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They are found in the tonsillar fossa of the lateral oropharyngeal wall, between
the palatoglossal arch (anterior) and the palatopharyngeal arch (posterior). The
medial surface is the free mucosal part of the tonsil facing the oropharynx. The
epithelium of the tonsil is the stratied squamous, nonkeratinized epithelium,
which contains blind tubules from the epithelium on the surface of the tonsil and
extends deep into this tissue, leading into tonsillar crypts [1]. About 10–30 branching and anastomosing crypts increase the tonsils’ surface area for interactions
between antigens and the nodular lymphoid tissue [1, 5, 6]. They increase the
surface area of the tonsil up to 300cm2 [2, 6, 7]. The tonsil is surrounded by a
capsule of loose connective tissue and is separated from the superior pharyngeal
constrictor fascia on the deep surface of the tonsil [1, 3]. The surface epithelia are
underlined by a band of thick connective tissue containing many vessels, nerves,
and lymphatics [1].
The arterial blood supplies of the tonsils are the anterior tonsillar artery, from
dorsal lingual branches of the lingual artery, the posterior tonsillar artery, and the
ascending palatine branch of the facial. Ascending pharyngeal arteries, a superior
tonsillar artery from a more signicant palatine branch of maxillary artery, and inferior tonsillar artery (main artery) from facial artery [1, 3, 4]. The venous drainage is
via the tonsillar vein (drains into the facial vein), and paratonsillar veins, which
drain into the pharyngeal plexus and then internal jugular vein [1, 3, 4]. The palatine
tonsils receive innervation from the maxillary nerve and glossopharyngeal nerve.
The lymphatic drainage of the palatine tonsils through to the jugulodigastric and
upper deep cervical lymph nodes located behind the angle of the mandible [1, 3, 4].
38.2.2 Lingual Tonsil
The lingual tonsil comprises numerous lymphoid nodules within the posterior third
of the tongue. A stratied nonkeratinized squamous epithelium covers the lingual
tonsil. The lingual artery’s dorsal and the lingual vein’s dorsal lingual branches
perform the vascular supply. Innervation is from the glossopharyngeal nerve.
Lymphatic uid from the lingual tonsil drains into the jugulodigastric and deep
cervical lymph nodes [1, 3, 4].
38.2.3 Adenoids (Pharyngeal Tonsil)
The pharyngeal tonsil, also known as the adenoid, is composed of lymphoid tissue
within the mucosa of the roof of the nasopharynx. The pharyngeal tonsil is lined by
pseudostratied ciliated columnar epithelium (respiratory epithelium) that is plicated to form numerous surface folds. The arterial supply of the adenoids is from
the basisphenoid artery, the ascending pharyngeal artery, the ascending palatine
artery, the pharyngeal branch of the maxillary artery, the tonsillar branch of the
facial artery, and the artery of the pterygoid canal. Venous drainage is to the pharyngeal plexus, which communicates with the pterygoid plexus and drains into the
38 Meeting Organ forENT andPediatric Pulmonology: Tonsils
internal jugular and facial veins. The nerve supply is from the pharyngeal plexus.
The efferent lymphatic drainage of the adenoids is to the retropharyngeal and pharyngomaxillary space lymph nodes [1, 3, 4].
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38.2.4 Tubal Tonsils
The tubal tonsils are the small aggregates of lymphoid tissue around the Eustachian
tube’s opening in the nasopharynx’s lateral wall. They form the lateral aspect of
Waldeyer’s ring. The epithelial covering of the tubal tonsils is ciliated pseudostratied epithelium with no crypts. Arterial supply is from the ascending pharyngeal
artery, and venous drainage is to the pharyngeal plexus. Innervation is via the maxillary and glossopharyngeal nerves. The retropharyngeal and the deep cervical lymph
nodes drain the tubal tonsils [1, 3, 4].
38.3 Embryology oftheTonsils
Tonsils are derived from the second pharyngeal pouch. Tonsilla palatina begins to
develop in the 14th gestational week and is characterized by the development of
invaginations of the epithelium in the underlying mesenchymal cells and the inltration of the stroma by lymphoid cells [8, 9]. About the 16th gestational week,
epithelial crypts develop into connective tissue and are inltrated with T lymphocytes [8, 9]. A progressive development of complex epithelial invagination (tubules
and crypts) occurs with the parallel development of lymphocytic tissue. Primary
follicles contain precursors of dendritic reticulum cells and lymphoid cells that
belong to the B-cell line and are considered the rst B-cell regions in fetal lymphoid
tissue [8, 9]. In embryonic life, no germinal center is observed in the lymphatic follicles of the tonsil [9]. Present at birth, the tonsils tend to reach their full size between
the sixth and eighth years of life. Between the 4th and 12th year of life, tonsils and
adenoids are found to be the most immunologically active and begin to involute/
atrophy shortly after the rst decade, directly proportional to the bacterial load and
the number of B and T cells [1, 3, 10].
38.4 Immunology oftheTonsils
Tonsils are lymphoid tissue structures positioned close to the entrance of the digestive and respiratory tracts and play a key role in our immune system as part of secondary lymphoid organs [2]. The mucosal-associated lymphoid tissues (MALT) are
considered a special type of secondary lymphoid organ concerned with immunity at
mucosal surfaces of the aerodigestive tract [7, 11]. The MALT includes Peyer’s
patches, appendix, and tonsils as nasopharynx-associated lymphoid tissue (NALT),
known as Waldeyer’s ring [2, 6, 7, 11].
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Tonsils are designed to carry foreign bodies from the outside to lymphoid cells.
This contrasts with the lymph nodes, which depend on antigenic administration via
the lymphatic pathway [1]. In the tonsils, immune-reactive lymphoid cells are found
in four separate areas: the reticular cell epithelium, the extrafollicular area, the mantle zone of the lymphoid follicle, and the germinal center of the lymphoid follicle
[1]. The germinal center and the mantle zone dene the lymphoid follicle.
Mature B lymphocytes make up the mantle zone surrounding the germ center. It
is surrounded by T cells in the extrafollicular area [2, 12, 13].
The reticulated crypt epithelium, also known as lymphoepithelium [2], plays a
vital role in beginning immune responses in the palatine tonsils when antigens are
inhaled or ingested [1, 2]. The antigen is transported by specialized membranous (M)
cells at the base of the reticulated crypt epithelium [7, 10–12]. After detecting an
antigen, M cells activate T and B cells in the tonsils, triggering an immunological
response [1–3]. B lymphocytes and T helper cells (CD4+) make up the majority of
lymphoid cells detected in the spaces of the reticulated crypt epithelium of the human
palatine tonsil. Approximately 50–90% of the intraepithelial lymphocytes are B
cells. Antigens enter the extrafollicular area of lymphoid follicles after passing
through the crypt epithelium. T cells (mainly of the CD4+ helper phenotype), interdigitating dendritic cells (IDC), macrophages, and specialized venules known as
high endothelial venules (HEV) are found in the extrafollicular region. HEV is necessary to enter T and B cells from the blood into the tonsils. Activated T cells produce
and release biologically active protein cytokines. T helper lymphocytes (CD4) stimulate B cells and facilitate their transformation into plasma cells (producing antibodies), and T cytotoxic lymphocytes (CD8) kill antigen-containing cells by direct
contact and by release of cytokines. B memory cells develop and are maintained at
the germinal center for repeated antigen exposure, whereas antibody-producing
plasma cells migrate from the germinal zone to the mantle zone. The palatine tonsils
produce a variety of Ig isotypes (IgD, IgM, IgG, and IgA) [2, 7, 12, 13].
IgA is an antibody that functions as a mucosal antiseptic’ and plays a vital role
in mucus immune activity [1, 3, 11, 12]. The J-chain is required for the epithelial
transport of Ig polymers and is produced by Ig-producing cells. The presence of the
J-chain in the IgA polymer is needed in a stable complex. IgA binds to pathogens
and other molecules, either blocking or rendering them harmless, allowing them to
be absorbed, transported as an immunological complex, and dealt with by the reticuloendothelial system. J-chain is also found in IgM, allowing it to be secreted in the
same way as IgA.In patients with selective IgA deciency, secretory IgA (sIgA) is
lacking but may be replaced by secretory IgM, which is also protective.
Immunoregulatory compensation occurs in other IgA-decient patients, resulting in
many IgD-producing cells in the respiratory mucosa. Because this cannot function
as a secretory antibody, these people are prone to repeated respiratory tract infections. Tonsillectomy specimens show an increase in IgD-bearing cells [2, 7, 11].
The number of lymphocytes in children’s tonsils is higher than in adults’ tonsils,
and the number of helper and cytotoxic T lymphocytes is higher in sick tonsils.
Also, the persistent antigenic stimulation from infected tonsils causes increased levels of immunoglobulins throughout the pretonsillectomy period [2, 11].
38 Meeting Organ forENT andPediatric Pulmonology: Tonsils
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38.5 Etiology andPathogenesis
Normal ora in the upper respiratory tract is established from birth. After birth, the
tonsils are one of the rst organs to accept external antigenic stimuli with respiration and digestion. The pathophysiology of disease in the tonsils is likely multifactorial [4]. Multiple organisms, including aerobic and anaerobic bacteria, viruses,
fungi, and parasites, can infect tonsils; some are part of the normal oral pharyngeal
ora, while others are external pathogens [1, 4, 14].
The mostly found aerobic bacteria in tonsils and adenoids are Streptococci
(groups A, B, C, G), Hemophilus inuenza, Streptococcus pneumoniae, Branhamella
cattarhalis, Staphylococcus aureus, Mycobacterium sp., and Neisseria sp. [4]. As
anaerobic, we may list Bacteroides sp., Actinomycosis sp., Peptococcus sp., and
Peptostreptococcus sp. [4].
38.5.1 Viral Tonsillitis
The most prevalent viral causes are rhinovirus, respiratory syncytial virus, adenovirus, and coronavirus, which all cause the common cold. These are typically lowvirulent, mild, and self-limiting infections that do not require special treatment and
rarely cause complications. The majority of patients have a fever and erythematous
pharyngeal mucosa. Although the tonsils may be swollen, no associated exudate
usually exists [1]. Tonsilitis can be caused by various viruses, including EpsteinBarr (which causes mononucleosis), CMV, herpesvirus, hepatitis A, rubella, and
HIV [1, 13, 15]. Coxsackievirus, herpesvirus, and Epstein-Barr virus may affect the
tonsils and produce symptoms of exudative and nonexudative tonsils [1, 13, 15–17].
High fever, general malaise, large, palatal petechia, swollen, dirty-gray tonsils,
posterior cervical lymphadenopathy, hepatosplenomegaly, and exhaustion are all
symptoms of mononucleosis caused by EBV [1, 13, 15, 16]. The diagnosis of
Epstein-Barr virus can be conrmed by laboratory testing in conjunction with physical exam ndings. A differential blood count indicating lymphocytosis (50% lymphocytes with 10% atypical cells) supports a diagnosis, as are heterophil antibody
titers [1, 15, 16]. The disease may still be present if the heterophil antibody agglutination test is negative. Only 60% of individuals with infectious mononucleosis have
a positive result during the rst 2weeks of illness onset; 90% have a positive impact
one month later [1]. Patients should avoid contact sports during their sickness due
to the link between hepatosplenomegaly and mononucleosis syndrome, since they
risk splenic rupture [13]. Symptomatic treatment is used to treat this condition.
When given to mononucleosis patients, amoxicillin-related drugs have been reported
to trigger an immune-mediated rash. Antibiotics should not be used in patients diagnosed with EBV tonsillitis or suspected of having it [1, 13]. Upper airway obstruction from severely enlarged tonsils can be life-threatening and should be managed
promptly with the insertion of a nasopharyngeal airway and short-term high-dose
steroid therapy. Tonsillectomy or tracheotomy may be indicated if the obstruction is
severe and these methods do not relieve it [1, 13].
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Small vesicles with erythematous bases form ulcers and extend over the anterior
pillar tonsils, palate, and posterior pharynx in Herpangina caused by coxsackievirus
[1, 13]. It could be a part of the hand, foot, and mouth syndrome, with blisters on the
palms and soles. Hydration, antipyretics, and analgesics are commonly supportive
treatments [1, 13, 17].
38.5.2 Bacterial Tonsillitis
GABHS (group A beta-hemolytic Streptococcus) is the most common cause of bacterial infections, though Staphylococcus aureus, Streptococcus pneumoniae, and
Haemophilus inuenzae have all been cultured. Symptoms of acute bacterial tonsillitis include throat soreness, swollen erythematous or exudative tonsils, stinking
breath, and painful cervical lymph nodes. It might be difcult to distinguish between
bacterial and viral causes of tonsillitis and pharyngitis. At the same time, supportive
care treats viral infections, pain management, and antibiotics (amoxicillin or macrolides). They are used to treat ordinary, moderate bacterial tonsillitis [1, 4, 13]. The
most prevalent bacterial cause of acute tonsillitis is Group A B-hemolytic streptococcus. Because this organism is a known precursor of acute rheumatic fever and
glomerulonephritis, which develops due to an autoimmune response, it is a severe
infectious condition [1, 4, 13, 17]. As a result, most authorities advise that microbio-
logic testing be used to conrm or rule out a diagnosis of group A-hemolytic streptococcal (GABHS) tonsillitis. Selective use of throat cultures is a time-honored
medical practice, the usefulness of which is somewhat limited by the delay in
obtaining results [1, 4, 17]. The use of throat cultures is a long-honored medical
practice, but its utility is restricted by the time it takes to get results [1, 4, 17]. The
18- to 36-h wait for positive cultures may cause the patient extra suffering and
lengthen the clinical course [1, 4, 17]. The development of rapid strep detection
tests for detecting the group A streptococcal antigen has represented a helpful
advance. Rapid streptococcus antigen tests are very specic but less sensitive than a
throat culture [1, 18]. This test is particular (ranging from 88 to 100%). However, it
is not exposed (61–95%) [14]. The quick strep test is the most accurate and costeffective way to diagnose acute GABHS infection. A standard throat culture is performed in individuals with a negative immediate strep test result and a strong
suspicion of streptococcal tonsillitis [1, 4, 13, 17, 18].
Other bacteria, such as Streptococci of Group C and G, Haemophilus inuenzae,
Nocardia, Corynebacteria, and Neisseria gonorrhoeae, must be evaluated more sel-
dom. Vincent’s angina is caused by the bacterial symbiosis of Fusobacterium
nucleatum and Borrelia vincentii, characterized by a generally unilateral, ulcerating
tonsillitis with halitosis. Patients complain of a high headache, fever, sore throat,
cervical lymphadenopathy, and a membrane on the tonsil that, when removed,
reveals an ulcer that is restricted to the surrounding tissue and resolves in 7–10days.
Treatment usually involves debridement, antiseptic mouthwashes such as chlorhexidine, pain control, and antibiotics, including clindamycin, penicillin, or erythromycin [1, 13, 17].
38 Meeting Organ forENT andPediatric Pulmonology: Tonsils
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Diphtheria tonsillitis has decreased dramatically since the introduction of diphtheria toxin immunization. This organism produces a thick pharyngeal membrane
and early exudative pharyngotonsillitis. When this membrane is removed, it causes
bleeding. After that, the infection might spread to the throat, palate, tonsils, and
larynx [1, 13]. Airway obstruction can occur when laryngeal inammation is accompanied by an exudative, necrotic gray pharyngeal membrane [1, 13].
The organisms of C. diphtheriae also release a fatal exotoxin that can damage
cells in distant organs. Myocarditis and neurologic sequelae resembling features of
poliomyelitis may result [1, 13]. Fluorescent antibody studies are used to identify
the organism. Gram staining can detect the presence of Klebs-Löfer bacillus in the
membrane. Because diphtheria is a life-threatening condition, antitoxin must be
administered within 48h of the onset of symptoms. Airway obstruction should be
managed with tracheotomy. Penicillin should be given in high dosages [1, 13].
One of the most common sexually transmitted bacterial infections is gonorrhea.
While oral-genital infections are most commonly transferred through sexual contact,
transmission from mother to fetus during pregnancy might result in systemic or ophthalmic diseases. As a result, N. gonorrhoeae and C. trachomatis are uncommonly
found in pediatric patients [13]. Unfortunately, because the physical ndings in the
pharynx are not specic enough to reveal the etiology, the diagnosis is frequently made
clinically, depending on the patient’s history and risk factors. Mild pharyngeal pain and
dysphagia are among the pharyngeal symptoms. Despite the start of empiric antibiotic
treatment, pharyngeal culture explicitly aimed at identifying gonorrhea is frequently
conducted. Notably, C. trachomatis, a gram-negative intracellular bacterium, is known
to be capable of causing a similar pharyngeal infection and often coexists with pharyngeal gonorrhea in patients. Despite signs of systemic disease, chlamydial conditions
are rarely found in pharyngeal culture, unlike gonorrhea. As a result, both N. gonor-
rhoeae and C. trachomatis should be treated. Intramuscular ceftriaxone in combination
with azithromycin or doxycycline is the preferred treatment [1, 13, 19].
Oral pharyngeal lesions have been linked to Treponema pallidum infections in
both the primary and later stages of syphilis. Oral chancres are common in primary
syphilis, while grayish supercial mucous membrane patches with an erythematous
border are standard in secondary syphilis. A dark-eld microscope inspection of the
lesions and a serological test are used to conrm the diagnosis [1, 19].
38.5.3 Candida
Although thrush is frequent in newborns, Candida albicans infection of the pharynx
is uncommon in healthy children and adults. Candidiasis can cause severe pharyngitis, especially in immunocompromised patients or those treated with antimicrobial drugs. The lesions are patchy white “in color,” and when the exudate is removed,
a shallow reddish ulcer is revealed. The usual yeast forms in stained smears and
cultures are used to conrm the diagnosis. In resistant cases, Nystatin or uconazole
are used to treat the infection [1, 19].
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38.6 Complications ofTonsillitis
The complications of tonsillitis can be divided into suppurative and nonsuppurative
difculties [1].
38.6.1 Suppurative Complications
38.6.1.1 Peritonsillar Abscess (Quincy Tonsil)
Peritonsillar abscess is the most common complication of acute tonsillitis. It is a
purulent uid in the space surrounding the tonsils between the tonsillar capsule and
the superior constrictor muscle [3]. Patients with recurrent tonsillitis or chronic tonsillitis that has not been appropriately treated are more likely to develop peritonsillar abscess [1, 15, 20]. Patients usually present with unilateral pain that causes
odynophagia, ipsilateral otalgia, and classic “hot potato” or mufed voice [1, 3].
The odynophagia may be so acute that the patient cannot swallow, resulting in dehydration. Oropharyngeal asymmetry can be demonstrated clinically by moving the
affected side’s tonsil toward the median [1, 20, 21]. Trismus is frequently present
due to irritation of the pterygoid musculature by the pus and inammation [1].
Peritonsillar abscess cultures typically reveal a polymicrobial infection, both aerobic and anaerobic. In recent studies, Fusobacterium necrophorum, also responsible
for Lemierre’s syndrome, is a prominent and prevalent pathogen in peritonsillar
abscesses [22]. In some circumstances, a single needle aspirate or a series of needle
aspirates may be sufcient to resolve abscess formation.
In some cases, broader drainage may be required to clear the infection. If there has
been a previous history of tonsillitis, a Quinsy tonsillectomy may be highly benecial in circumstances where incision and drainage cannot be performed without general anesthesia. Although tonsillectomy is not required for all peritonsillar abscesses,
it is the preferred treatment for recurrent infection [1, 15, 20, 21, 23]. Intratonsillar
abscesses are usually found in association with peritonsillar abscesses [20, 22, 23].
Peritonsillar abscess complications are relatively uncommon. Parapharyngeal and
retropharyngeal abscesses, upper airway obstruction [13], Lemierre’s syndrome [24,
25], mediastinitis [26], and other abnormal conditions are among them.
38.6.1.2 Parapharyngeal andRetropharyngeal Space Abscess
Parapharyngeal abscess is located between the superior constrictor muscle and the
deep cervical fascia [1, 20]. A patient with a parapharyngeal space infection typically has fever, leukocytosis, and pain. Tonsil displacement is found in the anteriormedial direction. A CT scan with contrast enhancement should be conducted if this
is suspected to be a parapharyngeal abscess. Aggressive antibiotic medication, uid
replacement, and close observation should all be used to treat lateral pharyngeal
space infections [1, 20]. The resolution of these infections frequently necessitates
surgical intervention. Intraoral methods should be utilized to treat peritonsillar
abscesses; they should not be utilized to treat lateral pharyngeal space abscesses due
to insufcient exposure in the event of heavy bleeding [1, 15, 20].
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In pediatric populations, retropharyngeal abscesses represent the predominant
deep neck infections after peritonsillar infections. Infection arises from the lymph
nodes that drain the upper airway and oropharynx. The abscess infectious process
may progress down the carotid sheath and into the mediastinum. Infections of the
retropharyngeal space are most frequent in children under the age of two. Irritability,
fever, dysphagia, airway obstruction, unilateral pain, torticollis, and cervical lymphadenopathy are common symptoms in children with retropharyngeal infections. A CT
scan is an excellent way to determine the size and extent of an abscess invasion [1, 15,
21, 23]. A transoral approach is recommended for incision and drainage of retropha-
ryngeal space abscesses. An external approach should be performed if the abscess
extends inferiorly below the hyoid bone (as revealed on the CT scan) [1].
Lemierre’s Syndrome
Lemierre syndrome commonly presents as sepsis following a sore throat with associated thrombosis of the internal jugular vein and septic emboli. It is most often linked
to Fusobacterium necrophorum, although it has also been linked to Staphylococcal
and Streptococcal infections. It most commonly affects healthy teenagers and young
adults. At the onset of the disease, patients present with nonspecic symptoms such
as exudative tonsillitis, high fever, oropharyngeal ulcers, cervical lymphadenopathy,
and pharyngeal hyperemia. Internal jugular vein thrombophlebitis, which commonly
manifests as pain and unilateral swelling around the angle of the jaw and along the
sternocleidomastoid muscle and is sometimes associated with trismus, is caused by
the second stage of the infection, which involves invasion of the anterior compartment. Invasion of the posterior compartment, on the other hand, can cause Horner
syndrome or cranial nerve X–XII palsies [27]. The third stage is the metastatic stage,
in which septic emboli can induce characteristic clinical signs and symptoms depending on the location of the embolism. The most prevalent location of metastatic dissemination is the lungs, where embolic illness causes symptoms similar to an aseptic
pulmonary embolism [25, 27]. Accurate diagnosis necessitates a high level of clinical suspicion. Early CT/US imaging and polymerase chain reaction–based serological screening are recommended to reduce diagnostic delays. The effective treatment
of Lemierre syndrome requires a combination of early diagnosis and aggressive antimicrobial therapy. Despite being a rare clinical entity today, Lemierre syndrome is
nevertheless a condition with signicant morbidity and death [24, 25, 27].
38.6.2 Nonsuppurative Complications
38.6.2.1 Acute Rheumatic Fever
Rheumatic fever (RF) is an inammatory, immunological condition caused by group
A Streptococcus infection. Patients aged 5–18 years old are the most typically
affected. While rare in the developed world, the incidence is high in developing
nations. RF usually appears 2–3weeks after a rheumatogenic streptococcus throat
infection, but it can present as early as 1week and as late as 5weeks. Multiple organ
systems are affected, and the presentation can have different degrees of severity. A
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diagnosis of acute rheumatic fever cannot be made using a specic laboratory test. It
is a clinical diagnosis based on the Jones criteria (table) and supported by clinical
immunology and microbiology lab data [1, 14, 15, 25]. For diagnosis of ARF, accord-
ing to Jones Criteria, two major or one signicant and two minor manifestations must
be present, plus evidence of antecedent group A streptococcus infection. Chorea and
carditis do not require evidence of antecedent group A streptococcus infection [14].
Cardiac manifestations such as pericarditis, myocarditis, and endocarditis are
common. Carditis affects approximately half of all patients and is frequently associated with valvular disease, particularly the mitral valve. Arthralgia, arthritis, skin
lesions, and central nervous system involvement (chorea) may be seen. Arthritis in
the major joints is frequently migratory, asymmetrical, and painful. Involuntary
movements of the limbs and facial muscles and speech and gait problems characterize Sydenham chorea. Patients may present with a rash called erythema marginatum
and subcutaneous nodules [1, 15, 25].
Elevated streptococcal antibody titers or demonstration of bacteria in the throat
are required to diagnose acute rheumatic fever. The ASO test may be administered
rst. Anti-DNAse B, antistreptokinase, or antihyaluronidase tests may be obtained if
the titer is not increased. To monitor disease activity, the preferred tests are C-reactive
protein and erythrocyte sedimentation rate to inammatory activity [1, 14, 15].
The use of antimicrobial medicines has reduced the incidence of rheumatic fever.
A single dose of penicillin, 1.2 million units intramuscularly for individuals weighing more than 27kg and 600,000units for those weighing less than 27kg, is suggested. Penicillin V is the preferred oral antibiotic, which should be taken twice to
thrice daily [1, 14, 15, 25]. For those allergic to penicillin, erythromycin (20–40mg/
kg/day for 10days) is a good option. Patients allergic to penicillin who do not have
acute hypersensitivity to beta-lactam antibiotics may benet from rst- or secondgeneration cephalosporins [1, 14]. Azithromycin and clarithromycin, two newer
macrolides, show fewer side effects in the stomach than erythromycin and have
similar sensitivity patterns to group A streptococcus. The inammatory process
involving numerous organ systems should be targeted for symptomatic treatment of
rheumatic fever. Because it has a higher risk of morbidity, the duration and kind of
therapy are determined mainly by the existence and severity of carditis during the
initial attack. The routine use of corticosteroids is not recommended. They should
only be used in the case of severe carditis, where they appear to help reduce mortality during an acute episode. The drug of choice is prednisone, given at 1–2mg/kg/
day for 2–3weeks. Rest for at least 4weeks is recommended. Arthritis caused by
acute rheumatic fever responds well to salicylates, with signicant clinical improvement. Treatment should last at least 2weeks and up to 6weeks to avoid rebound.
Sydenham’s chorea (SC) is not a self-limited or benign disease. SC mainly affects
children between 5 and 15years old and appears to predominate in girls. After Group
A B-hemolytic streptococcal pharyngitis, the condition usually takes 6–8weeks to
manifest. It does not happen as a result of a skin disease. Family investigations in both
SC and RF patients have indicated a signicant incidence of a favorable family history. The main feature of SC is the involuntary movements. These might be general or
unilateral, with the most commonly affected areas of the extremities and face. The
signs occur at rest, may start gradually or abruptly, and are exacerbated by stress. They
38 Meeting Organ forENT andPediatric Pulmonology: Tonsils
501
disappear during sleep, however. Depression, anxiety, personality changes, emotional
lability, OCD, tics, and attention decit disorder are some psychological and psychiatric symptoms of patients with SC.Cases of disability and social isolation have been
reported. It has been suggested that haloperidol be used to treat chorea. However,
sodium valproate has also been proven helpful. In this situation, there is no evidence
that steroids or nonsteroidal anti-inammatory medicines are benecial [1, 14].
38.6.2.2 Poststreptococcal Glomerulonephritis
Post-streptococcal glomerulonephritis (PSGN) is an immune-mediated disorder
following infection with Group A streptococcus. PSGN usually appears 1–2weeks
after a streptococcal throat infection or 6weeks after a streptococcal skin infection
(impetigo) in children. PSGN clinical symptoms are more prevalent in males than
females, with a 2:1 ratio. Patients present with hypertension, edema, abnormalities
on urine sediment, elevated inammatory markers, hypoproteinemia, and low complement levels. The situation is secondary to the presence of a common antigen of
the glomerulus with the streptococcus. Approximately 50% of children with PSGN
are asymptomatic and are discovered accidentally during routine urine analysis.
In most cases, PSGN is a self-limiting disease that only requires symptomatic
treatment. During the acute phase of the disease, supportive treatment aims to control the complications of volume overload, such as hypertension and edema. There
is no indication that antibiotic medication modies the natural history of glomerulonephritis, and penicillin management may not reduce the attack rate. A tonsillectomy may be required to eradicate the cause of infection [1, 25].
38.6.2.3 Scarlet Fever
Scarlet fever is related to the production of endotoxins by the group A streptococcal
bacteria. An erythematous rash, acute lymphadenopathy with a painful throat, vomiting, headache, fever, erythematous tonsils, pharynx, tachycardia, and a yellow exudate across the tonsils, pharynx, and nasopharynx are the most common symptoms
of scarlet fever. A strawberry tongue with a rash and large glossal papillae is a good
diagnostic sign. Diagnosis of scarlet fever is made by culture and positive result of
the Dick test, which is an intradermal injection of dilute streptococcal toxin. The rash
is not harmful, but it is a sign of group A streptococcus infection, which can cause
suppurative and non-suppurative problems. To avoid severe problems, it is necessary
to treat the acute infection. Penicillin is the rst-line therapy of choice [1, 15, 17].
38.6.2.4 Pediatric Autoimmune Neuropsychiatric Disorder
Associated withStreptococcal Infection (PANDAS)
Anxiety disorders, obsessive-compulsive characteristics, and pathologic compulsive tics associated with streptococcal tonsillitis and pharyngitis are increasingly
being recognized as a single entity. The symptoms start within weeks after the pharyngeal or tonsillar infection, and it is limited to the pediatric group by denition
[13]. Antibasal ganglia antibodies (ABGA) were detected in 95–100% of Sydenham
Corea (SC) patients and 64–94% of PANDAS patients [28]. Streptococcal infections may trigger an autoimmune response to the basal ganglia through a molecular
mimicry mechanism [13, 28, 29]. A tonsillectomy is an option for treatment [13].