Peritonsillar Abscess: Complication of Acute Tonsillitis or Weber's Glands Infection?
Peritonsillar Abscess: Complication of Acute Tonsillitis or Weber's Glands Infection?
Peritonsillar Abscess: Complication of Acute Tonsillitis or Weber's Glands Infection?
Otolaryngology
Head and Neck Surgery
S
No sponsorships or competing interests have been disclosed for this article. trategically located in the oropharynx, the palatine
tonsils are exposed to inhaled and ingested antigens
and are involved in the initiating immune responses
Abstract
against pathogens. This frequent exposure to potential
Objective. To review the literature concerning the 2 primary pathogens and involvement in local processing of microor-
hypotheses put forth to explain the pathogenesis of periton- ganisms may be the basis for the high incidence of tonsillar
sillar abscess: the acute tonsillitis hypothesis (peritonsillar infections. A small group of salivary glands, the Webers
abscess is a complication of acute tonsillitis) and the glands, is located in the supratonsillar space. The common
Weber gland hypothesis (peritonsillar abscess is an infec- duct from these glands penetrates the tonsillar capsule and
tion of Webers glands). opens into tonsillar crypts.
Data Sources. PubMed, EMBASE. Peritonsillar abscess (PTA), or quinsy, refers to a collection
of pus located between the tonsillar capsule and the pharyngeal
Review Methods. Data supporting or negating one hypothesis constrictor muscle. It is the most common deep neck space
or the other were elicited from the literature. infection1 with mean annual incidence rates in the range of 9
Conclusions. Several findings support the acute tonsillitis to 41 cases of 100 000 population per year.2-6 Teenagers and
hypothesis. First, the 2 main pathogens in peritonsillar young adults are most commonly affected,7 and smokers are at
abscess have been recovered from pus aspirates and bilat- increased risk of PTA.8Fusobacterium necrophorum and group
eral tonsillar tissues with high concordance rates, suggesting A streptococci (GAS) have been shown to be significant
that both tonsils are infected in patients with peritonsillar pathogens in PTA.9,10
abscess. Second, studies report signs of acute tonsillitis in Despite the relatively high prevalence of PTA, substan-
the days prior to and at the time of peritonsillar abscess. tial controversy exists regarding its pathogenesis.
Third, antibiotic treatment reduces the risk of abscess The classical acute tonsillitis hypothesis states that PTA
development in patients with acute tonsillitis. However, is a complication of acute tonsillitis. Bacteria are thought to
some findings suggest involvement of the Webers glands in spread from the tonsillar mucosa to the peritonsillar tissue.
peritonsillar abscess pathogenesis. First, high amylase levels Left untreated and occasionally even in spite of antibiotic ther-
have been found in peritonsillar pus. Second, the majority of apy, diffuse peritonsillar inflammation may evolve and prog-
peritonsillar abscesses are located at the superior tonsillar ress into abscess formation.11 The hypothesis does not describe
pole in proximity of the Webers glands. We propose a uni- how the bacteria penetrate the tonsillar capsule.
fied hypothesis whereby bacteria initially infect the tonsillar In 1994, Passy argued that the Weber gland hypoth-
mucosa and spread via the salivary duct system to the peri- esis explained the clinical, epidemiologic, and histologic
tonsillar space, where an abscess is formed. findings better.12 This hypothesis suggests that blockage of
the common duct from the Webers glands results in a loca- Table 1. Location of Peritonsillar Abscesses in Relation to the
lized, suppurative salivary gland infectiona 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
Webers 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 Webers 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
Webers 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 textperitonsillar abscess, the midportion or lower tonsillar pole. In contrast to the
quinsy, acute tonsillitis, pathogenesis, and Webers 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 Webers 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 Webers
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 Webers 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
histologic findings of the Webers glands and ducts during are at even greater risk of recurrent PTA, especially if \40
infection. years old.32-34,39
These findings suggest that scarring or other anatomic
PTA is associated with previous PTA and recurrent tonsillitis.
changes of the tonsil or the Webers glands, as inflicted by
Passy12 speculated that chronic infection of the Webers
infection within the tonsil or the peritonsillar tissues, increase
glands or attacks of peritonsillar cellulitis induced fibrosis
the risk of recurrent tonsillar disease in general and PTA in
of the salivary duct system, leading to increased risk of
particular. However, there is a lack of histologic studies sup-
PTA. To our knowledge, selective chronic or recurrent
porting this hypothesis and indicating the precise location of
infection of Webers glands has never been described. We
significant histologic alterations.
suggest that fibrosis could also be secondary to recurrent
There may be an increased risk of PTA in patients with
tonsillitis or previous PTA, which could lead to increased
recurrent tonsillitis (without previous PTA), but the magni-
risk of PTA.
tude of this association is not clear from the current litera-
PTA recurrence rates (excluding patients with residual dis-
ture (Table 3).
ease) were in the range of 1.8% to 25.3% in 14 studies reporting
Nevertheless, only a minority of PTA patients has had a
on the question (Table 2),29-42 with a cumulative average of
history of recurrent tonsillitis, peritonsillar cellulitis, or pre-
12.2% (95% CI: 11.2%-13.2%). The true number may be
vious PTA.
higher because recurrences can develop years after the initial
PTA and the mean follow-up period (when defined) ranged Tonsillectomy prevents future PTA. The risk of PTA is mark-
from 18 months to 17 years.29-31,33,35,39,40 Gavriel et al reported edly reduced after tonsillectomy. Passy argued that the
a mean time of 14 months between 2 PTA episodes.43 Weber gland hypothesis explains the reduced PTA risk
Studies report that patients with recurrent tonsillitis at the among tonsillectomized individuals, presumably due to the
time of initial PTA development are at increased risk of PTA removal of Webers glands at the time of tonsillectomy.12
recurrence.33,39,44 Kronenberg et al found that recurrent PTA However, it can be similarly argued that the removal of the
was 4 times more frequent in patients with previous recurrent tonsillar tissue is the reason for the reduced PTA risk.
tonsillitis (29 of 72, 40%) compared with patients without
(21 of 218, 9.6%).33 Similarly, in a study by Savolainen et al, Findings Supporting the Acute Tonsillitis Hypothesis
8 of 14 (47%) patients with .3 episodes of tonsillitis had
recurrence of PTA, compared with 13 of 77 (17%) patients Concurrent acute tonsillitis in PTA patients. Passy claimed that
with 3 acute tonsillitis episodes.44 only 4 of 100 consecutive patients with PTA had tonsillar
Hence, a previous episode of PTA significantly increases exudates.12 Accordingly, the majority of PTA patients did
the risk of recurrent PTA to approximately 12% (compared not have acute tonsillitis at the time of their PTA diagnosis.
with a 2%-3% lifetime risk of PTA in Denmark). Patients This argument against the acute tonsillitis hypothesis was
who also suffer from recurrent tonsillitis at the time of PTA made on the basis of a retrospective chart review, which raises
202 OtolaryngologyHead 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- 24% of patients (average across studies, 5.5%; 95% CI:
sillar mucosa description in the patient records. An accurate 4.7%-6.5%; Table 4).19,22,23,53-66 The majority of patients
description of the tonsillar mucosa in PTA patients is not with bilateral PTA were thought to have unilateral PTA, but
included in the majority of published PTA studies. However, an additional, contralateral abscess was discovered at the
in contrast to Passy, Spires et al reported tonsillar exudates in time of bilateral acute tonsillectomy. Unfortunately, none of
51% of patients with PTA.20 In a study of 275 acutely the studies report on bacterial findings from concurrent
removed tonsils due to PTA, acute or chronic inflammation abscesses. However, the fact that approximately 5% of PTA
was described in 68% of cases in routine histologic examina- patients have bilateral PTA suggests that PTA is secondary
tion.45 Blair et al conducted histopathologic examinations of to bilateral acute tonsillitis, and the finding is difficult to
tonsillar specimens from 6 patients with PTA, 4 with acute explain based on the Weber gland hypothesis alone.
tonsillitis, and 2 with intratonsillar abscess.11 In all 6 speci-
mens from PTA patients, the authors found erosion of the ton- Antibiotic treatment prior to PTA diagnosis. Studies report that
sillar surface epithelium and invasion of neutrophils, as 25% to 79% of PTA patients (collected average, 41%; 95%
observed in acute tonsillitis specimens. CI: 39.2%-43.6%) received antibiotics prior to diagnosis of
The limited evidence regarding signs of acute tonsillar PTA (Table 5).3,4,30,67-76 The indications for antibiotic
infection in patients with PTA favors the acute tonsillitis treatment were not described in any of the studies, and anti-
hypothesis. biotics may have been prescribed without signs and symp-
toms of acute tonsillitis. However, the fact that almost half
Common bacterial pathogens. GAS is commonly recognized as the PTA patients sought medical consultation and initiated
a significant pathogen in acute tonsillitis46 and PTA.9,47,48 antibiotic treatment in the days prior to abscess formation
Recent studies point to a major role of F necrophorum in suggests that acute tonsillitis prior to PTA development is
PTA,4,9,10 and this anaerobe may also play a pathogenic role common. The 60% of patients who did not take antibiotics
in acute tonsillitis.49-52 This concordance of 2 significant prior to PTA development may have had less severe symp-
pathogens between PTA and acute tonsillitis lends further sup- toms or a negative test result for the presence of GAS.
port to the acute tonsillitis hypothesis. However, it can be
argued that bacteria can exert their pathogenic potential at dif- Antibiotic treatment prevents PTA development. The findings
ferent anatomic sites without causal relationship. above indicate that antibiotic treatment does not prevent
abscess formation in all cases. However, studies suggest
Occasional bilateral PTA. In 14 studies reporting on the preva- that there could be a protective effect of appropriate antibio-
lence of bilateral PTA in patients undergoing bilateral tic treatment to patients with bacterial tonsillitis with avoid-
quinsy tonsillectomy, bilateral PTA was found in 2.0% to ance of suppurative complications.77,78 A Cochrane review
Klug et al 203
by Del Mar et al, based on 2433 patients from 8 studies, the number of patients presenting with initial PTA is
found a convincing 85% reduction in the risk of PTA if bac- unknown and that the number of patients with initial sore
terial acute tonsillitis was treated with antibiotics.77 This throat may constitute a minor part of all PTA patients.
percentage should be regarded with some reservation, as
72% (18 of 25) of the patients who developed PTA were Bacterial concordance rates between the 2 tonsils in patients
included in 2 nonrandomized and non-double-blinded stud- with PTA. The bacteriology of both tonsils (surface and core)
ies from 1951.79-86 At that time, the prevalence of PTA in and pus aspirates in patients with unilateral PTA undergoing
untreated patients was much higher than it is today. acute bilateral tonsillectomy was previously studied.9 GAS
Furthermore, some patients were treated with intramuscular was isolated from 7 of 36 patients. In all 7 patients, GAS
penicillin79 or antibiotics not presently recommended for was found in aspirated pus and the tonsillar core at the side
acute tonsillitis.82,83,85 Hence, it is largely unknown if the of the abscess. Similarly, F necrophorum was found in both
treatment of bacterial acute tonsillitis patients with the anti- pus and the tonsillar cores at the side of the abscess in 19
biotics used today reduces the risk of PTA. Nevertheless, patients. In addition, 2 F necrophorum isolates were recov-
the fact that a protective effect of antibiotics on PTA devel- ered solely from aspirated pus, and 1 F necrophorum isolate
opment exists is a strong indicator for the acute tonsillitis was found in the tonsillar core only.
hypothesis. The high concordance rates between tonsillar cores and
PTA pus make it rather unlikely that PTA is an isolated
Development of PTA after well-described initial sore throat. infection of the Webers glands independent of tonsillar
Recently, Little et al published the results of an impressive bacteriology. Moreover, the 7 GAS isolates were also recov-
study including 14,610 patients treated for sore throat in ered from the corresponding contralateral tonsils. Similarly,
616 general practices.87 They found that 47 of 13,288 20 of the 21 F necrophorum isolates were also found in the
patients (1322 patients had missing data) with well- contralateral tonsil. These findings confirm the nearly per-
described initial symptoms and findings of acute tonsillitis fect concordance between pus and ipsilateral tonsillar cores
developed PTA within a month of initial consultation. It can and show that the oropharyngeal infection in PTA patients
be argued that the development of PTA in a minority affects both tonsils with concurrent pathogens.
(0.5%) of patients could just be random or that the symp-
toms (throat pain and difficulty swallowing) in these 47 Findings Possibly Contradicting the Acute Tonsillitis
patients were due to incipient infection of the Webers Hypothesis
glands. Unfortunately, the authors did not state the initial
findings in patients with PTA alone but rather pooled all Acute tonsillitis is more frequent in childhood, and PTA is more
174 patients with complications (PTA, n = 47; sinusitis, n = prevalent among adults. The majority of PTA patients are
38; otitis media, n = 69; cellulitis, n = 20). In these patients, teenagers and young adults, while bacterial acute tonsillitis
34% had initial findings of purulent tonsils, and 21% had is more frequent among children.7,88-90 Researchers skepti-
severely inflamed tonsils. However, it can be argued that cal of the acute tonsillitis hypothesis argue that the age-
204 OtolaryngologyHead 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
related incidence rates of acute tonsillitis and PTA should However, some findings are difficult to explain from the
mirror each other if this hypothesis is true. However, factors acute tonsillitis hypothesis alone but suggest a role of the
other than age also contribute to the development of PTA. For minor salivary glands (Webers glands in particular) in PTA
instance, smoking is associated with an increased risk of PTA pathogenesis. First, elevated amylase levels have been
development.8 In a previous study of 847 PTA patients, F found in PTA pus compared with other neck abscesses.
necrophorum was significantly more prevalent among patients Second, the majority of PTAs are located at the superior
aged 15 to 24 years as compared with children and older tonsillar pole. Yet, a significant proportion of PTAs are
adults.7 Similarly, F necrophorum is more commonly associ- located at the midportion or lower tonsillar pole, and an
ated with acute tonsillitis in patients aged 15 to 30 years.49,50 extended version of the Weber gland hypothesis encompass-
The observed differences in age distribution of acute ton- ing all minor salivary glands in the tonsils may explain this
sillitis and PTA cases in children vs adults can potentially finding. In addition, the duct system of the minor salivary
be explained by additional risk factors for PTA development glands provides an explanation for how bacteria may pene-
and susceptibility to specific bacterial pathogens, which are trate the tonsillar capsule, when the infection progresses
unequally distributed between children and adults. from the tonsillar mucosa to the peritonsillar tissues.
Previous researchers have, for unknown reasons, thought
Conclusions of these 2 hypotheses as opposing.12,13,17,18 We propose
that, indeed, both hypotheses may be true and complemen-
More studies are needed before solid conclusions regarding
tary. We find it likely that, in the majority of PTA cases,
the pathogenesis of PTA can be drawn. Based on the current
bacteria infect the tonsillar mucosa (including the crypt
literature, however, there are more findings in favor of the
mucosa) and spread to the peritonsillar space via the sali-
acute tonsillitis hypothesis. First, the 2 main pathogens in
vary duct system, where an abscess is formed if the bacteria
PTAGAS and F necrophorumhave been recovered
are not overcome by the immune system and (in some
from PTA pus aspirates and bilateral tonsillar tissues with
high concordance rates. Second, also indicating bilateral cases) antibiotics. With the variations seen in the clinical
presentation of PTA patients, it is possible that PTA devel-
tonsillar infection, bilateral PTA has been found in approxi-
opment in some patients is solely an infection of the
mately 5% of PTA cases at the time of acute tonsillectomy.
Webers glands and in others a direct spread of the infection
Third, signs of acute tonsillitis in the days prior to and at
from the tonsillar mucosa.
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 Implications for Practice
antibiotics in the days prior to PTA diagnosis, possibly due PTA continues to be the most common deep neck abscess,
to signs and symptoms of acute tonsillitis. Last, antibiotic and antibiotic treatment directed against GAS in patients
treatment has been found to reduce the risk of PTA develop- with acute tonsillitis is currently the only intervention iden-
ment in patients with acute tonsillitis. tified to reduce the incidence. However, the use of antibiotic
Klug et al 205
therapy in patients with bacterial acute tonsillitis has abscesses in London, Ontario. J Otolaryngol Head Neck Surg.
recently been questioned by researchers skeptical to the 2013;42:5.
acute tonsillitis hypothesis. The findings in the current 7. Klug TE. Incidence of peritonsillar abscess: the influence of
review support the rationale for antibiotic treatment of season, age, and gender. Eur J Clin Microbiol Infect Dis.
patients with severe acute tonsillitis to reduce the risk of 2014;33:1163-1167.
PTA development. Little et al reported that the symptoms 8. Klug TE, Rusan M, Clemmensen KK, Fuurted K, Ovesen T.
and clinical findings in patients with acute tonsillitis were Smoking promotes peritonsillar abscess. Eur Arch Otorhinolaryngol.
unable to predict those who developed complications, includ- 2013;270:3163-3167.
ing PTA.87 Hence, the number of acute tonsillitis patients 9. Klug TE, Henriksen JJ, Fuursted K, Ovesen T. Significant
needed to treat to avoid one case of PTA is currently high. pathogens in peritonsillar abscesses. Eur J Clin Microbiol
Recent studies indicate a major role of F necrophorum in Infect Dis. 2011;30:619-627.
acute tonsillitis and PTA, and it is plausible that early detec- 10. Klug TE, Henriksen JJ, Rusan M, et al. Antibody development
tion and antibiotic therapy directed against this anaerobe may to Fusobacterium necrophorum in patients with peritonsillar
prevent PTA development in many teenagers and young abscess. Eur J Clin Microbiol Infect Dis. 2014;33:1733-1739.
adults. However, more studies are needed to substantiate this 11. Blair AB, Booth R, Baugh R. A unifying theory of tonsillitis,
assumption. intratonsillar abscess and peritonsillar abscess. Am J
Improved understanding of the PTA pathogenesis is Otolaryngol. 2015;36:517-520.
important for the development of more efficient prevention 12. Passy V. Pathogenesis of peritonsillar abscess. Laryngoscope.
strategies. Studies of the anatomy, distribution, microbiol- 1994;104:185-190.
ogy, and immunology of the minor salivary glands in the 13. Powell EL, Powell J, Samuel JR, Wilson JA. A review of the
tonsils are likely to provide valuable information. pathogenesis of adult peritonsillar abscess: time for a re-evaluation.
J Antimicrob Chemother. 2013;68:1941-1950.
Author Contributions 14. Krober MS, Bass JW, Michels GN. Streptococcal pharyngitis:
Tejs Ehlers Klug, initiating, designing, and drafting of the work; placebo-controlled double-blind evaluation of clinical response
identification and analysis of the studies; final approval of the to penicillin therapy. JAMA. 1985;253:1271-1274.
manuscript; accountable for all aspects of the work; Maria Rusan, 15. Bisno AL, Gerber MA, Gwaltney JM Jr, Kaplan EL, Schwartz
analysis and interpretation of the studies; critical revision and final RH. Diagnosis and management of group A streptococcal
approval of the manuscript; accountable for all aspects of the pharyngitis: a practice guideline. Infectious Diseases Society
work; Kurt Fuursted, designing the review; critical revision and of America. Clin Infect Dis. 1997;25:574-583.
final approval of the manuscript; accountable for all aspects of the 16. Del Mar CB, Glasziou PP, Spinks AB. Antibiotics for sore
work; Therese Ovesen, designing the review; critical revision and
throat. Cochrane Database Syst Rev. 2006;4:CD000023.
final approval of the manuscript; accountable for all aspects of the
17. Kordeluk S, Novack L, Puterman M, Kraus M, Joshua BZ.
work.
Relation between peritonsillar infection and acute tonsillitis: myth
Disclosures or reality? Otolaryngol Head Neck Surg. 2011;145:940-945.
Competing interests: None. 18. El-Saied S, Puterman M, Kaplan DM, Cohen-Lahav M, Joshua BZ.
Sponsorships: None. Involvement of minor salivary glands in the pathogenesis of periton-
sillar abscess. Otolaryngol Head Neck Surg. 2012;147:472-474.
Funding source: None.
19. Pham V, Gungor A. Bilateral peritonsillar abscess: case report
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