State of the Art Review
Otolaryngology–
Peritonsillar Abscess: Complication of
Acute Tonsillitis or Weber’s Glands
Infection?
Tejs Ehlers Klug, MD1, Maria Rusan, MD1,2,
Kurt Fuursted, DMsc3, and Therese Ovesen, DMsc1
No sponsorships or competing interests have been disclosed for this article.
Abstract
Objective. To review the literature concerning the 2 primary
hypotheses put forth to explain the pathogenesis of periton-
sillar abscess: ‘‘the acute tonsillitis hypothesis’’ (peritonsillar
abscess is a complication of acute tonsillitis) and ‘‘the
Weber gland hypothesis’’ (peritonsillar abscess is an infec-
tion of Weber’s glands).
Data Sources. PubMed, EMBASE.
Review Methods. Data supporting or negating one hypothesis
or the other were elicited from the literature.
Conclusions. Several findings support the acute tonsillitis
hypothesis. First, the 2 main pathogens in peritonsillar
abscess have been recovered from pus aspirates and bilat-
eral tonsillar tissues with high concordance rates, suggesting
that both tonsils are infected in patients with peritonsillar
abscess. Second, studies report signs of acute tonsillitis in
the days prior to and at the time of peritonsillar abscess.
Third, antibiotic treatment reduces the risk of abscess
development in patients with acute tonsillitis. However,
some findings suggest involvement of the Weber’s glands in
peritonsillar abscess pathogenesis. First, high amylase levels
have been found in peritonsillar pus. Second, the majority of
peritonsillar abscesses are located at the superior tonsillar
pole in proximity of the Weber’s glands. We propose a uni-
fied hypothesis whereby bacteria initially infect the tonsillar
mucosa and spread via the salivary duct system to the peri-
tonsillar space, where an abscess is formed.
Implications for Practice. Our findings support the rationale
for antibiotic treatment of patients with severe acute tonsil-
litis to reduce the risk of abscess development. Improved
understanding of peritonsillar abscess pathogenesis is impor-
tant for the development of efficient prevention strategies.
Keywords
pathogenesis, peritonsillar abscess, acute tonsillitis
Received January 5, 2016; revised February 22, 2016; accepted
February 26, 2016.
Head and Neck Surgery
2016, Vol. 155(2) 199–207
Ó American Academy of
Otolaryngology—Head and Neck
Surgery Foundation 2016
Reprints and permission:
sagepub.com/journalsPermissions.nav
DOI: 10.1177/0194599816639551
http://otojournal.org
S
trategically located in the oropharynx, the palatine
tonsils are exposed to inhaled and ingested antigens
and are involved in the initiating immune responses
against pathogens. This frequent exposure to potential
pathogens and involvement in local processing of microor-
ganisms may be the basis for the high incidence of tonsillar
infections. A small group of salivary glands, the Weber’s
glands, is located in the supratonsillar space. The common
duct from these glands penetrates the tonsillar capsule and
opens into tonsillar crypts.
Peritonsillar abscess (PTA), or quinsy, refers to a collection
of pus located between the tonsillar capsule and the pharyngeal
constrictor muscle. It is the most common deep neck space
infection1 with mean annual incidence rates in the range of 9
to 41 cases of 100 000 population per year.2-6 Teenagers and
young adults are most commonly affected,7 and smokers are at
increased risk of PTA.8Fusobacterium necrophorum and group
A streptococci (GAS) have been shown to be significant
pathogens in PTA.9,10
Despite the relatively high prevalence of PTA, substan-
tial controversy exists regarding its pathogenesis.
The classical ‘‘acute tonsillitis hypothesis’’ states that PTA
is a complication of acute tonsillitis. Bacteria are thought to
spread from the tonsillar mucosa to the peritonsillar tissue.
Left untreated and occasionally even in spite of antibiotic ther-
apy, diffuse peritonsillar inflammation may evolve and prog-
ress into abscess formation.11 The hypothesis does not describe
how the bacteria penetrate the tonsillar capsule.
In 1994, Passy argued that the ‘‘Weber gland hypoth-
esis’’ explained the clinical, epidemiologic, and histologic
findings better.12 This hypothesis suggests that blockage of
1
Department of Otorhinolaryngology, Head and Neck Surgery, Aarhus
University Hospital, Aarhus, Denmark
2
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard
Medical School, Boston, Massachusetts, USA
3
Department of Microbiology and Infection Control, Statens Serum Institut,
Copenhagen, Denmark
Corresponding Author:
Tejs Ehlers Klug, MD, Department of Otorhinolaryngology, Head and Neck
Surgery, Aarhus University Hospital, NBG, Building 10, Noerrebrogade 44,
Aarhus C, DK-8000, Denmark.
Email: tejsehlersklug@hotmail.com
200 Otolaryngology–Head and Neck Surgery 155(2)

the common duct from the Weber’s glands results in a loca- Table 1. Location of Peritonsillar Abscesses in Relation to the
lized, suppurative salivary gland infection—a PTA. It has Tonsillar Poles.a
furthermore been proposed that a blockage of the duct could
Study Upper Pole Middle Lower Pole
be secondary to recurrent tonsillitis or other inflammatory
processes.12,13
Bateman (1959)21 57 (72) 12 (14) 13 (14)
Antibiotic treatment is generally recommended for patients Beeden (1970)22 35 (56) 9 (14) 19 (30)
with GAS-positive acute tonsillitis. The benefits of treatment
Brandow (1973)23 109 (70) 34 (22) 13 (8)
are reduced duration of symptoms, halting of infectious
Bonding (1973)24 30 (35) 24 (28) 31 (37)
spread, and decreased risk of immunologic and suppurative
Yung (1976)25 38 (76) 6 (12) 6 (12)
complications.14-16 The mean reduction of symptoms is
Maisel (1982)26 38 (85) 7 (15) —
approximately only 1 day, and immunologic complications
Total 307 (64) 92 (19) 82 (17)
have become rare in Western countries. Hence, a major
a
reason for antibiotic treatment of patients with acute tonsilli- Values presented in n (%). Dash (—) indicates none.
tis is based on the belief that PTA is a complication of acute
tonsillitis, which can be averted by timely antibiotic treatment
of the causative bacteria. If PTA is rather an infection of the
Weber’s glands, the reasoning behind antibiotic treatment of the abscess following abscess formation from the adjacent
acute tonsillitis may be questioned. salivary glands. Hence, the finding of elevated amylase
Recent studies have added important new information levels may not signify that the Weber’s glands are the
regarding these 2 hypotheses. The Weber gland hypothesis source of the infection or even that these are part of the
has gained support by researchers over the last few route of bacterial spread.
years,13,17-19 while several findings supportive of the acute
tonsillitis hypothesis have been disproved. This shift Supratonsillar location of PTAs. In a retrospective review of
prompted the current review of the literature reporting on 100 consecutive PTA patients, Passy reported that 99% of
findings supporting or contradicting these 2 leading hypoth- abscesses were located in the supratonsillar space, and he
eses of PTA pathogenesis. argued that this finding supported the involvement of the
Weber’s glands.12 Only a few researchers have described
Methods the precise location of PTAs in relation to the tonsillar
The current narrative review is based on a comprehensive liter- poles.20-26 A meta-analysis of the literature confirms that
ature search in PubMed and EMBASE. No restrictions on pub- the most frequent location for PTAs is behind the upper ton-
lication year were used. Only articles in English were sillar pole (Table 1). However, 36% (95% confidence inter-
considered. The last search was performed September 9, 2015, val [95% CI]: 31.7%-40.4%) of PTAs were located behind
using MeSH terms including free text—peritonsillar abscess, the midportion or lower tonsillar pole. In contrast to the
quinsy, acute tonsillitis, pathogenesis, and Weber’s glands— acute tonsillitis hypothesis, the Weber gland hypothesis can
along with others in text format: hypothesis, theory, etiology, explain why the abscess is most commonly located at the
antibiotics, histology, location, amylase, recurrence, findings, superior tonsillar pole. However, the Weber gland hypoth-
pathogens, and epidemiology. Furthermore, an extensive esis cannot explain how or why 36% of PTAs arise inferior
manual search was performed through the reference lists (from to the upper tonsillar pole, far from the Weber’s glands.
articles included). Articles were read with the aim to identify Kraitrakul et al examined the distribution of minor salivary
and elicit data supporting or negating the 2 hypotheses. Given glands in 55 tonsils.27 They found salivary glands at the
review of the available data, we synthesized a unified upper (in 82% of patients), middle (80%), and lower (82%)
hypothesis. parts of the peritonsillar space. Hence, an extended version
of the Weber gland hypothesis, taking all minor salivary
Discussion glands in the tonsils into account, could explain the distribu-
tion of PTAs. This more general minor salivary gland
Findings Possibly Supportive of the Weber Gland hypothesis remains to be more thoroughly investigated.
Hypothesis
Concurrent PTA and inflammation and fibrosis of the Weber’s
Detection of amylase in pus from PTA. El-Saied et al reported glands. Passy argued that the histologic finding of destruc-
significantly elevated (median, 62 U/L) and occasionally tive and inflammatory changes of the salivary glands sur-
highly elevated (.500 U/L) amylase levels in PTA pus rounding the PTA supported the Weber gland hypothesis.12
compared with pus from neck abscesses with other loca- However, Passy studied only 1 patient, and the findings
tions.18 Amylase levels .20 U/L were found in 31 of 41 were not compared with tonsils removed for other reasons.
(76%) PTA pus specimens, compared with none of 6 control According to Powell et al,13 Chen and colleagues28 found
pus specimens.18 As a PTA is bound by the tonsillar capsule smooth and healthy tonsils but inflammation and minor
and the pharyngeal musculature (and not an impermeable fibrosis of the Weber’s glands in acutely removed tonsils
abscess capsule), it can be argued that amylase may enter because of PTA. More studies are needed concerning the
Klug et al 201

Table 2. Patients with Recurrent PTA after Treatment with Aspiration or Incision.
Patients with Recurrent PTA after Treatment With Aspiration or Incision

Patients Treated with

Study Aspiration or Incision, n n %

Muller (1978)38 42 3 7.1

Herbild (1981)32 166 37 22.3
Fried (1981)31 57 1 1.8
Nielsen (1981)34 44 10 22.7
Litman (1987)37 87 22 25.3
Kronenberg (1987)33 218 50 22.9
Harris (1991)39 36 8 22.2
Sorensen (1991)36 536 33 6.1
Wolf (1994)35 160 14 14.4
Ophir (1988)29 75 11 14.7
Ong (2004)30 185 14 7.6
Chung (2014)41 172 24 13.9
Bovo (2015)42 2667 312 11.7
Shaul (2015)40 117 17 14.5
Total 4562 556 12.2

Abbreviation: PTA, peritonsillar abscess.

histologic findings of the Weber’s glands and ducts during
infection.
PTA is associated with previous PTA and recurrent tonsillitis.
Passy12 speculated that chronic infection of the Weber’s
glands or attacks of peritonsillar cellulitis induced fibrosis
of the salivary duct system, leading to increased risk of
PTA. To our knowledge, selective chronic or recurrent
infection of Weber’s glands has never been described. We
suggest that fibrosis could also be secondary to recurrent
tonsillitis or previous PTA, which could lead to increased
risk of PTA.
PTA recurrence rates (excluding patients with residual dis-
ease) were in the range of 1.8% to 25.3% in 14 studies reporting
on the question (Table 2),29-42 with a cumulative average of
12.2% (95% CI: 11.2%-13.2%). The true number may be
higher because recurrences can develop years after the initial
PTA and the mean follow-up period (when defined) ranged
from 18 months to 17 years.29-31,33,35,39,40 Gavriel et al reported
a mean time of 14 months between 2 PTA episodes.43
Studies report that patients with recurrent tonsillitis at the
time of initial PTA development are at increased risk of PTA
recurrence.33,39,44 Kronenberg et al found that recurrent PTA
was 4 times more frequent in patients with previous recurrent
tonsillitis (29 of 72, 40%) compared with patients without
(21 of 218, 9.6%).33 Similarly, in a study by Savolainen et al,
8 of 14 (47%) patients with .3 episodes of tonsillitis had
recurrence of PTA, compared with 13 of 77 (17%) patients
with 3 acute tonsillitis episodes.44
Hence, a previous episode of PTA significantly increases
the risk of recurrent PTA to approximately 12% (compared
with a 2%-3% lifetime risk of PTA in Denmark). Patients
who also suffer from recurrent tonsillitis at the time of PTA
are at even greater risk of recurrent PTA, especially if \40
years old.32-34,39
These findings suggest that scarring or other anatomic
changes of the tonsil or the Weber’s glands, as inflicted by
infection within the tonsil or the peritonsillar tissues, increase
the risk of recurrent tonsillar disease in general and PTA in
particular. However, there is a lack of histologic studies sup-
porting this hypothesis and indicating the precise location of
significant histologic alterations.
There may be an increased risk of PTA in patients with
recurrent tonsillitis (without previous PTA), but the magni-
tude of this association is not clear from the current litera-
ture (Table 3).
Nevertheless, only a minority of PTA patients has had a
history of recurrent tonsillitis, peritonsillar cellulitis, or pre-
vious PTA.
Tonsillectomy prevents future PTA. The risk of PTA is mark-
edly reduced after tonsillectomy. Passy argued that the
Weber gland hypothesis explains the reduced PTA risk
among tonsillectomized individuals, presumably due to the
removal of Weber’s glands at the time of tonsillectomy.12
However, it can be similarly argued that the removal of the
tonsillar tissue is the reason for the reduced PTA risk.
Findings Supporting the Acute Tonsillitis Hypothesis
Concurrent acute tonsillitis in PTA patients. Passy claimed that
only 4 of 100 consecutive patients with PTA had tonsillar
exudates.12 Accordingly, the majority of PTA patients did
not have acute tonsillitis at the time of their PTA diagnosis.
This argument against the acute tonsillitis hypothesis was
made on the basis of a retrospective chart review, which raises
202 Otolaryngology–Head and Neck Surgery 155(2)

Table 3. Studies of Patients with PTA and Information Concerning Previous Episodes of Acute Tonsillitis, Recurrent Tonsillitis, Chronic
Tonsillitis, and Tonsillar Diseases in General.a
Study Description

Grahne (1958)54 79% (of 725) of patients had a history of 1 previous episodes of tonsillitis or peritonsillitis
Bateman (1959)21 34 of 120 (28%) patients had repeated tonsillitis in the past
Beeden (1970)22 56 of 111 (50%) patients had previous episodes of tonsillitis
Brandow (1973)23 79 of 156 (51%) patients previously had 1 attacks of tonsillitis
Bonding (1973)24 83 of 317 (26%) patients previously had repeated tonsillitis with fever 3 times per year; 38 of 317 (12%) patients
had symptoms of chronic tonsil affection or previously had 1 or 2 episodes of acute tonsillitis per year
Herbild (1981)32 51 of 256 (20%) patients previously had recurrent episodes of tonsillitis and 7% previously had symptoms of
pharyngitis in varying degrees
Fried (1981)31 12 of 41 (29%) patients had had 1 episodes of sore throat symptoms
Schechter (1982)91 29 of 74 (39%) patients had a history of tonsillar disease, including 4 patients with previous PTA
Stegehuis (1986)92 22 of 83 (27%) patients previously had 2 attacks of tonsillitis per year over the last 2 y
Stringer (1988)93 10 (36%) patients had a history of tonsillitis, including 5 patients with a history of PTA
Savolainen (1993)94 34 of 98 (35%) and 21 of 98 (21%) patients previously had 1-3 and .3 episodes of tonsillitis, respectively
Wolf (1994)35 34 of 160 (21%) patients had a medical history of recurrent tonsillitis
Matsuda (2002)95 75 of 724 (10%) patients had a history of tonsillar disease, including 48 with prior PTA
Ong (2004)30 23 of 185 (12%) patients gave a history of recurrent tonsillitis
Segal (2009)96 45 of 127 (35%) children previously had tonsillar infection in the past
Abbreviation: PTA, peritonsillar abscess.
a
The wording used by the original study authors is employed.

concerns regarding the accuracy and completeness of the ton-
sillar mucosa description in the patient records. An accurate
description of the tonsillar mucosa in PTA patients is not
included in the majority of published PTA studies. However,
in contrast to Passy, Spires et al reported tonsillar exudates in
51% of patients with PTA.20 In a study of 275 acutely
removed tonsils due to PTA, acute or chronic inflammation
was described in 68% of cases in routine histologic examina-
tion.45 Blair et al conducted histopathologic examinations of
tonsillar specimens from 6 patients with PTA, 4 with acute
tonsillitis, and 2 with intratonsillar abscess.11 In all 6 speci-
mens from PTA patients, the authors found erosion of the ton-
sillar surface epithelium and invasion of neutrophils, as
observed in acute tonsillitis specimens.
The limited evidence regarding signs of acute tonsillar
infection in patients with PTA favors the acute tonsillitis
hypothesis.
Common bacterial pathogens. GAS is commonly recognized as
a significant pathogen in acute tonsillitis46 and PTA.9,47,48
Recent studies point to a major role of F necrophorum in
PTA,4,9,10 and this anaerobe may also play a pathogenic role
in acute tonsillitis.49-52 This concordance of 2 significant
pathogens between PTA and acute tonsillitis lends further sup-
port to the acute tonsillitis hypothesis. However, it can be
argued that bacteria can exert their pathogenic potential at dif-
ferent anatomic sites without causal relationship.
Occasional bilateral PTA. In 14 studies reporting on the preva-
lence of bilateral PTA in patients undergoing bilateral
quinsy tonsillectomy, bilateral PTA was found in 2.0% to
24% of patients (average across studies, 5.5%; 95% CI:
4.7%-6.5%; Table 4).19,22,23,53-66 The majority of patients
with bilateral PTA were thought to have unilateral PTA, but
an additional, contralateral abscess was discovered at the
time of bilateral acute tonsillectomy. Unfortunately, none of
the studies report on bacterial findings from concurrent
abscesses. However, the fact that approximately 5% of PTA
patients have bilateral PTA suggests that PTA is secondary
to bilateral acute tonsillitis, and the finding is difficult to
explain based on the Weber gland hypothesis alone.
Antibiotic treatment prior to PTA diagnosis. Studies report that
25% to 79% of PTA patients (collected average, 41%; 95%
CI: 39.2%-43.6%) received antibiotics prior to diagnosis of
PTA (Table 5).3,4,30,67-76 The indications for antibiotic
treatment were not described in any of the studies, and anti-
biotics may have been prescribed without signs and symp-
toms of acute tonsillitis. However, the fact that almost half
the PTA patients sought medical consultation and initiated
antibiotic treatment in the days prior to abscess formation
suggests that acute tonsillitis prior to PTA development is
common. The 60% of patients who did not take antibiotics
prior to PTA development may have had less severe symp-
toms or a negative test result for the presence of GAS.
Antibiotic treatment prevents PTA development. The findings
above indicate that antibiotic treatment does not prevent
abscess formation in all cases. However, studies suggest
that there could be a protective effect of appropriate antibio-
tic treatment to patients with bacterial tonsillitis with avoid-
ance of suppurative complications.77,78 A Cochrane review
Klug et al 203

Table 4. Studies Reporting on the Prevalence of Bilateral Peritonsillar Abscess.

Patients with Bilateral Peritonsillar Abscess

Study Acute Bilateral Tonsillectomies, n n %

Grahne (1958)54 676 49 6.5

Bateman (1959)21 120 13 10.8
Beeden (1970)22 100 6 6.0
Bonding (1973)24 317 10 3.1
Brandow (1973)23 156 3 1.9
Lee (1973)63 29 7 24.1
Sumner (1973)65 114 4 3.5
Trzcinski (1973)66 50 1 2.0
Yung (1976)25 50 4 8.0
Templer (1977)53 119 3 2.5
Leek (1980)64 15 3 20.0
Maisel (1982)26 45 1 2.2
Lehnerdt (2005)57 541 21 3.9
Watanabe (2010)60 371 24 6.5
Total 2703 149 5.5

by Del Mar et al, based on 2433 patients from 8 studies,
found a convincing 85% reduction in the risk of PTA if bac-
terial acute tonsillitis was treated with antibiotics.77 This
percentage should be regarded with some reservation, as
72% (18 of 25) of the patients who developed PTA were
included in 2 nonrandomized and non-double-blinded stud-
ies from 1951.79-86 At that time, the prevalence of PTA in
untreated patients was much higher than it is today.
Furthermore, some patients were treated with intramuscular
penicillin79 or antibiotics not presently recommended for
acute tonsillitis.82,83,85 Hence, it is largely unknown if the
treatment of bacterial acute tonsillitis patients with the anti-
biotics used today reduces the risk of PTA. Nevertheless,
the fact that a protective effect of antibiotics on PTA devel-
opment exists is a strong indicator for the acute tonsillitis
hypothesis.
Development of PTA after well-described initial sore throat.
Recently, Little et al published the results of an impressive
study including 14,610 patients treated for sore throat in
616 general practices.87 They found that 47 of 13,288
patients (1322 patients had missing data) with well-
described initial symptoms and findings of acute tonsillitis
developed PTA within a month of initial consultation. It can
be argued that the development of PTA in a minority
(0.5%) of patients could just be random or that the symp-
toms (throat pain and difficulty swallowing) in these 47
patients were due to incipient infection of the Weber’s
glands. Unfortunately, the authors did not state the initial
findings in patients with PTA alone but rather pooled all
174 patients with complications (PTA, n = 47; sinusitis, n =
38; otitis media, n = 69; cellulitis, n = 20). In these patients,
34% had initial findings of purulent tonsils, and 21% had
severely inflamed tonsils. However, it can be argued that
the number of patients presenting with initial PTA is
unknown and that the number of patients with initial sore
throat may constitute a minor part of all PTA patients.
Bacterial concordance rates between the 2 tonsils in patients
with PTA. The bacteriology of both tonsils (surface and core)
and pus aspirates in patients with unilateral PTA undergoing
acute bilateral tonsillectomy was previously studied.9 GAS
was isolated from 7 of 36 patients. In all 7 patients, GAS
was found in aspirated pus and the tonsillar core at the side
of the abscess. Similarly, F necrophorum was found in both
pus and the tonsillar cores at the side of the abscess in 19
patients. In addition, 2 F necrophorum isolates were recov-
ered solely from aspirated pus, and 1 F necrophorum isolate
was found in the tonsillar core only.
The high concordance rates between tonsillar cores and
PTA pus make it rather unlikely that PTA is an isolated
infection of the Weber’s glands independent of tonsillar
bacteriology. Moreover, the 7 GAS isolates were also recov-
ered from the corresponding contralateral tonsils. Similarly,
20 of the 21 F necrophorum isolates were also found in the
contralateral tonsil. These findings confirm the nearly per-
fect concordance between pus and ipsilateral tonsillar cores
and show that the oropharyngeal infection in PTA patients
affects both tonsils with concurrent pathogens.
Findings Possibly Contradicting the Acute Tonsillitis
Hypothesis
Acute tonsillitis is more frequent in childhood, and PTA is more
prevalent among adults. The majority of PTA patients are
teenagers and young adults, while bacterial acute tonsillitis
is more frequent among children.7,88-90 Researchers skepti-
cal of the acute tonsillitis hypothesis argue that the age-
204 Otolaryngology–Head and Neck Surgery 155(2)

Table 5. Studies Stating the Percentage of Patients Who Received Antibiotics prior to Peritonsillar Abscess Diagnosis.
Patients Receiving Antibiotics prior to Diagnosis

Study Peritonsillar Abscess Patients, n n %

Bateman (1959)21 120 36 30

Hoffmann (1987)74 65 37 57
Brook (1991)67 34 18 53
Snow (1991)68 91 54 59
Muir (1995)69 74 22 30
Prior (1995)70 44 27 61
Mitchelmore (1995)71 44 27 61
Ong (2004)30 185 72 37
Sakae (2006)72 30 19 63
Sunnergren (2008)3 89 26 29
Al Yaghchi (2008)76 41 32 79
Segal (2009)73 126 95 67
Ehlers Klug (2009)4 776 293 38
Risberg (2010)75 274 67 25
Total 1993 825 41

related incidence rates of acute tonsillitis and PTA should
mirror each other if this hypothesis is true. However, factors
other than age also contribute to the development of PTA. For
instance, smoking is associated with an increased risk of PTA
development.8 In a previous study of 847 PTA patients, F
necrophorum was significantly more prevalent among patients
aged 15 to 24 years as compared with children and older
adults.7 Similarly, F necrophorum is more commonly associ-
ated with acute tonsillitis in patients aged 15 to 30 years.49,50
The observed differences in age distribution of acute ton-
sillitis and PTA cases in children vs adults can potentially
be explained by additional risk factors for PTA development
and susceptibility to specific bacterial pathogens, which are
unequally distributed between children and adults.
Conclusions
More studies are needed before solid conclusions regarding
the pathogenesis of PTA can be drawn. Based on the current
literature, however, there are more findings in favor of the
acute tonsillitis hypothesis. First, the 2 main pathogens in
PTA—GAS and F necrophorum—have been recovered
from PTA pus aspirates and bilateral tonsillar tissues with
high concordance rates. Second, also indicating bilateral
tonsillar infection, bilateral PTA has been found in approxi-
mately 5% of PTA cases at the time of acute tonsillectomy.
Third, signs of acute tonsillitis in the days prior to and at
the time of PTA development have been described in multi-
ple studies. These findings are in agreement with the finding
that approximately 40% of PTA patients were treated with
antibiotics in the days prior to PTA diagnosis, possibly due
to signs and symptoms of acute tonsillitis. Last, antibiotic
treatment has been found to reduce the risk of PTA develop-
ment in patients with acute tonsillitis.
However, some findings are difficult to explain from the
acute tonsillitis hypothesis alone but suggest a role of the
minor salivary glands (Weber’s glands in particular) in PTA
pathogenesis. First, elevated amylase levels have been
found in PTA pus compared with other neck abscesses.
Second, the majority of PTAs are located at the superior
tonsillar pole. Yet, a significant proportion of PTAs are
located at the midportion or lower tonsillar pole, and an
extended version of the Weber gland hypothesis encompass-
ing all minor salivary glands in the tonsils may explain this
finding. In addition, the duct system of the minor salivary
glands provides an explanation for how bacteria may pene-
trate the tonsillar capsule, when the infection progresses
from the tonsillar mucosa to the peritonsillar tissues.
Previous researchers have, for unknown reasons, thought
of these 2 hypotheses as opposing.12,13,17,18 We propose
that, indeed, both hypotheses may be true and complemen-
tary. We find it likely that, in the majority of PTA cases,
bacteria infect the tonsillar mucosa (including the crypt
mucosa) and spread to the peritonsillar space via the sali-
vary duct system, where an abscess is formed if the bacteria
are not overcome by the immune system and (in some
cases) antibiotics. With the variations seen in the clinical
presentation of PTA patients, it is possible that PTA devel-
opment in some patients is solely an infection of the
Weber’s glands and in others a direct spread of the infection
from the tonsillar mucosa.
Implications for Practice
PTA continues to be the most common deep neck abscess,
and antibiotic treatment directed against GAS in patients
with acute tonsillitis is currently the only intervention iden-
tified to reduce the incidence. However, the use of antibiotic
Klug et al
therapy in patients with bacterial acute tonsillitis has
recently been questioned by researchers skeptical to the
acute tonsillitis hypothesis. The findings in the current
review support the rationale for antibiotic treatment of
patients with severe acute tonsillitis to reduce the risk of
PTA development. Little et al reported that the symptoms
and clinical findings in patients with acute tonsillitis were
unable to predict those who developed complications, includ-
ing PTA.87 Hence, the number of acute tonsillitis patients
needed to treat to avoid one case of PTA is currently high.
Recent studies indicate a major role of F necrophorum in
acute tonsillitis and PTA, and it is plausible that early detec-
tion and antibiotic therapy directed against this anaerobe may
prevent PTA development in many teenagers and young
adults. However, more studies are needed to substantiate this
assumption.
Improved understanding of the PTA pathogenesis is
important for the development of more efficient prevention
strategies. Studies of the anatomy, distribution, microbiol-
ogy, and immunology of the minor salivary glands in the
tonsils are likely to provide valuable information.
Author Contributions
Tejs Ehlers Klug, initiating, designing, and drafting of the work;
identification and analysis of the studies; final approval of the
manuscript; accountable for all aspects of the work; Maria Rusan,
analysis and interpretation of the studies; critical revision and final
approval of the manuscript; accountable for all aspects of the
work; Kurt Fuursted, designing the review; critical revision and
final approval of the manuscript; accountable for all aspects of the
work; Therese Ovesen, designing the review; critical revision and
final approval of the manuscript; accountable for all aspects of the
work.
Disclosures
Competing interests: None.
Sponsorships: None.
Funding source: None.
References
1. Rusan M, Klug TE, Ovesen T. An overview of the microbiol-
ogy of acute ear, nose and throat infections requiring hospitali-
sation. Eur J Clin Microbiol Infect Dis. 2009;28:243-251.
2. Risberg S, Engfeldt P, Hugosson S. Incidence of peritonsillar
abscess and relationship to age and gender: retrospective
study. Scand J Infect Dis. 2008;18:1-5.
3. Sunnergren O, Swanberg J, Mölstad S. Incidence, microbiol-
ogy and clinical history of peritonsillar abscesses. Scand J
Infect Dis. 2008;40:752-755.
4. Ehlers Klug T, Rusan M, Fuursted K, Ovesen T.
Fusobacterium necrophorum: most prevalent pathogen in peri-
tonsillar abscesses in Denmark. Clin Infect Dis. 2009;49:1467-
1472.
5. Marom T, Cinamon U, Itskoviz D, Roth Y. Changing trends
of peritonsillar abscess. Am J Otolaryngol. 2010;31:162-167.
6. Sowerby LJ, Hussain Z, Husein M. The epidemiology, antibio-
tic resistance and post-discharge course of peritonsillar
205
abscesses in London, Ontario. J Otolaryngol Head Neck Surg.
2013;42:5.
7. Klug TE. Incidence of peritonsillar abscess: the influence of
season, age, and gender. Eur J Clin Microbiol Infect Dis.
2014;33:1163-1167.
8. Klug TE, Rusan M, Clemmensen KK, Fuurted K, Ovesen T.
Smoking promotes peritonsillar abscess. Eur Arch Otorhinolaryngol.
2013;270:3163-3167.
9. Klug TE, Henriksen JJ, Fuursted K, Ovesen T. Significant
pathogens in peritonsillar abscesses. Eur J Clin Microbiol
Infect Dis. 2011;30:619-627.
10. Klug TE, Henriksen JJ, Rusan M, et al. Antibody development
to Fusobacterium necrophorum in patients with peritonsillar
abscess. Eur J Clin Microbiol Infect Dis. 2014;33:1733-1739.
11. Blair AB, Booth R, Baugh R. A unifying theory of tonsillitis,
intratonsillar abscess and peritonsillar abscess. Am J
Otolaryngol. 2015;36:517-520.
12. Passy V. Pathogenesis of peritonsillar abscess. Laryngoscope.
1994;104:185-190.
13. Powell EL, Powell J, Samuel JR, Wilson JA. A review of the
pathogenesis of adult peritonsillar abscess: time for a re-evaluation.
J Antimicrob Chemother. 2013;68:1941-1950.
14. Krober MS, Bass JW, Michels GN. Streptococcal pharyngitis:
placebo-controlled double-blind evaluation of clinical response
to penicillin therapy. JAMA. 1985;253:1271-1274.
15. Bisno AL, Gerber MA, Gwaltney JM Jr, Kaplan EL, Schwartz
RH. Diagnosis and management of group A streptococcal
pharyngitis: a practice guideline. Infectious Diseases Society
of America. Clin Infect Dis. 1997;25:574-583.
16. Del Mar CB, Glasziou PP, Spinks AB. Antibiotics for sore
throat. Cochrane Database Syst Rev. 2006;4:CD000023.
17. Kordeluk S, Novack L, Puterman M, Kraus M, Joshua BZ.
Relation between peritonsillar infection and acute tonsillitis: myth
or reality? Otolaryngol Head Neck Surg. 2011;145:940-945.
18. El-Saied S, Puterman M, Kaplan DM, Cohen-Lahav M, Joshua BZ.
Involvement of minor salivary glands in the pathogenesis of periton-
sillar abscess. Otolaryngol Head Neck Surg. 2012;147:472-474.
19. Pham V, Gungor A. Bilateral peritonsillar abscess: case report
and literature review. Am J Otolaryngol. 2012;33:163-167.
20. Spires JR, Owens JJ, Woodson GE, Miller RH. Treatment of
peritonsillar abscess: a prospective study of aspiration vs inci-
sion and drainage. Arch Otolaryngol Head Neck Surg. 1987;
113:984-986.
21. Bateman GH, Kodicek J. Primary quinsy tonsillectomy. Ann
Otol Rhinol Laryngol. 1959;68:315-321.
22. Beeden AG, Evans JN. Quinsy tonsillectomy: a further report.
J Laryngol Otol. 1970;84:443-448.
23. Brandow EC Jr.Immediate tonsillectomy for peritonsillar abscess.
Trans Am Acad Ophthalmol Otolaryngol. 1973;77:ORL412-
ORL416.
24. Bonding P. Tonsillectomy à chaud. J Laryngol Otol. 1973;87:
1171-1182.
25. Yung AK, Cantrell RW. Quinsy tonsillectomy. Laryngoscope.
1976;86:1714-1717.
26. Maisel RH. Peritonsillar abscess: tonsil antibiotic levels in
patients treated by acute abscess surgery. Laryngoscope. 1982;
92:80-87.
206
27. Kraitrakul S, Sirithunyaporn S, Yimtae K. Distribution of
minor salivary glands in the peritonsillar space. J Med Assoc
Thai. 2001;84:371-378.
28. Chen Z, Zhou C, Chen J. Investigation of the infectious route
of peritonsillar abscess [in Chinese]. Zhonghua Er Bi Yan Hou
Ke Za Zhi. 1997;32:245-246.
29. Ophir D, Bawnik J, Poria Y, Porat M, Marshak G.
Peritonsillar abscess: a prospective evaluation of outpatient
management by needle aspiration. Arch Otolaryngol Head
Neck Surg. 1988;114:661-663.
30. Ong YK, Goh YH, Lee YL. Peritonsillar infections: local
experience. Singapore Med J. 2004;45:105-109.
31. Fried MP, Forrest JL. Peritonsillitis: evaluation of current ther-
apy. Arch Otolaryngol. 1981;107:283-286.
32. Herbild O, Bonding P. Peritonsillar abscess. Arch Otolaryngol.
1981;107:540-542.
33. Kronenberg J, Wolf M, Leventon G. Peritonsillar abscess:
recurrence rate and the indication for tonsillectomy. Am J
Otolaryngol. 1987;8:82-84.
34. Nielsen VM, Greisen O. Peritonsillar abscess: I. Cases treated
by ID: a follow-up investigation. J Laryngol Otol. 1981;95:
801-805.
35. Wolf M, Even-Chen I, Kronenberg J. Peritonsillar abscess:
repeated needle aspiration versus ID. Ann Otol Rhinol
Laryngol. 1994;103:554-557.
36. Sorensen JA, Godballe C, Andersen NH, Jørgensen K.
Peritonsillar abscess: risk of disease in the remaining tonsil
after unilateral tonsillectomy à chaud. J Laryngol Otol. 1991;
105:442-444.
37. Litman RS, Hausman SA, Sher WH. A retrospective study of
peritonsillar abscess. Ear Nose Throat J. 1987;66:53-55.
38. Muller SP. Peritonsillar abscess: a prospective study of patho-
gens, treatment, and morbidity. Ear Nose Throat J. 1978;57:
439-444.
39. Harris WE. Is a single quinsy an indication for tonsillectomy?
Clin Otolaryngol Allied Sci. 1991;16:271-273.
40. Shaul C, Koslowsky B, Rodriguez M, et al. Is needle aspira-
tion for peritonsillar abscess still as good as we think? A long-
term follow-up. Ann Otol Rhinol Laryngol. 2015;124:299-304.
41. Chung JH, Lee YC, Shin SY, Eun YG. Risk factors for recur-
rence of peritonsillar abscess. J Laryngol Otol. 2014;128:
1084-1088.
42. Bovo R, Barillari MR, Martini A. Hospital discharge survey on
4,199 peritonsillar abscesses in the Veneto region: what is the
risk of recurrence and complications without tonsillectomy [pub-
lished online January 11, 2015]? Eur Arch Otorhinolaryngol.
43. Gavriel H, Vaiman M, Kessler A, Eviatar E. Microbiology of
peritonsillar abscess as an indication for tonsillectomy.
Medicine (Baltimore). 2008;87:33-36.
44. Savolainen S, Jousimies-Somer HR, Mäkitie AA, Ylikoski JS.
Peritonsillar abscess: clinical and microbiologic aspects and
treatment regimens. Arch Otolaryngol Head Neck Surg. 1993;
119:521-524.
45. Rokkjaer MS, Klug TE. Tonsillar malignancy in adult patients
with peritonsillar abscess: retrospective study of 275 patients
and review of the literature. Eur Arch Otorhinolaryngol. 2015;
272:2439-2444.
Otolaryngology–Head and Neck Surgery 155(2)
46. Krober MS, Bass JW, Michels GN. Streptococcal pharyngitis:
placebo-controlled double-blind evaluation of clinical response
to penicillin therapy. JAMA. 1985;253:1271-1274.
47. Flodström A, Hallander HO. Microbiological aspects on peri-
tonsillar abscesses. Scand J Infect Dis. 1976;8:157-160.
48. Mazur E, Czerwińska E, Korona-G1owniak I, Grochowalska
A, Kozio1-Montewka M. Epidemiology, clinical history and
microbiology of peritonsillar abscess. Eur J Clin Microbiol
Infect Dis. 2015;34:549-554.
49. Kjaerulf AM, Thomsen MK, Ovesen T, Klug TE. Clinical
and biochemical characteristics of patients with Fusobacterium
necrophorum-positive acute tonsillitis. Eur Arch Otorhinolar-
yngol. 2015; 272:1457-1463.
50. Centor RM, Atkinson TP, Ratliff AE, et al. The clinical pre-
sentation of fusobacterium-positive and streptococcal-positive
pharyngitis in a university health clinic: a cross-sectional
study. Ann Intern Med. 2015;162:241-247.
51. Hedin K, Bieber L, Lindh M, Sundqvist M. The aetiology of
pharyngotonsillitis in adolescents and adults: Fusobacterium
necrophorum is commonly found. Clin Microbiol Infect. 2015;
21(3):263.e1-e7.
52. Jensen A, Hansen TM, Bank S, Kristensen LH, Prag J.
Fusobacterium necrophorum tonsillitis: an important cause of
tonsillitis in adolescents and young adults. Clin Microbiol
Infect. 2015;21(3):266.e1-e3.
53. Templer JW, Holinger LD, Wood RP 2nd, Tra NT, DeBlanc
GB. Immediate tonsillectomy for the treatment of peritonsillar
abscess. Am J Surg. 1977;134:596-598.
54. Grahne B. Abscess tonsillectomy: seven hundred twenty-five
cases. AMA Arch Otolaryngol. 1958;68:332-336.
55. Dalton RE, Abedi E, Sismanis A. Bilateral peritonsillar
abscesses and quinsy tonsillectomy. J Natl Med Assoc. 1985;
77:807-812.
56. Mobley SR. Bilateral peritonsillar abscess: case report and pre-
sentation of its clinical appearance. Ear Nose Throat J. 2001;
80:381-382.
57. Lehnerdt G, Senska K, Fischer M, Jahnke K. Bilateral periton-
sillar abscesses. Eur Arch Otorhinolaryngol. 2005;262:573-
575.
58. Simons JP, Branstetter BF 4th, Mandell DL. Bilateral periton-
sillar abscesses: case report and literature review. Am J
Otolaryngol. 2006;27:443-445.
59. Edinger JT, Hilal EY, Dastur KJ. Bilateral peritonsillar
abscesses: a challenging diagnosis. Ear Nose Throat J. 2007;
86:162-163.
60. Watanabe T, Suzuki M. Bilateral peritonsillar abscesses: our
experience and clinical features. Ann Otol Rhinol Laryngol.
2010;119:662-666.
61. Lin YY, Lee JC. Bilateral peritonsillar abscesses complicating
acute tonsillitis. CMAJ. 2011;183:1276-1279.
62. Kanesada K, Mogi G. Bilateral peritonsillar abscesses. Auris
Nasus Larynx. 1981;8:35-39.
63. Lee KJ, Traxler JH, Smith HW, Kelly JH. Tonsillectomy:
treatment of peritonsillar abscess. Trans Am Acad Ophthalmol
Otolaryngol. 1973;77:ORL417-ORL423.
64. Leek JH. Stat tonsillectomy for peritonsillar abscess. Minn
Med. 1980;63:699-700.
Klug et al
65. Sumner E. Quinsy tonsillectomy: a safe procedure.
Anaesthesia. 1973;28:558-561.
66. Trzcinski WK. Peritonsillar abscess: a rationale for treatment.
Northwest Med. 1973;72:139-141.
67. Brook I, Frazier EH, Thompson DH. Aerobic and anaerobic
microbiology of peritonsillar abscess. Laryngoscope. 1991;
101:289-292.
68. Snow DG, Campbell JB, Morgan DW. The microbiology of
peritonsillar sepsis. J Laryngol Otol. 1991;105:553-555.
69. Muir DC, Papesch ME, Allison RS. Peritonsillar infection in
Christchurch 1990-2: microbiology and management. N Z Med
J. 1995;108:53-54.
70. Prior A, Montgomery P, Mitchelmore I, Tabaqchali S. The
microbiology and antibiotic treatment of peritonsillar
abscesses. Clin Otolaryngol Allied Sci. 1995;20:219-223.
71. Mitchelmore IJ, Prior AJ, Montgomery PQ, Tabaqchali S.
Microbiological features and pathogenesis of peritonsillar
abscesses. Eur J Clin Microbiol Infect Dis. 1995;14:870-877.
72. Sakae FA, Imamura R, Sennes LU, Araújo Filho BC, Tsuji
DH. Microbiology of peritonsillar abscesses. Braz J
Otorhinolaryngol. 2006;72:247-251.
73. Segal N, El-Saied S, Puterman M. Peritonsillar abscess in chil-
dren in the southern district of Israel. Int J Pediatr
Otorhinolaryngol. 2009;73:1148-1150.
74. Hoffmann S, Sørensen CH, Vimpel T. Influence of antibiotic
treatment on the isolation rate of group A streptococci from
peritonsillar abscesses. Acta Otolaryngol. 1987;104:360-362.
75. 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;42:747-
751.
76. Al Yaghchi C, Cruise A, Kapoor K, Singh A, Harcourt J. Out-
patient management of patients with a peritonsillar abscess.
Clin Otolaryngol. 2008;33:52-55.
77. Del Mar CB, Glasziou PP, Spinks AB. Antibiotics for sore
throat. Cochrane Database Syst Rev. 2006;4:CD000023.
78. Dunn N, Lane D, Everitt H, Little P. Use of antibiotics for
sore throat and incidence of quinsy. Br J Gen Pract. 2007;57:
45-49.
79. Bennike T, Brøchner-mortensen K, Kjaer E, Skadhauge K,
Trolle E. Penicillin therapy in acute tonsillitis, phlegmonous
tonsillitis and ulcerative tonsillitis. Acta Med Scand. 1951;139:
253-274.
80. Pichichero ME, Disney FA, Talpey WB. Adverse and benefi-
cial effects of immediate treatment of group A beta-hemolytic
streptococcal pharyngitis with penicillin. Pediatr Infect Dis J.
1987;6:635-643.
81. De Meyere M, Mervielde Y, Verschraegen G, Bogaert M.
Effect of penicillin on the clinical course of streptococcal
pharyngitis in general practice. Eur J Clin Pharmacol. 1992;
43:581-585.
207
82. Dagnelie CF, van der Graaf Y, De Melker RA. Do patients
with sore throat benefit from penicillin? A randomized double-
blind placebo-controlled clinical trial with penicillin V in gen-
eral practice. Br J Gen Pract. 1996;46:589-593.
83. Howe RW, Millar MR, Coast J, Whitfield M, Peters TJ,
Brookes S. A randomized controlled trial of antibiotics on
symptom resolution in patients presenting to their general
practitioner with a sore throat. Br J Gen Pract. 1997;47:280-
284.
84. Zwart A, Sachs PE, Ruijs GJHM, Gubbels JW, Hoes AW, de
Melker RA. Penicillin for acute sore throat: randomised
double blind trial of seven days versus three days treatment or
placebo in adults. Br Med J. 2000;320:150-154.
85. Landsman JB, Grist NR, Black R, McFarlane D, Blair W,
Anderson T. ‘‘Sore throat’’ in general practice. Br Med J.
1951;1:326-329.
86. Little P, Gould C, Williamson I, Warner G, Gantley M,
Kinmonth AL. Reattendance and complications in a rando-
mised trial of prescribing strategies for sore throat: the medica-
lising effect of prescribing antibiotics. Br Med J. 1997;315:
350-352.
87. Little P, Stuart B, Hobbs FD, et al. Predictors of suppurative
complications for acute sore throat in primary care: prospec-
tive clinical cohort study. Br Med J. 2013;347:f6867.
88. McIsaac WJ, Goel V, To T, Low DE. The validity of a sore
throat score in family practice. CMAJ. 2000;163:811-815.
89. Fine AM, Nizet V, Mandl KD. Large-scale validation of the
Centor and McIsaac scores to predict group A streptococcal
pharyngitis. Arch Intern Med. 2012;172:847-852.
90. McIsaac WJ, White D, Tannenbaum D, Low DE. A clinical
score to reduce unnecessary antibiotic use in patients with sore
throat. CMAJ. 1998;158:75-83.
91. Schechter GL, Sly DE, Roper AL, Jackson RT. Changing face
of treatment of peritonsillar abscess. Laryngoscope. 1982;92:
657-659.
92. Stegehuis HR, Schousboe M. Peritonsillar infection in
Christchurch 1981-1984. N Z Med J. 1986;99:536-538.
93. Stringer SP, Schaefer SD, Close LG. A randomized trial for out-
patient management of peritonsillar abscess. Arch Otolaryngol
Head Neck Surg. 1988;114:296-298.
94. Savolainen S, Jousimies-Somer HR, Mäkitie AA, Ylikoski JS.
Peritonsillar abscess: clinical and microbiologic aspects and
treatment regimens. Arch Otolaryngol Head Neck Surg. 1993;
119:521-524.
95. Matsuda A, Tanaka H, Kanaya T, Kamata K, Hasegawa M.
Peritonsillar abscess: a study of 724 cases in Japan. Ear Nose
Throat J. 2002;81:384-389.
96. Segal N, El-Saied S, Puterman M. Peritonsillar abscess in chil-
dren in the southern district of Israel. Int J Pediatr
Otorhinolaryngol. 2009;73:1148-1150.