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Suppurative Lymphadenitis
Iain P. Fraser, MD, DPhil
Corresponding author
Iain P. Fraser, MD, DPhil
Clinical Pharmacology, Merck Research Laboratories,
126 East Lincoln Avenue, RY34-A500, Rahway, NJ 07065, USA.
E-mail: iain_fraser@merck.com
Current Infectious Disease Reports 2009, 11:383–388
Current Medicine Group LLC ISSN 1523-3847
Copyright © 2009 by Current Medicine Group LLC
Suppurative lymphadenitis is an important and com-
mon form of soft tissue infection. Most acute cases
of suppurative lymphadenitis are caused by Staphy-
lococcus aureus or by Streptococcus pyogenes.
Empiric antibiotic therapy is frequently successful in
the early stages of the disease process, but increas-
ing prevalence of methicillin-resistant S. aureus in
particular has necessitated a shift in antibiotic choice
that is dictated primarily by speci c local resistance
patterns. Several other organisms and noninfectious
in ammatory processes may give rise to a clinical
syndrome suggestive of suppurative lymphadenitis.
Failure to respond to empiric antibiotics should trig-
ger a diagnostic re-evaluation to determine the need
for surgical intervention and/or the possibility of
alternative microbiologic diagnoses.
Introduction
Lymph nodes along with other secondary lymphoid tis-
sues are the site of almost all primary immune responses.
These tissues provide a microenvironment that facilitates
interactions between antigens carried from the periphery
by antigen-presenting cells (APCs) and their cognate
T lymphocytes. Lymph nodes are grouped together phys-
ically to provide drainage of anatomically de ned areas
and facilitate host protection against microbial invasion
by 1) limiting the spread of pathogens when speci c
immune responses are generated (cellular and humoral
macrophage effector functions of the innate immune
system), 2) co-localizing APCs and low-frequency,
pathogen-speci c lymphocytes to facilitate speci c
immune interactions, and 3) providing the appropriate
microenvironment for lymphocyte activation, prolifera-
tion, and maturation [1•]. Given these critical functions
in host defense, it is not surprising that pathogens may
occasionally overwhelm these mechanisms and establish
an infection in the very organs intended to facilitate their
control and elimination.
Even though lymph nodes are well-de ned, encapsu-
lated structures with exquisite microarchitectural features,
they undergo developmental and temporal changes
during the lifespan of an individual. In most healthy
newborn infants, lymph nodes are not usually clinically
palpable, but grow in size through puberty (rising to peak
prominence between the ages of 4 and 8 years), and then
undergo steady atrophy. [2]. Atrophy of lymph nodes with
age may be a major reason for the decrease in the inci-
dence of lymphadenitis that occurs with age.
Lymphadenitis refers to in ammation of lymph nodes
and can be quali ed further. Suppurative lymphadenitis
is characterized by invasion of the lymph node by neu-
trophils, resulting in rapid swelling leading to capsular
distention, edema, and ultimately tissue necrosis and
liquefaction. When super cial lymph nodes are involved,
the increased size of the nodes may be appreciated clini-
cally, and the rapid capsular distention causes local pain.
Suppurative lymphadenitis refers conventionally to acute,
localized infections caused by pyogenic bacteria (eg,
Staphylococcus aureus and Streptococcus pyogenes).
However, several organisms (see below) are not typically
pyogenic, and yet may produce localized lymphadenitis
that progresses to necrosis and/or liquefaction, thereby
resembling the clinical presentation of suppurative lymph-
adenitis. Suppurative lymphadenitis constitutes a major
subset of soft tissue infections. In a retrospective analysis
of 242 children hospitalized with soft tissue infections
(2000–2004), 26% had cervical lymphadenitis and 20%
had cervical abscess (often a complication of suppurative
lymphadenitis) [3].
Clinical Presentations and Microbiology
Suppurative lymphadenitis affecting super cial lymph
nodes typically presents acutely as a localized in am-
matory mass with associated mild systemic symptoms.
Whereas bilateral or multifocal lymphadenitis is more
likely caused by viral pathogens, acute bacterial lymphad-
enitis occasionally may present in this fashion. The size of
the affected nodes, the extent to which the overlying skin
is in amed, and the ability of the examiner to elicit clinical
uctuance vary. In childhood, the cervical lymph nodes
(draining the head, neck, oropharynx and nasopharynx)
are the most common anatomic group of lymph nodes to
undergo suppurative infection. Whereas acute in amma-
tory masses in the neck region arise most frequently from
infected lymph nodes, the clinical differential diagnosis
384 I Skin, Soft Tissue, Bone, and Joint Infections
includes in ammation in other structures (eg, suppurative
parotitis, thyroiditis, and infected cysts—thyroglossal
duct, branchial cleft, dermoid, and epidermoid cysts) [4].
Suppurative lymphadenitis affecting deep lymph nodes
(eg, retropharyngeal lymphadenitis in children) produces
signs and symptoms indicative of a deep-seated in amma-
tory process, usually without clinical features to implicate
lymph nodes as the anatomic source. The clinical differ-
ential diagnosis in this setting is therefore considerably
broader than that of super cial lymphadenitis. Differen-
tiating retropharyngeal lymphadenitis (intact lymph node
with liquefactive necrosis and surrounding edema) from
abscess (extension of purulence beyond the node and into
the retropharyngeal space) may help determine the most
appropriate therapy (especially with respect to medical
vs surgical management), but even with modern imaging
technology, this may be dif cult to achieve without surgi-
cal exploration [5•].
Microbial Etiology
For several decades, studies conducted to determine
the causative agents of suppurative lymphadenitis have
consistently indicated a predominance of S. aureus over
S. pyogenes [6,7,8•]. However, these results may not
accurately represent all cases of suppurative lymphad-
enitis in the community, because only cases suf ciently
severe to merit hospitalization and/or surgical interven-
tion undergo the necessary microbiologic evaluation.
Furthermore, prior empiric antibiotic therapy may
confound culture results. In a retrospective review of
65 children undergoing incision and drainage of super-
cial head and neck abscesses (presumed to have arisen
from suppurating lymph nodes) in the United Kingdom
(1991–1996), bacterial cultures were positive in 78%
of children, with the most common organisms being
S. aureus and S. pyogenes (57% and 12% of positive
cultures, respectively) [9]. In a similar analysis involving
62 children in Philadelphia, PA (2000–2006), bacterial
cultures were positive in 79% of children, with the most
common organisms again being S. aureus and S. pyo-
genes (63% and 22% of positive cultures, respectively)
[10]. In a review of 284 Canadian children (1996–2001)
admitted to the hospital with adenitis, 86% of 57
bacterial cultures were positive, with the most com-
mon organisms once again being S. aureus and
S. pyogenes (70% and 9% of positive cultures, respec-
tively) [8•]. Several other organisms have been cultured
from the lymph nodes of patients presenting with a clin-
ical diagnosis of suppurative lymphadenitis. Examples
include Haemophilus in uenzae, Bacteroides spp, [9],
Streptococcus intermedius [11], and Fusobacterium
necrophorum [12]. In newborn infants, Streptococcus
agalactiae (group B streptococcus, GBS) is associated
with a syndrome of cellulitis-adenitis, an infrequent but
well-characterized manifestation of neonatal infection
with this organism [13]. The growth in culture of mixed
skin ora and/or of coagulase-negative staphylococci
from the lymph nodes of otherwise healthy patients are
of doubtful etiologic signi cance.
Changes in Antimicrobial Susceptibility
Although the main organisms causing suppurative
lymphadenitis appear not to have changed in prominence
over several decades, the antimicrobial susceptibility of
the primary agent, S. aureus, most certainly has. In their
British series of 65 patients from the early 1990s, Simo
et al. [9] reported that all 29 isolates of S. aureus were
susceptible to β-lactamase–resistant antibiotics ( ucloxa-
cillin). During the past several years, however, infections
caused by methicillin-resistant S. aureus (MRSA) have
increased in prevalence. Whereas these organisms pre-
viously were associated primarily with nosocomial
acquisition in large medical centers, community-acquired
MRSA (CA-MRSA) infections in children and adults
without identi ed predisposing risk factors have become
increasingly prevalent [14]. In a retrospective chart
review of radiologically con rmed neck abscesses in 228
children (1999–2007), S. aureus was isolated as the caus-
ative organism in 48%, and 29% of these were identi ed
as CA-MRSA [15]. The methicillin-resistant phenotype
of CA-MRSA isolates is conferred by a staphylococ-
cal cassette chromosome, SCCmec IV, that is smaller
and contains fewer antibiotic-resistance genes than the
SCCmec elements associated with hospital-associated
MRSA isolates [16]. As a result, these CA-MRSA strains
may retain susceptibility to non–β-lactam antibiotics
(eg, clindamycin, trimethoprim-sulfamethoxazole, and
tetracyclines). Unfortunately, many of these CA-MRSA
isolates have been found to harbor a phage bearing
Panton-Valentine leukocidin (PVL) genes, which in turn
appear to be associated with increased virulence [17•].
The PVL virulence factor appears to be associated with
S. aureus infections that generate a more proin amma-
tory host response, are more likely to result in abscess
formation, are more likely to give rise to positive blood
cultures, and are more likely associated with venous
thrombophlebitis and septic embolism [18]. Therefore,
inappropriate selection of empiric antibiotic therapy for
infections caused by S. aureus is now likely to be more
frequent than previously, and is more likely associated
with infections of greater clinical severity. Appropriate
selection of empiric antibiotics to treat presumed sup-
purative lymphadenitis therefore needs to encompass
a careful assessment of clinical severity (to ensure that
parenteral antibiotics are administered in preference to
oral, if clinically indicated), may need a more aggressive
approach to obtaining samples for bacterial culture (eg,
by lymph node aspiration), and requires detailed knowl-
edge of antibiotic resistance patterns in the patient’s local
community. Local microbiology laboratory panels should
include a wide range of antibiotics for susceptibility
testing of S. aureus isolates, and in communities where
Suppurative Lymphadenitis I Fraser I 385
clindamycin remains an important therapeutic option,
detection of inducible macrolide-lincosamide-strepto-
gramin B (MLSB) phenotypes should be available [18].
Differential Diagnosis
Some organisms, although less frequently isolated from
suppurating lymph nodes, bear special mention because
they may lead to a clinical picture resembling suppurative
lymphadenitis. Failure to respond to treatment directed
toward the common bacterial causes of suppurative
lymphadenitis should provoke inter alia a consideration
of these organisms in the ongoing diagnostic evaluation
of such patients.
Nontuberculous mycobacteria (NTM) are a cause of
unilateral cervical lymphadenitis in otherwise healthy,
immunocompetent children (predominantly between
1 and 5 years of age) [19]. With few clinical features to
distinguish NTM from suppurative lymphadenitis in the
early phases, this microbiologic diagnosis frequently is
only entertained after the adenitis has failed to respond
to therapy directed against S. aureus and S. pyogenes.
The natural history of untreated NTM lymphadenitis
involves progression to liquefaction, violaceous discolor-
ation of the overlying skin, and then drainage through the
skin. Clinical features suggestive of a diagnosis of suppu-
rative lymphadenitis include redness (different from the
violaceous hue associated with NTM infection), warmth
of the overlying skin, tenderness, and fever [19]. Radio-
logic imaging (CT or MRI scans) features, especially a
lack of in ammatory stranding of the subcutaneous fat,
may help to distinguish NTM from suppurative lymph-
adenitis [20]. Surgical excision has long been considered
the curative therapy of choice, although cases responsive
to antimicrobial chemotherapy have been described [21].
A recent clinical trial randomly assigned patients with
culture-proven NTM lymphadenitis to either surgical
excision or antimicrobial chemotherapy [22]. In this
study, surgical excision was more effective than medical
therapy (cure rates of 96% vs 66%, respectively) in an
intent-to-treat analysis.
Bartonella henselae, the cause of cat scratch disease
(CSD), typically leads to a chronic form of lymphade-
nopathy in the lymph nodes draining the site of the
inoculating scratch. On occasion, CSD may present with
a suppurative lymphadenopathy, which may progress to
abscess formation, the etiology of which only becomes
apparent following biopsy and molecular diagnostics
and/or serologic conformation [23]. In a study of 454
patients with undiagnosed head and neck masses in Ger-
many (1997–2001), about 13% were ultimately diagnosed
with CSD, with about 12% diagnosed with other primary
infectious etiologies (including S. aureus and S. pyo-
genes) [24]. Antibiotic therapy for uncomplicated CSD
in immunocompetent patients remains controversial, but
macrolides/azalides as well as combination rifampin and
doxycycline have been used [25].
Tularemia is a zoonosis caused by the gram-negative
pleomorphic coccobacillus Francisella tularensis. The
common forms of the disease in humans are ulceroglan-
dular and glandular, both of which affect the lymph
nodes. In nonendemic areas, the bacterial etiology may
become apparent only after antibiotics directed toward
suppurative lymphadenitis have failed to resolve the
infection, or when bacterial cultures of aspirates from
apparently suppurating lymph nodes return nega-
tive [26]. In the absence of a clear exposure history,
general laboratory investigations, radiology, and even
histopathology may not contribute additional diagnostic
information. The organism is dif cult (and potentially
dangerous) to culture in the microbiology laboratory,
and serologic testing is the diagnostic modality of choice.
Treatment with aminoglycosides (particularly strepto-
mycin) has long been the medical treatment of choice for
nonmeningitic tularemia, but recent reports suggest that
quinolones may be safe and effective alternatives [27].
Several other infectious agents may produce a
clinical picture consistent with a diagnosis of suppu-
rative lymphadenitis, but concomitant epidemiologic,
anatomic, and clinical features usually are suf ciently
obvious to steer the clinician toward the appropri-
ate diagnosis. Examples of these infectious conditions
include tuberculous lymphadenopathy [28], bubonic
plague (Yersinia pestis) [29], Yersinia enterocolitica
infection [30], focal nontyphoid Salmonella infection
[31], Legionella pneumophila infection [32•], and
sexually transmitted infections such as syphilis [33],
chancroid [34], and lymphogranuloma venereum [35].
Noninfectious causes of in amed, enlarged lymph
nodes further complicate the diagnosis and therapy
of suppurative lymphadenitis. Neoplasia, particularly
lymphomas and metastatic carcinomas may cause
lymph node swelling that could be mistaken for sup-
purative lymphadenitis. These diagnoses tend to be
more frequent in adults than in children. Histiocytic
necrotizing lymphadenitis (Kikuchi-Fujimoto disease)
is an in ammatory disorder of unknown etiology that
occurs predominantly in young women. It is benign
and self-limiting, and is diagnosed most frequently by
histopathologic evaluation of an affected lymph node
[36]. In children, lymphadenitis is a component of the
periodic fever, aphthous stomatitis, pharyngitis, and
adenitis (PFAPA) syndrome (also known as Marshall
syndrome) [37]. In PFAPA, the periodic fevers should
provide an important diagnostic clue; however, the
fever pattern may not be apparent early in the disease
process, and a negative workup for infectious etiologies
frequently precedes the diagnosis. Kawasaki disease
is another in ammatory pediatric disorder associated
with localized cervical lymphadenitis [38]. A careful
evaluation of the pediatric patient with cervical adenitis
for other diagnostic features of Kawasaki disease may
help ensure that this important condition is not over-
looked or treated inappropriately.
386 I Skin, Soft Tissue, Bone, and Joint Infections
Host Susceptibility: Role of Immunode ciency
Although suppurative lymphadenitis clearly can and does
occur in immunocompetent individuals, this infectious
syndrome may be the presenting feature or a manifesta-
tion of genetic immunode ciency. The relative frequency
with which patients with chronic granulomatous disease
(CGD) develop suppurative lymphadenitis speaks to the
importance of oxidative killing mechanisms in this infec-
tious process. In a review of 368 patients in the US national
CGD registry in 2000, 53% of patients had experienced at
least one episode of suppurative lymphadenitis, with only
pneumonia (79%) and abscess (of any kind, 68%) as more
frequent infectious manifestations [39]. In this US series,
S. aureus was the most common lymphadenitis pathogen
(isolated from 26% of suppurative lymphadenitis cases),
followed by Serratia, Candida, and Klebsiella species.
Given the relative infrequency with which the latter three
organisms are cultured from immunocompetent individu-
als with suppurative lymphadenitis, their isolation should
prompt an evaluation for underlying immunode ciency,
particularly CGD. In a cohort of 429 European patients
with CGD, 213 patients (50%) experienced at least one
episode of suppurative lymphadenitis [40]. Of these
patients with lymphadenitis, 80% either did not undergo
bacterial culture or had negative cultures of their infected
lymph nodes. As in the US cohort, S. aureus was the most
frequent pathogen cultured from these lymph nodes (12%
of all lymphadenitis cases). In contrast to the US cohort
(with no cases reported), bacille Calmette-Guérin (BCG)
represented 2% of the positive lymphadenitis cultures in
the European cohort, with BCG exposure by vaccination
thought to explain the difference between the cohorts.
Interestingly, BCG infections (including lymphadenitis)
have been described in other series of CGD patients,
again likely representative of different bacterial exposures
in geographic regions [41]. Recently, a novel gram-nega-
tive bacillus (now named Granulobacter bethesdensis, of
the family Acetobacteraceae) was isolated from a CGD
patient with fever and lymphadenitis, thereby adding to
the list of organisms associated with bacterial infection of
the lymph nodes [42•].
Several other genetic immunode ciencies result in
pyogenic infections that can include suppurative lymph-
adenitis, although their clinical presentation is unlikely
that of isolated adenitis in an otherwise well-appear-
ing patient. Some examples include interleukin (IL)-12
de ciency (BCG, Salmonella enteritidis adenitis) [43];
IL-12/-23 receptor de ciency (BCG adenitis) [44]; inter-
feron-γ receptor de ciency (BCG and Mycobacterium
abscessus adenitis) [45]; and IL-1 receptor–activated
kinase 4 (IRAK-4) de ciency (S. aureus adenitis with
paratracheal abscess) [46].
Diagnosis and Treatment
Several diagnostic and therapeutic questions face the
clinician confronted with a patient with apparently
in amed, enlarged lymph nodes. The duration and tempo
of the illness, known sick contacts, local trauma, animal
exposures, travel, associated local and systemic symp-
toms, and family history (particularly with respect to
immunode ciency) are all key features to be probed in the
medical history. The physical examination should include
an assessment of the overall health of the patient and the
presence of systemic signs of in ammation. The number
of affected anatomic regions (localized vs generalized)
should be determined, and a clinical exclusion of other
anatomic structures (eg, parotid gland, thyroid, blood
vessel) should be attempted. Careful examination of the
affected tissue should include an assessment of overlying
skin and of lymph node size, consistency, mobility, and
uctuance. The anatomic regions drained by the in amed
lymph nodes should be evaluated (including dentition and
oropharynx for cervical adenopathy, and the perineal
region for inguinal adenopathy).
The utility of laboratory investigations depends on the
clinical assessment provided by the history and physical
examination. For most patients with suppurative lymph-
adenitis encountered in primary care practice, a trial of
empiric antibiotic therapy without further laboratory
evaluation is likely appropriate, provided the antibiotic
regimen includes appropriate coverage for CA-MRSA
as described earlier. More severe cases may require early
surgical consultation to allow for appropriate timing of
radiologic examination and initiation of antibiotic therapy.
Close follow-up of patients treated with empiric antibiot-
ics for suppurative lymphadenitis is required to identify
nonresponders. For these patients, re-evaluation should
include anatomic reassessment (has the in ammatory
process progressed to abscess formation requiring surgical
drainage?) and microbiologic reassessment (could this pro-
cess be caused by a previously unanticipated organism?).
When the suppurative lymphadenitis is cervical,
percutaneous aspiration can provide diagnostic and
therapeutic bene t [47], but may not be adequate to
avoid the need for formal surgical drainage [48••]. In a
Canadian study of 284 children hospitalized with acute
unilateral lymphadenitis, younger patients (especially
those younger than 2 years of age) and longer duration of
symptoms (> 48 hours before presenting to the hospital)
were features associated with an increased risk of surgi-
cal drainage [8]. For patients with concern for neoplastic
disease rather than in ammation in super cial affected
lymph nodes, measurement of resistive index by power
Doppler may be helpful [49].
Conclusions
Suppurative lymphadenitis is a common diagnosis, espe-
cially in the pediatric age group. For several decades,
S. aureus and S. pyogenes have remained the major bacte-
rial causes of this infectious syndrome. Although many
patients with moderate to mild disease of recent onset are
cured by empiric oral antibiotics, changes in the antibiotic
Suppurative Lymphadenitis I Fraser I 387
resistance pro le of S. aureus in particular have made the
selection of appropriate empiric antibiotics more challeng-
ing. Clinicians should ensure that their chosen antibiotics
maintain activity against the MRSA strains circulating in
their community. Enlarged, in amed lymph nodes may
have many other infectious and noninfectious causes.
Accordingly, patients who do not respond to empiric
antibiotic therapy and patients who present with sugges-
tive clinical features on history or physical examination
should undergo more extensive evaluation to assess the
need for surgical intervention or alternatively directed
antimicrobial therapy. Some patients may also require a
directed evaluation of their immune system to exclude
possible immunode ciency.
Disclosure
The author is a full-time employee of Merck & Co. and
owns stock and/or stock options in the company.
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