table 256.2). The causative agents tend to fall into one of these two categories, although they may overlap. Overall, approximately three-fourths of all the infections have an acute presentation. The duration of lymph node swelling is less than 3 days in one-half of all children with acute adenitis and less than 1 week in the majority. Generally, acute bilateral cervical adenitis is associated with upper respiratory tract viral infection, including EBV and CMV, or with acute streptococcal pharyngitis. Lymph nodes may be tender, but no other signs of inflammation are found. The appearance of such an enanthem as gingivostomatitis or of such an exanthem as scarlatina should suggest either a viral or a streptococcal cause.

Generally, children with acute unilateral cervical lymphadenitis have a paucity of systemic manifestations. A history of upper respiratory tract symptoms, such as sore throat, earache, coryza, or impetigo, can be elicited from one-fourth to one-third of patients. Usually, the diameter of an infected node (or nodes) ranges from 2.5 to 6.0 cm; the nodes are tender and exhibit varying degrees of warmth and erythema. S. aureus and group A streptococci are the causative agents in approximately 50% to 90% of infections. Less commonly, other bacteria residing in the oropharynx are implicated (see Table 256.2). Streptococcal adenitis occurs in younger children, is accompanied more often by generalized adenopathy, has a shorter duration of symptoms (less than 5 days), and is less likely to suppurate than are nodes infected by S. aureus. Overall, one-fourth to one-third of involved nodes suppurate, and 90% of these become fluctuant within 2 weeks of onset. Concomitant lymphadenopathy at other sites is observed in as many as one-third of children with acute unilateral cervical adenitis, most commonly in association with a generalized viral process or a group A streptococcal infection in very young children.

Hepatomegaly or splenomegaly is rare, however; if found, either condition should suggest a generalized process (e.g., EBV, CMV, or HIV infection, tuberculosis, reticuloendotheliosis, lymphoma). Kawasaki disease may present as a febrile illness associated with bilateral or unilateral cervical lymphadenopathy.