J Antimicrob Chemother 2013; 68: 1941 1950

doi:10.1093/jac/dkt128 Advance Access publication 23 April 2013

A review of the pathogenesis of adult peritonsillar

abscess: time for a re-evaluation
Emily L. Powell1, Jason Powell2, Julie R. Samuel3 and Janet A. Wilson1,2*
1

Institute of Health and Society, Newcastle University, Newcastle upon Tyne NE1 7RU, UK; 2Department of Otolaryngology Head and
Neck Surgery, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK; 3Department of Medical Microbiology, Freeman Hospital,
Newcastle upon Tyne NE7 7DN, UK
*Corresponding author. Department of OtolaryngologyHead and Neck Surgery, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK.
Tel: +44-(0)191-223-1086; Fax: +44-(0)191-223-1246; E-mail: janet.wilson@ncl.ac.uk

Design: A literature review exploring key pathogens, predisposing host factors and current pathogenic hypotheses.
Methods: A PubMed search for articles published between January 1980 and January 2012 using the terms peritonsillar abscess AND microbiology, peritonsillar abscess AND pathophysiology and peritonsillar abscess AND
etiology.
Results: Major pathogens in PTA are opportunistic microflora. Group A streptococcal PTA infections present differently
from polymicrobial PTA. A number of host factors influence the conditions required for the pathogenesis of PTA.
Conclusions: PTA is clinically distinct from acute tonsillitis and occurs in people with a chronic underlying
susceptibility. Targeting host factors, including oral hygiene, antibiotic use and smoking, may prevent PTA. Reeducation of clinicians concerning the aetiology of PTA is necessary for appropriate disease management.
Keywords: quinsy, microbiology, aetiology

Introduction

Methods

Peritonsillar abscess (PTA)also known as quinsyis a localized

deep neck infection that develops between the tonsil and its
capsule.1 3 The infection can progress to airway obstruction,
abscess rupture and asphyxia by aspiration of pus and necrosis
resulting in septicaemia or haemorrhage.4,5 English data from
the year 2009 10 saw 7589 finished consultant episodes attributed to PTA, and the condition is on the rise.4,6,7
There is very little understanding of the diseases aetiology6,8
as highlighted by the lack of management protocols.7 Treatments vary greatly between clinicians, ranging across antibiotics
+ surgical drainage + removal of the palatine tonsils.7,9,10 PTA is
commonly stated to be a complication of acute tonsillitis (AT);11
recent reports, however, suggest that primary tonsillitis may not
always be the causative factor. The pathogenesis requires certain
microfloral compositions coinciding with oropharyngeal damage
and/or immunocompromise.12 14 This review attempts to
explore these controversies with a view to improving understanding of the disease, standardizing management and generating
strategies for its prevention.
We reviewed the literature to identify probable pathogens and
critically analysed the evidence behind current hypotheses on
the pathogenesis of PTA.

The literature was reviewed using the PubMed database, searching

for papers published between January 1980 and January 2012. Search
terms were peritonsillar abscess AND microbiology, peritonsillar
abscess AND pathophysiology and peritonsillar abscess AND etiology.
Of the 668 results obtained, 112 titles were deemed to be relevant to the
pathogenesis and incidence of PTA in adults. Relevance when reading
abstracts was further assessed using an inclusion criterion (Figure 1); this
resulted in 58 appropriate sources. References within the bibliographies
of these articles were then tracked.

Results
PTA microbiology
Microbiological overview
There is much inconsistency and controversy across the literature
in describing the microbiology of PTA. Table 1 displays the diverse
range of microbiological findings obtained from PTA pus samples
that were analysed in 15 papers.8,15 28 This is likely to reflect the
substantial diversity of natural flora within the oropharyngeal
spaces.29

# The Author 2013. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved.
For Permissions, please e-mail: journals.permissions@oup.com

1941

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

Objectives: To perform a multifactorial exploration of the aetiology of peritonsillar abscess (PTA) in adults, in
order to develop greater clinical understanding of the condition and improve management.

Review

Peritonsillar abscess AND

microbiology
197
Abstracts include
Titles include

Peritonsillar abscess AND

pathophysiology

29

Non-paediatric focus
Focus on PTA parameters
other than management
Focus on PTA parameters
other than disease
presentation

112

English language abstract

PTA as major disease focus
PTA specific to adults
Focus on PTA parameters
other than management
Focus on PTA parameters
other than disease
presentation

58

Papers
read

442

Figure 1. Flow chart demonstrating the search method used to identify the relevant literature. The numbers in bold represent the number of papers
found and carried over for assessment.

The majority of PTAs, in most series, are polymicrobial infections containing common oropharyngeal microflora,5,15,16,22,30,31
with an average of three isolates per specimen.15,16,19 However,
Megalamani et al.32 describe all their identified aerobic infections
(65% of their isolated cultures) as being monomicrobial, and
72.3% of the patients studied by Snow et al.17 also had monomicrobial infections.

Determination of PTA pathogens: methodological

considerations
The extreme variation observed in Table 1 may reflect methodological differences between the studies reviewed. Different culturing techniques, incubation times, sample origins and collection
methods could significantly alter the validity of the findings as a
true representation of the isolates found at the site of infection.21,33 The method of recording microbiological findings may
also influence the results. Whether facultative anaerobes were
classified as aerobes or anaerobes varied across studies.19,25
Some studies used species growth as a indication of pathogenesis
and recorded only those with moderate to heavy growth.19 More
virulent PTA pathogens with less growth might have been
overlooked.15,25,34
Alternatively, data variations could have occurred due to the
different geographical locations of the studies. The microflora
of individual populations may differ significantly owing to
native diets and lifestyles.21 Klug et al.26,35 and Rusan et al.8
recorded particularly high levels of Fusobacterium but gathered
all of their data from a Danish population, which may have
higher microfloral Fusobacterium levels than other populations.
Another important variable was that patients presenting with
PTA were at different stages of antimicrobial therapy. The majority
of patients had been prescribed antibiotics on primary presentation to their GP, which may have altered the findings. Some
studies have reported no significant difference in microflora
between patients with prior antibiotic treatment and those

1942

without.18,21,27,32 Microbiological analyses by Megalamani

et al.32 used only patients without prior antibiotic treatment and
gained percentages of isolates of group A streptococci (GAS)
similar to those noted in patients who had had antibiotic pretreatment. Conversely, some studies found that the incidence of GAS
infections was significantly reduced in patients pretreated with
antimicrobial agents.15,19 These studies suggest that GAS could
be the causative organism in far more cases of PTA than have
been recorded, but that the use of antimicrobials kills the pathogen, allowing resistant commensals to invade the damaged
tissue space.15,18,19,36

Major pathogens in PTA

In PTAs yielding a single isolate, GAS and Fusobacterium necrophorum
were the most commonly isolated organisms.8,17 19,26,27,31,32,35,36
Klug et al.26 and Rusan et al. 36 showed that F. necrophorum and
GAS were significantly more prevalent in the tonsils of their patients
with PTA than in tonsils excised electively from patients with chronic
tonsillar disease. Pure cultures containing Streptococcus milleri group
(SMG), Staphylococcus aureus, Nocardia asteroides, Haemophilus
influenzae, Arcanobacterium haemolyticum and Streptococcus pneumoniae have also been recorded.15 19,31,33,37,38 These findings
suggest a role for them as primary pathogens.
It is a difficult task to determine which of the identified strains
prevalent in polymicrobial samples is a significant pathogen. In the
literature, three opportunistic bacteria yielding heavy growth from
aspirates have been considered to be key causative organisms:
GAS, indigenous Fusobacterium species and SMG.8,15,18,25,26
While the heavy growth of group C streptococci, Peptostreptococcus and Prevotella species is commonly observed in PTA aspirates,
these organisms have received very little attention within the literature and hence will not be addressed in detail here.15,16,22,25,31
GAS Microbiological analyses show that between 20% and 30%
of PTAs are caused by GAS, while in some studies GAS have been

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

Peritonsillar abscess AND

etiology

Review

Table 1. Studies analysing the microbiological composition of PTAs 1980 2012

Positive
cultures Anaerobes Aerobes
(n)
(%)
(%)

Study
15

Mixed aerobes
and anaerobes
(%)

Average
isolates/
specimen

Common aerobes

Common anaerobes

Jokipii et al., 1988

42

66.7

90.5

61.9

3.2

Brook et al., 199116

34

94.1

82.4

76.0

3.1

Snow et al., 199117

55

34.5

78.1

27.3

1.2

122

82.3

86.3

71.3

4.4

Mitchelmore et al.,
199519
Muir et al., 199520
Sakae et al., 200621
Zagolski and Gajda,
200728
Sunnergren et al.,
200822

45

84.4

62.2

46.7

3.2

GAS

39
26
12

48.0
73.1
50

29.0
96.2
50

69.2
50

2.9
1.5

GAS
GAS, other streptococcal sp.
streptococcal sp.

83

36.1

38.6

13.0

Gavriel et al., 200923

137

51.8

57.7

9.5

1.1

GAS, group C streptococci, group

G streptococci, S. pneumoniae,
SMG
GAS, S. intermedius

Repanos et al.,
200924
Rusan et al., 20098
Hidaka et al., 201125

119

23.5

43.7

26.9

streptococcal sp.

464
65

33.2
30.8

26.9
84.6

26.2

1.4

Klug et al., 201126

Love et al., 201127

36
147

91.7
57

88.9
57.10

80.6
57.0

3.7

GAS, group C streptococci

Fusobacterium sp.
SMG, GAS, other streptococcal sp. Prevotella sp., Peptostreptococcus sp.,
F. necrophorum

GAS, group C streptococci, other F. nucleatum, Eikenella corrodens

b-haemolytic streptococcal
sp., S. aureus, H. influenzae

Weighted average

71

45

49

Jousimies-Somer
et al., 199318

GAS, non-haemolytic
streptococcal sp., S. aureus,
H. influenzae
GAS, SMG, H. influenza, viridans
streptococcal spp.

Peptostreptococcus sp., Bacteroides sp.,

Fusobacterium sp.
Prevotella sp., Porphyromonas sp.,
Peptostreptococcus sp.
Peptostreptococcus sp., Fusobacterium
sp., Bacteroides sp.,
F. necrophorum, Prevotella sp.,
Peptostreptococcus micros,
Fusobacterium nucleatum, Actinomyces
odontolyticus
SMG, Peptostreptococcus sp., Prevotella
sp., Fusobacterium sp.

Prevotella sp., Peptostreptococcus sp.

Bacteroides sp.
Bacteroides sp., microaerophilic
Streptococcus, Peptostreptococcus sp.,
Prevotella melaninogenica
Prevotella sp., Peptostreptococcus sp.,
Gemella morbillorum, Bacteroides
fragilis

Weighted averages that cannot be configured due to lack of data.

52.0
9.0

56.0

19.0
6.0

0.84

4.1

1943

JAC

GAS, other streptococcal sp.,

Neisseria sp.
S. aureus, GAS

b-Lactamaseproducing
cultures (%)

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

Review

reported in 45% of abscesses.15,16,18,21 23,26,27 Various

studies17,18,31,32 have observed GAS growing in pure culture
more often than in mixed culture: Lilja et al.31 found GAS to
be present only in monomicrobial PTA samples. GAS are consistently the isolate most commonly recovered from monomicrobial
PTAs. The prevalence of GAS in aspirates is higher than that in
patients with little or no history of sore throat: Jousimies-Somer
et al.18 found, in a series of 550 aspirates, that the rate of
previous peritonsillar or tonsillar infection was significantly
lower (P,0.01) in GAS-harbouring patients than in those with
anaerobic infections. Despite the high incidence of GAS in PTAs,
its causative relationship has not been fully identified. Risberg
et al.39 found that those presenting with PTA had no significant
excess of GAS-positive results compared with those presenting
with sore throat. This would suggest the involvement of other
co-factors in the pathogenesis of PTA.

SMG The facultative anaerobic group of commensal SMG consists of three species: Streptococcus intermedius, Streptococcus
anginosus and Streptococcus constellatus. SMG has been associated with a range of serious head and neck infections and is
commonly associated with abscess formation.45,46 Saiki et al.47
identified SMG isolates as making up 28% of their total isolates,
findings supported by Hidaka et al.,25 Jousimies-Somer et al.18
and Fujiyoshi et al.,48 for whom SMG was the most common
species isolated (25.8%).48 Mitchelmore et al.19 recorded SMG

1944

PTA pathogenesis
Current hypotheses
Two hypotheses are currently described to explain the pathogenesis of PTA. The predominant theorydescribed in the majority
of medical textbooks and hence well known among cliniciansstates that PTA is a complication of AT.11 There seems,
however, to be no scientific literature that provides direct supporting evidence for this. The second is a hypothesis that has
been slowly gathering more recognition and supporting evidence
over the last 20 years and highlights the association between
damaged tissue and abscess development: the Weber gland
hypothesis.

A complication of AT
Recurrent episodes of ATand sore throat are commonly reported in
PTA.19,50 Marom et al.50 found that 79% of patients in their study
reported a sore throat preceding the development of PTA.
However, other studies have reported that up to 68% of patients
with PTA have no preceding history of tonsillitis or sore
throat.22,50,51 Some other recent observations question the true involvement of AT in the development of PTA.12 14 First, Passy12
observed in a study of 100 consecutive PTA patients that 96% of
patients had no exudate on the tonsils and very little tonsillar swelling. Furthermore, a study of resected tonsils by Chen et al.14
showed that the tonsils of patients with PTA were smooth and
healthy, while fibrosis was noted in the surrounding tissue.
Considering the bacteriology, isolates commonly found in PTA
are also found in the oropharynx of patients with AT and recurrent AT.52 54 As in PTA, there is great variation in the oropharyngeal bacteriology related to AT and recurrent AT.52,53,55 GAS are
found in statistically similar numbers,52 and anaerobic microflora
are becoming more recognized as potential causes of these diseases.53,54 However, other studies indicate significantly more
growth of S. aureus and H. influenza in the tonsils of patients
with AT than in those with PTA.52,55
A further area of discrepancy concerns the modal peak of incidence groups with the highest diagnoses of AT and PTA. The incidence of PTA is highest from the mid-teens to 40 years

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

Fusobacterium species F. necrophorum is the anaerobe most

commonly found in pure culture in PTA.8,19,26,35 This obligate anaerobe has been linked to a variety of localized head and neck
infections as well as Lemierres syndrome.40,41 Studies have
observed Fusobacterium in 4%53% of samples, often reporting
higher isolate numbers than for GAS.8,18,19,25,26,33,35,40 The capability of Fusobacterium to be a significant pathogen in PTA has
been highlighted in a number of studies.35,40,42 Klug et al.35
observed that 81% of F. necrophorum isolates grew as a pure
culture, and that colonized patients harbouring these isolates
had significantly stronger inflammatory responses to the PTA infection. Brook et al.42 showed that F. nucleatum could be isolated
from the PTAs of 74% of a series of paediatric patients. Furthermore, this study found higher levels of antibodies to both
F. nucleatum and Prevotella intermedia in patients with PTA
than healthy controls, highlighting a probable pathogenic
interaction of these organisms with their host.42 This evidence
must take into the fact that microbial compositions and distributions may vary significantly with age due to growth, lifestyle and
hormonal changes.
Patients with a history of recurrent sore throat prior to the development of PTA were found to be more likely to have anaerobic
infections containing Fusobacterium.18 This bacterium has also
been isolated from patients presenting with recurrent AT, persistent sore throat syndrome, pharyngitis and hypertrophic
tonsils.41,43,44 It may be that the species favours conditions
that could potentially exist in all of these throat problems.
Fusobacterium species clearly have a pathogenic role in the
development of PTA, especially within polymicrobial infections.
Their apparent involvement as pathogens in other throat infections suggests that co-factors are necessary to promote the
localized tissue invasion required for PTA.

in 51% of samples. SMG most commonly coexists with anaerobes. Jousimies-Somer et al.18 observed that SMG was always
in mixed culture, although Hidaka et al.25 obtained aspirate cultures with pure SMG isolates. SMG thrives within polymicrobial
infections and is thought to promote virulence and accelerate inflammation.19,25,45 Given these findings, SMG is likely to have a
pathogenic role in the development of PTA.
We have clearly identified three key opportunistic bacteria
that are likely to be causative organisms in PTA: GAS, indigenous
Fusobacterium species and SMG. There seem to be predominantly two pathogenically different PTA subtypes. Type 1 contains a
pure culture of a single organism, most often GAS. Type 2 displays heavy polymicrobial growth, often containing a variety of
facultative and obligate anaerobes. Clinically, type 2 PTA often
appears to be more severe, probably due to synergistic microbial
interactions.15,49 The history of recurrent sore throat observed in
patients presenting with type 2 PTA is possibly representative of a
chronic underlying microfloral imbalance.18,23

JAC

Review

old.4,12,22,27,56 58 AT, on the other hand, has its highest incidence

at ages 5 15.12 One would have expected an overlap between
these age bands if PTA was indeed a direct complication of AT.
Furthermore, the average times to onset of symptoms are
similar in PTA and AT (3 5 days), which also makes it seem
unlikely that PTA is a progression of AT.12,25 Investigating the
seasonal incidence of PTA in relation to AT, Kordeluk et al.59
found no correlational lag between outbreaks of AT and PTA.
Rather, AT and PTA were observed to peak simultaneously.
However, this could be due to a common causal factor such as
an environmental condition or pathogen that has the capability
to induce both throat conditions.59 Ong et al.58 found no consistent seasonal correlation between the incidence of PTA and other
upper respiratory tract infections.

Blocked Weber glands

Host factors associated with PTA

The key pathogens in PTA are resident microflora. In order to
cause PTA, opportunists need to overcome the homeostatic
nature of the commensalhost relationship within the oropharynx. There are several host factors that may promote PTA, such
as age (mid-teens to 40 years), male gender, periodontal
disease, smoking, compromised immunity and previous
antibiotic use4 6,8,10,12,14,19,22,23,25,27,35,40,41,43,46,48,50 52,56 60,62 89
(Table 2). These in turn influence other factors: conditions for
the growth of opportunists, local humoral immunity, routes for
microbial invasion and niches for trapped debris, microbial
growth and localized suppuration.

Host immunity and PTA

PTA has been identified as a comorbidity factor often associated
with viral infection suppressing or compromising host immunity,
allowing for opportunistic secondary infection.50,84,89 91
Between January 2006 and December 2007, Ahmad and
Anari84 recorded infectious mononucleosis (IM) in 4% of patients
with PTA admitted to the Freeman Hospital, Newcastle upon
Tyne. Some small-scale studies have shown comorbidity rates
of IM with PTA to be as high as 20%.84 The compromised

PTA pathogens may produce proteolytic enzymes that outcompete and over-ride host local immunity.31
There is possible support for Passys Weber gland hypothesis.
These glands secrete IgA; blockage may lead to decreased
IgA production, which may subsequently allow for growth of
and invasion by pathogens.31
There appears to be no other literature investigating the expression or interaction of local immune system components and the
development of PTA. There is, however, evidence relative to other
throat infections. Tonsillar human b-defensin (HBD) levels, for
example, have been shown to be significantly reduced in patients
with recurrent tonsillitis.60,74,87
Besides producing immunomodulatory proteins, the tonsillar
tissue also acts as a site for antigen sampling.93 Damage or blockage of these sampling sitesas a result of debris or damaging
habits such as smokingmay affect the ability of receptors to recognize pathogens and manifest an immune response.68,70,79,93

Implications for clinical practice

This review supports the current practice of administering combined antibiotics to patients with PTA.7 Furthermore, it supports
guidelines from the Scottish Intercollegiate Guidelines Network
not to prescribe antibiotics to patients presenting with uncomplicated sore throat, with the risk of promoting a polymicrobial anaerobic (type 2) PTA or switching a streptococcal infection into an
infection with more severe type 2 characteristics.94
Patients presenting with a history of chronic sore throat
should be monitored following management of PTA and steps
should be taken to address lifestyle choices that may potentially
be promoting microfloral imbalance and susceptibility to infection. We suggest attempting this non-invasive, cost-effective
form of management before considering more interventional
procedures such as tonsillectomy.
Understanding factors that promote the growth and colonization of key PTA pathogens should not only lead to a more effective and standardized management of PTA, but also provide

1945

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

Passy12 hypothesized that PTA results from damage to the salivary glands of the upper soft palate known as the Weber glands.
These glands are proximal to the palatine tonsils and help to
keep the peritonsillar niche and tonsil crypts clean. The resected
tonsil study of Chen et al.14 found that although the upper tonsils
were smooth and healthy, there was inflammation and minor fibrosis of the adjacent Weber glands. Both Brook5 and Passy12
suggest that localized Weber gland infection or poor dental
hygiene could lead to scarring and subsequent blockage of the
gland or the draining duct. A reduction in the production of
saliva could increase the chances of suppuration within the tonsillar crypts and oral scar tissue, providing opportunity for localized peritonsillar infection. Saliva is also known to contain
elements of the innate immune system that control the resident
microflora;60 a blockage could potentially result in less control
over opportunists. Although this is a plausible theory, Dang
et al.61 performed a prospective cohort study that found no
correlation between salivary flow rate and PTA.

humoral immunity of these patients allows opportunists to

adhere to the hosts tonsillar tissue and subsequently invade
the epithelia, clinically seen as the progression of membranous
tonsillitis to PTA.89 It has been hypothesized that patients reporting non-exudative tonsillitis prior to the development of PTA may
have a localized viral infection, compromising the local immune
system and allowing bacterial invasion. A report of entirely viral
PTA supports this hypothesis.92 However, the recent study of
Rusan et al.36 investigating viral incidence and PTA showed no
significant difference in the viral load of patients with PTA compared with that in the tonsils of patients with chronic tonsillar
disease.
Lilja et al.31 found that most bacteria recovered from PTA pus
were not opsonized by complement components or immunoglobulin (Ig). In comparison, bacteria from the surfaces of
healthy tonsils were coated by surface IgA. None of the infecting
organisms from monomicrobial PTA samples was host immunelabelled. The group consistently noticed build-ups of deformed
and apoptotic host immune cells at the PTA site, occurring
with particular severity when GAS were also present. Their justification for their findings includes:

Review

Relation to pathogen
Host factor

Relation to PTA
incidence

Age:
highest PTA incidence
post-puberty
mid-teens to
40 years of age

Reference
(4, 8, 22, 23, 27, 41,
56 58, 62, 63)

Contributing effects
hormonal effect on local
immunity and/or microfloral
composition (8, 57)

GAS
lower incidences of GAS
infections in those over
40 years of age (8)

lifestyle
tonsillar crypt size (41)

Gender

higher PTA incidence in

males than females
in a 3: 1 ratio
retrospectively

Periodontal
disease

high incidence of
periodontal disease
coinciding with PTA

for: (27, 58, 63, 65)

males have larger oropharyngeal

features (41)
against (gender as a females have better
non-significant
oropharyngeal immunity prior
factor): (36, 56, 57,
to middle age (66)
59, 62)
lifestyle (25)
(67 70)
build-ups of infectious fibrosis
and altered oropharyngeal
architecture (5, 12, 14, 69, 71,
72)

ear/nose/throat GAS
infections are more
common in males than
females (8)

Fusobacterium sp.

Smoking

in comparison with
population groups, a
high proportion of
PTA sufferers are
smokers

predisposes to other head and

neck infections (67, 68)
(5, 10, 25, 36, 51, 69, linked to periodontal disease and
77 79)
other head and neck infections
(25, 71, 80)
suppresses local humoral
immunity (81)
lower densities of normal flora
(82, 83)
disruption of mucosal barrier (5,
69, 71, 72, 80)
build-up of infectious fibrosis and
altered oropharyngeal
architecture (5, 69, 71, 72, 80)

SMG

highest incidence of
fusobacterial PTA
infections is in
young adults (35)
high incidence of other
fusobacterial
infections in young
adults (8, 42, 44,
64)
fusobacterial infections high incidence of SMG
suggested to be
infections in males
more common in
(25, 47)
males (8, 64)

common organism
identified in
periodontal disease
and caries (69, 70,
76)

disrupts mucosal barrier

alters oral conditions, local
immunity and microfloral
growth (73 75)

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

1946

Table 2. Host factors correlating with PTA incidence and, where possible, identified relationships to pathogens

common organism
identified in
periodontal disease
and caries (69, 70,
76)
SMG takes advantage
of established
infectious damage
(47)

promotes growth (84)

promotes growth (25)

JAC

Review

suggested that
antibiotic use
promotes
pathogenicity (49)

opportunity for disease prevention. Re-educating clinicians about

the pathogenesis of PTA will increase awareness of the risk
factors, identifying high-risk groups while dismissing misconceptions that PTA is purely a complication of AT. Individuals presenting to primary care with chronic throat problems are potentially
identifiable as being at high risk of PTA. By addressing the
patients lifestyle, steps can be taken to monitor and reduce
the risk of abscess development.
With increasing evidence of links between poor oral hygiene
and throat infections such as PTA, it is perhaps time for a more
communal approach to the monitoring, care and education of
patients in which dentists and doctors collaborate further.

Parentheses denote reference numbers for sources of evidence.

Antibiotic use

increased incidence of
PTA correlates with
increased prescribed
antibiotics for sore
throat

(19, 51)

poor humoral response to

pathogen, allowing growth
(30, 60, 88)
pathogen switch: kill/inhibit
original pathogen allowing
resistant, potentially more
virulent species to invade
promote growth and
pathogenesis of b-lactamase
opportunists (19)
encourages bacteria to invade
tonsillar tissue (51)

inflammation as a result of
superficial infection can lead
to increased access of
pathogens (87)

compromised humoral immunity

allowing tissue invasion (90)

comorbidity factor: high (36, 85 87)

incidence of PTA in
patients with IM and
Kawasakis disease
(60, 75, 88, 89)
evidence of genetic
susceptibility to other
throat infections
such as recurrent
tonsillitis
Compromised
immunity

Standardizing PTA pus sample analysis would provide more comparable, reliable microbiological data. The use of highly sensitive,
modern analytic tests such as PCR should identify the true PTA
microfloral composition more reliably.95 PCR of peritonsillar
swabs from healthy volunteers could provide comparative
control data to then determine the probable pathogenspossibly a more valid method than investigating the microflora of
tonsils excised from elective tonsillectomy patients, samples
that are unlikely to be representative of healthy individuals.
Immune assays of patients with PTA may allow for a more conclusive identification of pathogenic species.42 More data from a
wider cultural and populational spread would permit for a
more viable dataset and fairer analysis.
Investigating patients symptoms, sore throat experience and
history in relation to the microbiology of PTA could provide more
conclusive evidence in support of our proposal that there are
subtypes of PTA. Grouping patients into microbiologically similar
subtypes might allow for a more appropriate and more efficient
management.
Designing a tool that assesses throat health could be of use
both for disease prevention and for monitoring the efficacy of
PTA management. Our team have recently explored the use of
the Tonsillectomy Outcome Inventory 14 as such a tool, with positive outcomes for scoring throat-related quality of life.96

Conclusions
We have identified pathogens in PTA that are opportunistic species
native to the oropharynx. With the rapid evolution of generational
behaviour and lifestyle, it is likely that microfloral compositions are
continually changing. Therefore, it is probable that the organisms
considered to be major pathogens associated with PTA will fluctuate and change. For example, it has been suggested that the
increased prescription and dosage of b-lactamases is encouraging
pathogenic behaviour on the part of anaerobes.19 It is unclear
whether the rise in anaerobic infections seen in recent years
is linked to changes such as these or whether it is related to
more sensitive tests that actively search and identify species that
have been ever-present. Patients experience and history of
sore throat appear to differ according to whether their PTA is a
monomicrobial aerobic infection or a polymicrobial infection
containing anaerobes. This leads us to propose that there may
be pathogenically distinct PTA subtypes.
The establishment of PTA ultimately requires the disruption
of oropharyngeal commensal host homeostasis followed by

1947

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

contrary to control data,

HBD-1 expression in tonsils
from patients with
recurrent AT is not
significantly increased
when challenged with GAS
(88)

Further research

Review

Viral tonsillitis

Smoking
Poor oral hygiene

Infectious
mononucleosis

Immunocompromised/deficient

Microfloral imbalance

Antibiotics

Gender*

Genetics

Age

Poor oral hygiene

Age
Tissue damage

Bacterial niche

Smoking

Gender*
Suppurative infection

Genetics

Acute tonsillitis

PTA

Figure 2. Summary of the effect of the interaction of host factors on the development of PTA. Solid outlined, non-shaded text indicates uncontrollable
factors. Dark grey outlined shading indicates factors that can be addressed and controlled. Light grey shading indicates factors that there may be
some control over. *Contradictory evidence.

localized tissue invasion. Certain host factors influence the development of PTA; some are controllable and therefore clinically targetable, whereas others are uncontrollable risk factors that may
be used by clinicians to indicate overall patient susceptibility
(Figure 2).
Current hypotheses concerning the pathogenesis of PTA are
likely to have some validity. Mild suppurative infection, such as
AT, could spread and result in tissue damage allowing localized
invasion by the already established pathogen. Blocked Weber
glands could lead to increased debris in the tonsillar crypts, subsequent poor oral hygiene and niches for suppuration. The
number of factors and variables affecting the development of
PTA, however, suggests that the combination of a variety of circumstances can trigger pathogenesis. It would seem that PTA
is, more often than not, a pathogenically separate entity from AT.
With the incidence of PTA rising worldwide and an increased
understanding of its aetiology, it is important to focus attention
on disease prevention in addition to appropriate management.
Re-education concerning the range of factors that promote
pathogenesis and invasion in PTA may facilitate disease
prevention.

Transparency declarations
None to declare.

References
1 Stedman J. Stedmans Medical Dictionary. Philadelphia, USA: Lippincott
Williams & Wilkins, 2006.
2 Rahn R. Quinsy (peritonsillar abscess). Can J Rural Med 2009; 14: 25 6.

1948

3 Hett GS. The anatomy of the capsule of the tonsil, and its significance
in the treatment of diseases of the tonsil. J Laryngol Otol 1910; 25:
56170.
4 Galioto N. Peritonsillar abscess. Am Fam Physician 2008; 77: 199202.
5 Brook I. Microbiology and management of peritonsillar,
retropharyngeal, and parapharyngeal abscesses. J Oral Maxillofac Surg
2004; 62: 1545 50.
6 National Health Service. Hospital Episode Statistics for England.
Inpatient Statistics, 201011. Primary Diagnosis: 3 Character. London,
UK: Health and Social Care Information Centre, 2012.
7 Powell J, Wilson J. An evidence-based review of peritonsillar abscess.
Clin Otolaryngol 2012; 37: 13645.
8 Rusan M, Klug T, Ovesen T. An overview of the microbiology of acute
ear, nose and throat infections requiring hospitalisation. Eur J Clin
Microbiol Infect Dis 2009; 28: 24351.
9 Mehanna H, Al.-Bahnasawu L, White A. National audit of the
management of peritonsillar abscess. Postgrad Med J 2002; 78: 5457.
10 Herzon F, Martin A. Medical and surgical treatment of peritonsillar,
retropharyngeal, and parapharyngeal abscesses. Curr Infect Dis Rep
2006; 8: 196202.
11 Ellis M. Infectious Diseases of the Respiratory Tract. Cambridge, UK:
Cambridge University Press, 1998.
12 Passy V. Pathogenesis of peritonsillar abscess. Laryngoscope 1994; 104:
18590.
13 Farmer S, Khatwa M, Zeitoun H. Peritonsillar abscess after
tonsillectomy: a review of the literature. Ann R Coll Surg Engl 2011; 93:
3537.
14 Chen Z, Zhou C, Chen J. [Investigation of the infectious route of
peritonsillar abscess.] Zhonghua Er Bi Yan Hou Ke Za Zhi 1997; 32: 245 6.
15 Jokipii A, Jokipii L, Sipila P et al. Semiquantitative culture results and
pathogenic significance of obligate anaerobes in peritonsillar abscesses.
J Clin Microbiol 1988; 26: 957 61.

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

Peritonsillar cellulitis

Review

16 Brook I, Frazier E, Thompson D. Aerobic and anaerobic microbiology of

peritonsillar abscess. Laryngoscope 1991; 101: 289 92.
17 Snow D, Campbell J, Morgan D. The microbiology of peritonsillar
sepsis. J Laryngol Otol 1991; 105: 5535.
18 Jousimies-Somer H, Savolainen S, Makitie A et al. Bacteriologic
findings in peritonsillar abscesses in young adults. Clin Infect Dis 1993;
16: S2928.
19 Mitchelmore I, Prior A, Montgomery P. Microbiological features and
pathogenesis of peritonsillar abscesses. Eur J Clin Microbiol Infect Dis
1995; 14: 8707.
20 Muir D, Papesch M, Allison R. Peritonsillar infection in Christchurch
1990 2: microbiology and management. N Z Med J 1995; 108: 53 4.
21 Sakae F, Imamura R, Sennes L. Microbiology of peritonsillar abscesses.
Braz J Otorhinolaryngol 2006; 72: 24751.

23 Gavriel H, Lazarovitch T, Pomortsev A et al. Variations in the

microbiology of peritonsillar abscess. Eur J Clin Microbiol Infect Dis
2009; 28: 27 31.
24 Repanos C, Mukherjee P, Alwahab Y. Role of microbiological studies in
management of peritonsillar abscess. J Laryngol Otol 2009; 123: 877 9.
25 Hidaka H, Kuriyama S, Yano H et al. Precipitating factors in the
pathogenesis of peritonsillar abscess and bacteriological significance of
the Streptococcus milleri group. Eur J Clin Microbiol Infect Dis 2011; 30:
52732.
26 Klug T, Henriksen J, Fuursted K et al. Significant pathogens in
peritonsillar abscesses. Eur J Clin Microbiol Infect Dis 2011; 30: 61927.
27 Love R, Allison R, Chambers S. Peritonsillar infection in Christchurch
2006 2008: epidemiology and microbiology. N Z Med J 2011; 124:
16 23.

39 Risberg S, Engfeldt P, Hugosson S. Peritonsillar abscess and cellulitis

and their relation to a positive antigen detection test for streptococcal
infection. Scand J Infect Dis 2010; 42: 74751.
40 Hagelskjaer K, Prag J. Localised Fusobacterium necrophorum
infections: a prospective laboratory-based Danish study. Eur J Clin
Microbiol Infect Dis 2008; 27: 7339.
41 Batty A, Wren M, Gal M. Fusobacterium necrophorum as the cause of
recurrent sore throat: comparison of isolates from persistent sore throat
syndrome and Lemierres disease. J Infect 2004; 51: 299306.
42 Brook I, Foote P, Slots J. Immune-response to Fusobacterium
nucleatum and Prevotella intermedia in patients with peritonsillar
cellulitis and abscess. Clin Infect Dis 1995; 20: s220 1.
43 Aliyu S, Marriott R, Curran M et al. Real-time PCR investigation into the
importance of Fusobacterium necrophorum as a cause of acute
pharyngitis in general practice. J Med Microbiol 2004; 53: 1029 35.
44 Klug T, Henriksen J, Fuursted K et al. Similar recovery rates of
Fusobacterium necrophorum from recurrently infected and non-infected
tonsils. Dan Med Bull 2011; 58: A4295.
45 Hirai T, Kimura S, Mori N. Head and neck infections caused by
Streptococcus milleri group: an analysis of 17 cases. Auris Nasus Larynx
2005; 32: 55 8.
46 Han J, Kerschner J. Streptococcus milleri: an organism for head and
neck infections and abscess. Arch Otolaryngol Head Neck Surg 2001; 127:
6504.
47 Saiki T, Sakaki M, Watanabe F. [Clinical study of 215 cases of peritonsillar
abscess]. Pract Otorhinolaryngolog (Basel) 2010; 103: 1021 7.
48 Fujiyoshi T, Inaba T, Udaka T et al. [Clinical significance of the
Streptococcus milleri group in peritonsillar abscesses]. Nihon Jibiinkoka
Gakkai Kaiho 2001; 104: 866 71.

28 Zagolski O, Gajda M. [The microbiology of peritonsillar abscesses].

Przeglad Lekarski 2007; 64: 545 8.

49 Brook I, Hunter V, Walker R. Synergistic effect of Bacteroides,

Clostridium, Fusobacterium, anaerobic cocci, and aerobic bacteria on
mortality and induction of subcutaneous abscesses in mice. J Infect Dis
1984; 149: 9248.

29 McFarland L. Normal flora: diversity and functions. Microb Ecol Health

Dis 2000; 12: 193 207.

50 Marom T, Cinamon U, Itskoviz D et al. Changing trends of peritonsillar

abscess. Am J Otolaryngol 2010; 31: 1627.

30 Brook I, Foote P, Slots J. Immune response to anaerobic bacteria

in patients with peritonsillar cellulitis and abscess. Acta Otolaryngol
1996; 116: 88891.

51 Dunn N, Lane D, Everitt H et al. Use of antibiotics for sore throat and
incidence of quinsy. Br J Gen Pract 2007; 57: 459.

31 Lilja M, Raisanen S, Stenfors L. Immunoglobulin- and complementcoated bacteria in pus from peritonsillar abscesses. J Laryngol Otol
1998; 112: 6348.
32 Megalamani S, Suria G, Manickam U et al. Changing trends in
bacteriology of peritonsillar abscess. J Laryngol Otol 2008; 122: 92830.
33 Lilja M, Ralanen S, Jokinen K et al. Direct microscopy of effusions
obtained from peritonsillar abscesses as a complement to bacterial
culturing. J Laryngol Otol 1997; 111: 3925.

52 Zautner A, Krause M, Stropahl G et al. Intracellular persisting

Staphylococcus aureus is the major pathogen in recurrent tonsillitis.
PLoS One 2010; 5: e9452.
53 Brook I. The role of anaerobic bacteria in upper respiratory tract and
other head and neck infections. Curr Infect Dis Rep 2007; 9: 20817.
54 Jensen A, Hagelskjaer Kristensen L, Prag J. Detection of
Fusobacterium necrophorum subsp. funduliforme in tonsillitis in young
adults by real-time PCR. Clin Microbiol Infect 2007; 13: 695 701.

34 Barnham M, Bradwell R. Acute peritonsillar abscess caused by

Arcanobacterium haemolyticum. J Laryngol Otol 1992; 106: 10001.

55 Jeong J, Lee D, Ryu R et al. Bacteriologic comparison of tonsil core in

recurrent tonsillitis and tonsillar hypertrophy. Laryngoscope 2007; 117:
2146 51.

35 Klug T, Rusan M, Fuursted K et al. Fusobacterium necrophorum: most

prevalent pathogen in peritonsillar abscess in Denmark. Clin Infect Dis
2009; 49: 1467 72.

56 Hanna B, McMullan R, Gallagher G et al. The epidemiology of

peritonsillar abscess disease in Northern Ireland. J Infect 2006; 52:
24753.

36 Rusan M, Klung T, Henriksen J et al. The role of viruses in the

pathogenesis of peritonsillar abscess. Eur J Clin Microbiol Infect Dis
2012; 31: 2335 43.

57 Risberg S, Engfeldt P, Hugosson S. Incidence of peritonsillar abscess

and relationship to age and gender: retrospective study. Scand J Infect
Dis 2008; 40: 7926.

37 Bomke A, Steiner S, Podbielski A. [Multiple peritonsillar abscesses

caused by Arcanobacterium haemolyticum in a young female]. Dtsch
Med Wochenschr 2009; 134: 75 8.

58 Ong Y, Goh Y, Lee Y. Peritonsillar infections: local experience.

Singapore Med J 2004; 45: 1059.

38 Adair JC, Amber I, Johnston JM. Peritonsillar abscess caused by

Nocardia asteroides. J Clin Microbiol 1987; 25: 22145.

59 Kordeluk S, Novack L, Puterman M et al. Relation between peritonsillar

infection and acute tonsillitis myth or reality? Otolaryngol Head Neck Surg
2011; 145: 9405.

1949

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

22 Sunnergren O, Swanberg J, Molstad S. Incidence, microbiology and

clinical history of peritonsillar abscesses. Scand J Infect Dis 2008; 40:
7525.

JAC

Review

60 Ball S, Siou G, Wilson J et al. Expression and immunocolocalisation of

antimicrobial peptides within human palatine tonsils. J Laryngol Otol
2007; 121: 9738.

80 Shcheglov A, Oskolskii G, Lushnikova E et al. Morphological and

immunological analysis of the oral mucosa in tobacco smoking and
odontopreparation. Bull Exp Biol Med 2006; 142: 62832.

61 Dang J, Athavale SM, Teng J et al. Salivary flow rate and peritonsillar
abscess development: a prospective cohort study. Laryngoscope 2011; 121:
S244.

81 Brook I. The impact of smoking on oral and nasopharyngeal bacterial

flora. J Dent Res 2011; 90: 70410.

62 Matsuda A, Tanaka H, Kanaya T et al. Peritonsillar abscess: a study of

724 cases in Japan. Ear Nose Throat J 2002; 81: 384 9.

82 Kumar P, Mathews C, Joshi V et al. Tobacco smoking affects bacterial

acquisition and colonization in oral biofilms. Infect Immun 2011; 79:
4730 8.

63 Brazier J, Hall V, Yusuf E et al. Fusobacterium necrophorum infections

in England and Wales 1990 2000. J Med Microbiol 2002; 51: 26972.

83 van Winkelhoff A, Bosch-Tijhof C, Winkel E et al. Smoking affects the

subgingival microflora in periodontitis. J Periodontol 2001; 72: 66671.

64 Knipping S, Passmann M, Schrom T et al. Abscess tonsillectomy for

acute peritonsillar abscess. Rev Laryngol Otol Rhinol (Bord) 2002; 123:
13 6.

84 Ahmad U, Anari S. Infectious mononucleosis screening in quinsy

patients. Eur Arch Otorhinolaryngol 2009; 267: 1135.

65 Indrasingh I, Chandi G, Jeyaseelan L et al. Quantitative analysis of

CD1a (T6) positive Langerhans cells in human tonsil epithelium. Ann
Anat 1999; 181: 56772.

67 Agarwal A, Sethi A, Sethi D et al. Role of socioeconomic factors in

deep neck abscess: a prospective study of 120 patients. Br J Oral
Maxillofac Surg 2007; 45: 553 5.
68 Georgalas C, Kanagalingam J, Zainal A et al. The association between
periodontal disease and peritonsillar infection: a prospective study.
Otolaryngol Head Neck Surg 2002; 126: 914.
69 Shayani Nasab M, Behnod F, Farehani F et al. Association between
peritonsillar abscess and molar caries. J Res Med Sci 2006; 11: 1013.
70 Salvi G, Lawrence H, Offenbacher S et al. Influence of risk factors on
the pathogenesis of periodontitis. Periodontology 2000; 14: 173 201.
71 Eliasson L, Heyden G, Landahl S et al. Effects of tobacco and diuretics
on human palatal salivary glands. J Oral Pathol Med 1991; 20: 1269.
72 Wood D, Weinstein K, Podbielski A et al. Generation of metabolically
diverse strains of Streptococcus pyogenes during survival in stationary
phase. J Bacteriol 2009; 191: 6242 52.
73 Olsen R, Shelburne S, Musser J. Molecular mechanisms underlying
group A streptococcal pathogenesis. Cell Microbiol 2009; 11: 1 12.
74 Schwaab M, Hansen S, Pearson M et al. Human b-defensinsat the
front line of the peritonsillar abscess. Eur J Clin Microbiol Infect Dis
2009; 28: 74555.
75 Rajasuo A, Jousimies-Somer H, Savolainen S et al. Bacteriologic
findings in tonsillitis and pericoronitis. Clin Infect Dis 1996; 23: 51 60.
76 Dilkes M, Dilkes J, Ghufoor K. Smoking and quinsy. Lancet 1992; 339:
1552.
77 Kilty S, Gaboury I. Clinical predictors of peritonsillar abscess in adults.
J Otolaryngol Head Neck Surg 2008; 37: 1658.

86 Hathursinghe H, Patel S, Uppal H et al. Acute tonsillitis: an unusual

presentation of Kawasaki syndrome: a case report and review of the
literature. Eur Arch Otorhinolaryngol 2005; 263: 336 8.
87 Bell S, Howard A, Wilson J et al. Streptococcus pyogenes infection of
tonsil explants is associated with a human b-defensin 1 response from
control but not recurrent acute tonsillitis patients. Mol Oral Microbiol
2012; 27: 16071.
88 Jesic S, Stojilijkovic L, Stosic S et al. Enzymatic study of tonsil
tissue alkaline and acid phosphatase in children with recurrent
tonsillitis and tonsil hypertrophy. Int J Pediatr Otorhinlaryngol 2012;
74: 82 6.
89 Stenfors L, Bye H, Raisanen S et al. Bacterial penetration into tonsillar
surface epithelium during infectious mononucleosis. J Laryngol Otol
2000; 114: 84852.
90 Ryan C, Dutta C, Simo R. Role of screening for infectious
mononucleosis in patients admitted with isolated, unilateral
peritonsillar abscess. J Laryngol Otol 2004; 118: 3625.
91 Ravi K, Brooks J. Peritonsillar abscess an unusual presentation of
Kawasaki disease. J Laryngol Otol 1997; 111: 73 4.
92 Gonen C, Uner A, Cetinkaya Y et al. Tonsillar abscess formation due to
herpes simplex type-1 in a severely immunocompromised stem cell
transplant patient with chronic myeloid leukemia. Transpl Infect Dis
2006; 8: 16670.
93 Clark M, Wilson C, Sama A et al. Differential cytokeratin and
glycoconjugate expression by the surface and crypt epithelia of human
palatine tonsils. Histochem Cell Biol 2000; 114: 31121.
94 Scottish Intercollegiate Guidelines Network. Management of Sore
Throat and Indications for Tonsillectomy: A National Clinical Guideline.
Edinburgh, UK: SIGN, 2010.

78 Lehnerdt G, Senska K, Fischer M et al. [Smoking promotes the formation

of peritonsillar abscesses]. Laryngorhinootologie 2005; 84: 676 9.

95 Siqueira J, Rocas I, De Uzeda M et al. Comparison of 16S

rDNA-based PCR and checkerboard DNA DNA hybridisation for
detection of selected endodontic pathogens. J Med Microbiol 2002; 51:
10906.

79 Torre V, Bucolo S, Giordano C et al. Palatine tonsils in smoker and

non-smoker patients: a pilot clinicopathological and ultrastructural
study. J Oral Pathol Med 2005; 34: 3906.

96 Powell J, Powell E, Conroy K et al. Application of the adult tonsil

outcome inventory 14 (ATOI-14) to peritonsillar abscess patients.
J Laryngol Otol 2013; in press.

1950

Downloaded from http://jac.oxfordjournals.org/ by guest on August 21, 2015

66 Daramola O, Flanagan C, Maisel R et al. Diagnosis and treatment of

deep neck space abscesses. Otolaryngology Head Neck Surg 2009; 141:
12330.

85 Choi S, Kim H. A case of Kawasaki disease with coexistence of a

parapharyngeal abscess requiring incision and drainage. Korean J
Pediatr 2010; 53: 8558.