Chapter 26. Cervical Lymphadenitis

Lymphadenopathy, or enlarged lymph nodes, may be the result of acute inflammation, chronic inflammation, or infiltration via malignant cells. Lymphadenitis is the term used to describe inflammation of lymph nodes.

Most cases of acute cervical lymphadenitis are caused by either staphylococcal or streptococcal infections, and the changing epidemiology of acute unilateral cervical adenitis has been well documented in the literature. In 1944, Powers and Boisvert reported that 79% of cervical abscesses were caused by group A beta-hemolytic Streptococcus (GABHS; Streptococcus pyogenes) and only 17% were caused by Staphylococcus aureus (formerly S. pyogenes). In 1969, Scobie reported that Staphylococcus species caused most (67%) cases of cervical adenitis, and only 7% were caused by streptococci.1

Nontuberculosis mycobacterium (NTM) infections in the head and neck are common among children.2 NTM includes mycobacterial species Mycobacterium avium-intracellulare complex, Mycobacterium scrofulaceum, Mycobacterium fortuitum, and Mycobacterium chelonei. NTM are ubiquitous in the environment and can be found in soil, contaminated water, dairy products, eggs, and dust. NTM are endemic in certain regions of the United States such as the mid-west and southwest. Ingestion of contaminated materials is likely to be the main route for introduction of NTM. This explains why cervicofacial lymph nodes are the sites primarily affected by NTM infections.2 Until approximately 50 years ago, adenitis caused by Mycobacterium tuberculosis (TB) and Mycobacterium bovis were more common than NTM adenitis. However, as TB and M. bovis disease decreased in the United States and other developed countries, NTM became a major cause of chronic lymphadenitis in children. Cessation of Bacille Calmette–Guerin vaccination in the United States has decreased collateral immunity against NTM. Chlorination of water has also been attributed to decrease in number of infections caused by M. scrofulaceum.3

Peripheral tuberculous lymphadenitis involves mainly the cervical lymph nodes. It is the most common form of extrapulmonary tuberculosis in children from tuberculosis-endemic areas. Lymphadenitis is thought to occur secondary to a lymphatic spread of organisms from a primary pulmonary focus. However, it can occasionally occur from primary focus in the mouth, tonsils, oropharynx, or tissues of the head and neck.4

Cat-scratch disease (CSD) was first reported by Debre in 1950 as a syndrome of regional lymphadenopathy after a cat scratch. CSD is caused by infection with Bartonella henselae, a zoonotic disease.5,6 Cat fleas Ctenocephalides felis transmit B. henselae between cats who remain asymptomatic. Humans become infected after exposure to infected cats, usually after scratches or bites from kittens. Dogs have also been known to be the vector for transmitting the disease. The true incidence of CSD is unknown. Most cases occur in people younger than 20 years. More than 90% of patients with CSD have a history of recent contact with cats, often kittens.7 Infection is reported to occur more often during the autumn and winter. The incubation period from the time of the scratch to appearance of the primary cutaneous lesion is 7–12 days; the period from the appearance of the primary lesion to the appearance of lymphadenopathy is 5–50 days (median, 12 days).8

Toxoplasma gondii, a parasite, is distributed throughout the world. Cats are definitive hosts and acquire the infection by feeding on infected animals such as mice or uncooked meats.7,8 After the parasite sexually replicates in the intestine, it is excreted as a oocyst in stools. After excretion and maturation, the oocytes are capable of infecting if ingested by the oral route. Intermediate hosts such as sheep, pigs, and cattle can have tissues infected with the cysts, which are viable for the lifetime of the host. Humans become infected by consumption of raw or undercooked meat that contains cysts or by accidental ingestion of sporulated oocysts from soil or in contaminated food. Primary infection with T. gondii is usually benign. The most common presentation is nontender and nonsuppurative lymphadenopathy. Infection usually causes regional enlargement of lymph nodes (most commonly suboccipital and cervical) rather than generalized lymphadenopathy.7,8 The incubation period of acquired infection is estimated to be 7 days (range: 4–21 days).

Based on the location of infection, lymphatic vessels drain infectious agents and inflammatory mediators to regional lymph nodes. An initial inflammatory response involves hyperplasia of the lymphoid tissue and recruitment of phagocytic cells, cytokine release, and vascular edema. This leads to enlargement of the regional nodes. In acute adenitis, this rapid expansion increases pressure on the lymph node capsule, resulting in pain at the site of the swollen lymph node. Involvement of adjacent lymph nodes and surrounding soft tissue can lead to cellulitis, suppuration, necrosis, or fixation to nearby structures. In chronic adenitis, pain at the site of lymph node enlargement is less common because lymphoid hyperplasia is more gradual, inflammatory responses are less robust, and the body attempts to wall off the infection with fibrosis and granuloma formation.

Lymph Node Drainage in the Head

Figure 26–1 illustrates the regional lymph nodes affected in children with cervical adenitis. Five important lymph node groups found in the head include the postauricular (mastoid), occipital, preauricular, parotid, and facial nodes. The postauricular nodes drain temporal and parietal scalp and the posterior ear canal. Occipital nodes are responsible for the posterior scalp and neck. Scalp dermatitis or infection may cause regional occipital lymphadenitis. However, in generalized lymphadenopathy, occipital nodes are often enlarged. Preauricular nodes drain the anterior and temporal scalp, ear canal and pinna, and lateral conjunctivae. The parotid and facial nodes drain the midface, parotid gland, external auditory canal, middle ear, posterior palate, conjunctivae, eyelids, and nasopharynx.

Lymph Node Drainage in the Neck

Lymph tissue of the neck is divided into five regions of local drainage, which include the submental, submandibular (submaxillary), superficial cervical, and the superior and inferior deep cervical groups. Submental nodes lie on the inferior aspect of the chin and are responsible for draining the intraoral region. The submandibular lymph nodes lie next to the submandibular salivary gland and receive a large proportion of lymphatic drainage from the head, including from the lateral aspect of the lower lip, vestibule of the nose, cheeks, medial parts of the eyelids, and the forehead. The superficial cervical nodes are three vertical chains that lie along the posterior border of the sternomastoid muscle, external jugular vein, and midline from the chin to the suprasternal notch. These are responsible for draining the superficial anterior neck tissues, including the skin, lower larynx, thyroid, lower ear canal, and parotid regions. Deep cervical nodes of the neck lie deep to the sternomastoid muscle and are divided into the superior and inferior regions. The superficial deep nodes drain the palatine tonsils and submental nodes. The lower deep cervical nodes drain the larynx, trachea, thyroid, and esophagus. The supraclavicular nodes, also part of the inferior deep cervical chain, are responsible for draining the lungs and abdomen. Enlargement of supraclavicular nodes most often indicates thoracic or abdominal pathology, including Hodgkin and non-Hodgkin lymphomas. Prompt evaluation and biopsy are necessary with supraclavicular nodal enlargement.

The majority of the lymphatics of the head and neck drain to the deep cervical and submandibular nodes. Therefore, these are the nodes most often (80%) involved in cervical lymphadenitis in children.

Most normal infants and children have palpable cervical, inguinal, and axillary lymph nodes. In general, a lymph node measuring greater than 10 mm in longest diameter is considered enlarged. There are three exceptions to this rule: (1) epitrochlear nodes measuring more than 5 mm are abnormal; (2) inguinal nodes measuring more than 15 mm are abnormal; and (3) palpable supraclavicular, iliac, or popliteal nodes are always considered abnormal.9

Regarding cervical lymphadenopathy, it is important to classify the enlarged node as either acute or chronic and unilateral or generalized. These criteria can help guide the decision-making process in a differential diagnosis.

History

Important details of the history include location, onset, duration, and rate of enlargement of lymph node. Epidemiologic clues as to the etiology include exposure to animal bites or scratches, especially cats or kittens, risk factors for HIV infection, contact with tuberculosis infection, and travel outside of the geographical region of residence. Weight loss, protracted fever, rash, hepatosplenomegaly, and generalized lymphadenopathy signify systemic disease.

Asking if the patient received antibiotics and the clinical response with the prescribed antibiotics are important. Past history of tuberculin testing skin with results and date of test is an essential part of the history.

Physical Examination

A comprehensive physical examination is necessary to determine whether the lymphadenopathy is isolated or generalized. The skin and soft tissue near the enlarged lymph node should be evaluated for evidence of inflammation such as erythema, induration, tenderness, or fluctuance. Areas distal to the adenopathy may yield important information regarding scars, nodules, or papules.

Characteristics of the lymph node are important in helping to identity the etiology of the lymphadenopathy. Viral hyperplastic lymph nodes are typically small, discrete, mobile, nontender, and bilateral. No superficial cellulitis or periadenitis should be present. Pyogenic lymphadenitis is typically unilateral, warm, large, and tender with surrounding erythema and edema (Figure 26–2). Lymph node characteristics associated with specific infectious causes are discussed further in the “Differential Diagnosis” section of this chapter. Chronic lymphadenitis is characterized by discrete margins and adherence to underlying tissue with minimal signs of inflammation. Characteristic malignant lymphadenopathy is firm, discrete, and nontender, with a classic description of “rubbery texture” without inflammation. After a period of time, the surrounding tissue becomes matted together and fixed in place to the skin and underlying structures. Malignancy should not suppurate.

The rest of the physical examination should focus on a detailed head and neck examination including sources for infection—scalp, dental, oropharyngeal, otitic, and conjunctival sources. Range of motion of the neck should be evaluated. All lymph chains should be palpated for lymphadenopathy. Liver and spleen should be palpated. Inspection for rash and peripheral extremity changes could signal Kawasaki syndrome, malignancy, or viral etiology. See Table 26–1 for important aspects of the history and physical examination.

Infectious and noninfectious etiologies of cervical lymph- adenopathy are summarized in Tables 26–2 and 26–3.

Infectious Causes of Lymphadenitis by Lymph Node Location

Acute Bilateral Cervical Lymphadenitis

Acute bilateral lymphadenitis is commonly associated with other constitutional symptoms including fever, cough, rhinorrhea, conjunctivitis, or pharyngitis of upper respiratory or oropharyngeal infections. Viral etiologies include adenovirus, rhinovirus, parainfluenza, influenza, respiratory syncytial virus, and coronavirus. In adenoviral infections, anterior and posterior cervical nodal enlargements are more common than preauricular lymphadenopathy.9

Both Epstein–Barr Virus (EBV) and cytomegalovirus (CMV) can cause acute bilateral cervical adenitis associated with infectious mononucleosis. EBV is more commonly the cause of cervical adenitis than is CMV.9 In both EBV and CMV infections, posterior cervical nodes are more commonly enlarged than are anterior cervical nodes. Cervical lymphadenitis may present prior to generalized lymphadenopathy in many cases of EBV or CMV infectious mononucleosis.9

Other infectious etiologies responsible for bilateral cervical lymphadenitis include HIV, rubella, varicella, HSV, measles, coxsackie, and roseola (HHV-6) viruses. Associated symptoms are important factors in arriving at the correct diagnosis. Gingovistomatitis caused by HSV or herpangia from coxsackie virus infection is commonly associated with bilateral enlargement of the anterior cervical, submental, and submandibular nodes.9 In addition, many of these viral agents, which cause generalized infections, will also produce generalized lymphadenopathy.

Acute Unilateral Cervical Lymphadenitis

Acute, unilateral, suppurative bacterial cervical lymphadenitis is the classic form of cervical lymphadenitis brought to medical attention. S. aureus and GABHS are responsible for the majority of these infections. Reports of 40–80% of isolated organisms were S. aureus or GABHS in studies where fine needle aspiration or excision was performed.10–13 These infected lymph nodes may result from upper respiratory, throat, dental, or scalp infections. In children aged 1–4 years, S. aureus and GABHS are common etiological agents. In older children, GABHS and anaerobic infections are most frequently seen.9 Streptococcal infections in this age group appear to represent the natural incidence of streptococcal pharyngitis in this group. Anaerobic organisms associated with dental abscesses, gingival infections, and mucositis have been cultured from biopsied lymph nodes. Bacteroides,Peptostreptococcus,Proteus, Escherichia coli, Pseudomonas, mixed infections of both Staphylococcus and Streptococcus, coagulase-negative staphylococcal species, Actinomyces israelii, Streptococcus milleri group, Haemophilus influenzae, Francisella tularensis, Aspergillus spp., Nocardia spp., and NTM have all been isolated from pediatric patients with acute cervical adenitis or abscess.1,9,13–16

The primary sites of acute cervical lymphadenitis are submandibular (50–75%), cervical (13–39%), submental (5–8%), and occipital (2–3%).1,15 Suppuration occurs most commonly with Staph. aureus infection, with a rate of 25% of all acute bacterial cervical adenitis.15,16

Subacute or Chronic Unilateral Cervical Lymphadenitis

The most common causes of subacute or chronic lymphadenitis are mycobacterial infection, CSD, and toxoplasmosis.17

Cervical lymphadenitis is the most common mycobacterial infection found in children. These infections are typically caused by NTM rather than M. tuberculosis; M. avium-intracellulare complex is isolated most often. Adenitis caused by mycobacteria generally affects healthy children between the ages of 1 and 5 years. The involved cervical lymph nodes are frequently located in the submandibular and preauricular nodal groups. The size of the node can vary between 1 and 7 cm in diameter. Symptoms may have been ongoing for several weeks to months before seeking medical attention.2 In the early phase of the infection, the lymph nodes are firm with minimal tenderness, erythema, or warmth. Later, a necrotic center develops. Without treatment, the infection leads to progressive lymph node necrosis, overlying violaceous skin discoloration with a papyraceous or cigarette paper-like appearance, and, subsequently, draining skin sinus.2,18

CSD is usually a localized, self-limited disease but may be complicated by encephalitis, neuroretinitis, or Parinaud oculoglandular syndrome, a syndrome of unilateral conjunctivitis associated with regional lymphadenopathy and a characteristic neuroretinitis that occurs after conjunctival inoculation.6–8,19 The primary clinical feature is lymphadenitis, which is single or regional and restricted to the drainage area of the site of the inoculation. The involved nodes tend to be as large as several centimeters in diameter. These may be elastic, mobile, and tender. Spontaneous regression of the nodes usually occurs in 2 weeks to 2 months. A primary lesion or papule may be located at the site of a scratch. This lesion typically precedes the development of lymphadenitis. CSD is generally associated with systemic symptoms such as fever and malaise. There is usually a history of contact with a kitten or a cat.6–8

Lymphadenopathy without fever is the most frequent clinical manifestation of acute acquired infection with T. gondii in the immunocompetent individual. The majority of acquired T. gondii infections are asymptomatic. The adenopathy may be present for months and tends to be nonsuppurative and only occasionally tender. Toxoplasmic lymphadenitis most frequently involves a solitary lymph node in the head and neck regions, without systemic symptoms.8

Cervical lymphadenitis caused by TB is uncommon in the United States. However, in endemic areas, TB remains a significant cause of cervical lymphadenitis.4

Subacute or Chronic Bilateral Cervical Lymphadenitis

Viral etiologies such as EBV, CMV, and HIV infections can cause bilateral subacute chronic cervical lymphadenitis. Syphilis can also cause lymphadenitis. However, the above infections account for only a small proportion of the clinically diagnosed cervical lymphadenopathies.

Infectious Causes of Lymphadenitis by Demographic Characteristics and Epidemiologic Exposures

Age

The most common cause of acute cervical lymphadenitis in infants is S. aureus. However, group B Streptococcus can cause a late-onset cellulitis-adenitis syndrome in neonates. Presenting features of cellulitis-adenitis syndrome include poor feeding, irritability, fever, and unilateral facial, preauricular, or submandibular swelling with overlying erythema. Adenitis presents within 2–3 days after onset of soft-tissue infection. Reported cases have a male predominance (72%). Blood culture and culture of the soft tissue or lymph node are almost always positive. This syndrome had previously been thought not to be associated with meningitis, but, in 1998, two cases of meningitis were reported in association with group B Streptococcus cellulitis-adenitis syndrome in afebrile, well-appearing neonates.20,21

Staph. aureus and GABHS are the most common etiologies (80%) of acute cervical adenitis in children aged 1–4 years. The majority of cases of acute cervical lymphadenitis occur in this age group. Children aged 5 years and older are more likely to have lymphadenitis caused by NTM, T. gondii, B. henselae, EBV, CMV, and tularemia.9

Immunization Status

Lack of immunizations can predispose patients to preventable causes of cervical adenitis including measles, rubella, varicella, H. influenzae type b, and Corynebacterium diphtheriae. In rare cases, cervical lymphadenopathy has been reported following immunization with some vaccines (diphtheria–pertussis–tetanus, poliomyelitis, typhoid fever, and Bacille Calmette–Guerin).1,7,17

Contact with Animals

Zoonoses are a common cause of cervical lymphadenitis in children. History of exposure to animals is very important in the diagnosis of CSD, toxoplasma, tularemia, anthrax, brucellosis, and plague.

Pasturella multocida can cause acute adenitis following bites or scratches from animals.16 Tularemia results from infection with F. tularensis via insect vectors, direct contact with infected animals or carcasses, or ingestion of contaminated food or water. Approximately 250 animal species can be infected with tularemia including the rabbit. Occurrence is seasonal (June through September and November through February), which corresponds to vector and rabbit-hunting activities. Tularemia is highly infectious, with as few as 10 organisms being needed to cause infection. The ulceroglandular form is most common (75% cases) and causes ulcer at site of inoculation with regional lymphadenopathy. Exposure to F. tularensis through the conjunctiva can result in Parinaud oculoglandular syndrome, which is indistinguishable from that caused by B. henselae.22

Cutaneous anthrax begins as a focal pustule at the site of skin wound, and within 2–3 days, the lesion rapidly progresses with ulceration and eschar formation. Regional lymphadenitis may develop.22 Brucellosis is contracted via direct contact with animals or ingestion of unpasteurized dairy products. In rare cases, brucellosis causes chronic lymphadenopathy with chronic fatigue-like syndrome. Yersinia pestis is endemic in rodents and several notable outbreaks in the southwest United States have occurred in the recent years. Bubonic plague, the most common form of the disease, is transmitted to humans via flea bites, leading to regional lymphadenitis characteristic of the classic bubo.22

Contact with Sick Individuals

GABHS and the respiratory viral pathogens are all highly communicable via respiratory droplet transmission. History of a close contact with symptoms suggestive of TB, travel to endemic parts of the world, or history of incarceration should prompt evaluation for M. tuberculosis infection. Both congenital HIV and acute retroviral syndrome are characterized by lymphadenopathy.

Underlying Illness or Predisposing Condition

Patients with underlying undiagnosed immunodeficiency disease may present with lymphadenopathy or lymphadenitis. For example, suppurative lymphadenitis is one of the common initial presentations for patients with either chronic granulomatous disease or Job syndrome (hyperimmunoglobulin E syndrome). HIV infection may also present with generalized lymphadenopathy.

Noninfectious Causes of Lymphadenitis

PFAPA (periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis) is characterized by the onset of fever, malaise, chills, headaches, aphthous ulcers, pharyngitis, and tender cervical adenopathy. This cluster of symptoms cyclically recurs at 4–6-week intervals, and the episodes resolve spontaneously approximately 4–5 days.7 PFAPA is discussed further in the “Periodic Fever Syndromes” chapter (Chapter 61).

Kawasaki Syndrome (discussed in Chapter 62) manifests with nonsuppurative cervical lymphadenopathy (usually a single, large node). The other associated symptoms of fever, conjunctival injection, rash, and subsequent desquamation suggest the diagnosis. However, diagnosis may be difficult if unilateral lymphadenitis precedes mucocutaneous manifestations.23

Kikuchi disease (histocytic necrotizing lymphadenitis) is a self-limited condition characterized by cervical lymphadenopathy and fever. It usually occurs in women of Asian decent.7 Other inflammatory diseases such as juvenile rheumatoid arthritis may present with lymphadenopathy.

Infected congenital cysts such as bronchial cleft cysts, cystic hygromas, or thyroglossal duct cysts can mimic lymphadenitis. Congenital cysts should be considered, especially in cases when there appears to be recurrent cervical lymphadenitis.

Malignancy should be considered in the cases of indolent adenopathy, especially with a history of anorexia, weight loss, and other systemic symptoms.

The need for diagnostic evaluation depends on the history and clinical presentation. Most childhood cases of cervical lymphadenitis are benign and self-limited.

If the patient appears ill with systemic infection and has suggestive history, complete blood count, blood culture, liver enzymes, inflammatory markers such as erythrocyte sedimentation rate or c-reactive protein, and serologies for EBV, CMV, HIV, T. gondii, and Brucella spp. may be helpful.

Radiologic Studies

Ill-appearing patients with acute unilateral lymphadenitis should be evaluated for abscess via either ultrasound or CT. Ultrasound has a 90–95% sensitivity for identifying presence of liquefaction and abscess formation, and CT adds information about osseous involvement, in addition to the nature of the nodal tissue.13 Chest radiograph should be obtained to assess for pulmonary tuberculosis and hilar lymphadenopathy.

Tuberculin Skin Testing

A tuberculin skin test should be placed if NTM or TB is considered. Induration >5 mm in a low-risk population suggests NTM. TB should be considered if induration is >14 mm. However, usefulness of purified protein derivative (PPD) is limited even in the United States as subpopulations, such as those who live in major metropolitan areas, have a high risk of TB exposure.3

Serologic Studies

Serologic testing is available for B. henselae, T. gondii, HIV, EBV, CMV, tularemia, brucella, and plague. Details of testing for HIV (Chapter 52), EBV (Chapter 63), and CMV (Chapter 63) are discussed elsewhere in this text.

Specific serologic diagnostic tests can support the diagnosis of CSD. One of these, the indirect fluorescent antibody test, was shown to be 98% sensitive and 98% specific in a population of patients who met the classic case definition of CSD. Enzyme immunoassay testing for immunoglobulin (Ig) M and IgG antibodies to B. henselae is also commercially available. A high antibody titer (>1:64) suggests recent infection. An elevation in titer between acute and convalescent sera may be confirmatory. Paired sera are particularly useful in cat owners who may have a background rate of Bartonella antibody seropositivity greater than the general population (2–6%). The most sensitive technique currently available to diagnose B. henselae infection is polymerase chain reaction. This species-specific test detects B. henselae DNA in blood or tissue specimens (e.g., lymph nodes and bone). The Centers for Disease Control and Prevention and some commercial laboratories perform B. henselae polymerase chain reaction testing. This test should be considered when an atypical manifestation is suspected. It is also useful to diagnose CSD in immunocompromised patients who may not be able to mount a significant antibody response.

The presence of T. gondii-specific IgM antibodies suggests recent infection. IgM antibodies can be detected 2 weeks after infection. The concentration peaks in 1 month and is generally undetectable within 6–9 months. The lack of T. gondii-specific IgM antibodies indicates infection more than 6 months ago. Enzyme immunoassay tests are the more sensitive assays compared to indirect fluorescent antibody tests. False-positive IgM tests do occur, particularly with the use of commercial laboratory kits. This has been documented, particularly, in pregnant women. It is recommended that retesting be done by reference laboratory if there is a positive IgM test.24,25 IgG-specific antibodies achieve a peak concentration 1–2 months after infection and remain positive indefinitely.8

Throat Cultures

Viral cultures are expensive and not typically helpful. Throat culture for GABHS is warranted in cases of acute lymphadenitis. Patients have been reported to have negative throat cultures but positive nodal cultures with GABHS; therefore, a negative throat culture does not rule out GABHS, nor does a positive throat culture confirm the diagnosis.15 However, since approximately 15% of children have asymptomatic throat carriage of GABHS, detection of these bacteria from the throat does not necessarily mean that it is the cause of lymphadenitis.

Biopsy, Histology, and Culture

Up to 10% of patients with acute unilateral infection without abscess who are treated with oral antibiotics may still need incision and drainage as a result of progression to suppurative infection.26 Aspiration of the node is safe and reliable in both solid and cystic lesions (Table 26–4). Nodal aspirate should be sent for Gram stain, acid-fast bacilli (AFB) stain, and aerobic, anaerobic, and mycobacterial cultures. Complete blood count and throat and blood cultures should also be sent. However, yield of blood cultures in children with cervical abscesses is low, with rates of 3.8–10.5%.10,27

Definitive diagnosis of NTM adenitis depends on isolating the organisms.28 Excisional biopsy can help make the definitive diagnosis. Fine needle aspiration has been shown as an alternative mode for obtaining sample for diagnostic culture. Incision and drainage are contraindicated if NTM is suspected, as it may lead to chronically draining sinus tract. NTM is found in the environment and can commonly be a contaminant of specimens. However, its recovery from sterile site such as lymph node is considered diagnostic.

When the diagnostic suspicion is TB, mycobacterial culture remains the standard for definitive diagnosis of tuberculosis. A positive TB polymerase chain reaction, stain with AFB, and granulomas on histopathology may aid in the diagnosis but are not definitive.

In CSD, lymph node histology may also be helpful in suggesting the diagnosis. Histologically, lymphocytic infiltration is present in the early phase followed by polymorphonuclear leukocyte infiltration with necrotic granulomas.6,8,19 Warthin–Starry silver stain may show bacilli although not specific for B. henselae.

Strategies for the management of acute and subacute cervical lymphadenitis are summarized in Figures 26–3 and 26–4.

Treatment is based on presumed or known etiology. It is neither important nor possible to identify all etiologies for acute lymphadenitis. Empiric therapy is based on history and clinical presentation, assessment of risk factors, and review of the current antibiotic susceptibility patterns in the population.

Therapy for acute bacterial lymphadenitis should begin with oral or parenteral antistaphylococcal and streptococcal antibiotics based on patient's clinical appearance. Prevalence of community-acquired methicillin-resistant S. aureus (CA-MRSA) is important in deciding empiric antibiotic coverage. Many institutions in areas with a high MRSA prevalence use clindamycin or a combination of trimethoprim–sulfamethoxazole (to cover MRSA) and penicillin (to cover GABHS). The usual course of antibiotics is 7–14 days. Clinical response should be noted within 72 hours of starting the therapy. If no improvement is noted after 72 hours or symptoms worsen, this should prompt evaluation for abscess or reconsideration of the diagnosis. If abscess is identified, incision and drainage may be required. If a dental infection is present, empiric therapy should include coverage for Gram-positive cocci, anaerobes, and Gram-negative organisms. Once a specific etiology is identified, treatment should be based on review of current literature or a consultation with an infectious disease specialist (Table 26–5). If a patient completes a full antibiotic course and has no regression in nodal size, excisional biopsy should be considered.

Fine needle aspiration has been suggested as an initial step of the evaluation of chronic cervical lymphadenitis in patients who are stable. If the culture result yields NTM, surgery remains the best-established treatment, as it provides cure for localized NTM disease. If excision of the node is incomplete or the disease recurs, medical management with antimicrobials is recommended: clarithromycin or azithromycin plus ethambutol with rifampin or rifabutin.8 The utility of macrolide-based antimicrobial therapy as an alternative to surgery (or as an additive) has not been fully established. More recent studies suggest surgical excision to be more effective than antibiotic treatment.29 The study results showed that surgical excision was more effective than antibiotic therapy, with cure rates of 96% and 66%, respectively (95% confidence interval for the difference, 16–44%). Treatment failures in the antibiotic group could not be explained by noncompliance or development of resistance (to clarithromycin or rifabutin). Adverse events were also lower in the surgical group (28%) compared to the antimicrobial group (78%).

If TB is suspected, empiric antituberculosis therapy should be promptly started after the needle aspiration. Three-drug combination therapy is recommended for the first 2 months. Isoniazid, rifampin, and pyrazinamide (plus ethambutol or an aminoglycoside if resistance is suspected) are the initial choices of therapy. The fourth drug may be discontinued once susceptibility is known. Additional treatment for at least 4 months with isoniazid and rifampin is indicated for susceptible M. tuberculosis.8 The local Department of Health should be informed of cases of tuberculous lymphadenitis.

Treatment is supportive for lymphadenitis caused by B. henselae, as it is primarily a self-limited disease.6,8 Symptoms usually resolve in 2–4 months. A prospective, randomized, double-blind, placebo-controlled study to evaluate benefit of treatment (with azithromycin) showed that there is treatment benefit within the first month of treatment (defined by lymph node volume); after the 30 days, there was no significant difference between the two groups.30 Fine needle aspiration may be indicated to relieve pressure from painful suppurative lymph nodes. Antimicrobial therapy may be necessary for patients with severe or systemic disease or for those who are immunocompromised. Optimal choice of antimicrobial therapy or its length has not been established. Choices of antimicrobial therapies include erythromycin, azithromycin, gentamicin, trimethroprim–sulfamethoxazole, rifampin, and ciprofloxacin.7,8

Lymphadenitis caused by acquired T. gondii infection in a nonpregnant, immunocompetent host does not require antimicrobial therapy.8

Most cases of acute unilateral lymphadenitis resolve with appropriate antibiotic therapy. Up to 10% of patients may need incision and drainage despite appropriate management.26 Described risk factors that predict need for surgical intervention include patient aged <1 year and symptoms present approximately 48 hours prior to presentation.13,31 Abscess formation is a common complication of cervical lymphadenitis. Rapid progression or failure to treat adenitis can result in cellulitis, septicemia, or toxin-mediated sequelae. Poststreptococcal glomerulonephritis occurs occasionally. Rare complications include cervical fasciitis, carotid artery aneurysm with rupture, jugular vein thrombosis, septic embolization, mediastinal abscess, and purulent pericarditis.31 These complications stress the need for appropriate treatment with the first signs of lymphadenitis.