Atypical Forms of Tonsillitis: Classification, Clinical Manifestations, and Treatment

Acute tonsillitis is an inflammation of the palatine tonsils, which can manifest itself in various clinical forms. Atypical forms of tonsillitis differ in their etiology, course, as well as features of local and general symptoms.

Classification of acute tonsillitis

• Herpetic sore throat;
• Phlegmonous tonsillitis (intratonsillar abscess);
• Ulcerative plaque angina (Simanowsky-Plaut-Venson);
• Fungal form of tonsillitis;
• Tonsillitis in diphtheria;
• Tonsillitis in measles;
• Tonsillitis in scarlet fever;
• Tonsillitis in infectious mononucleosis;
• Tonsillitis in syphilis.

Comparative characterization of atypical forms of tonsillitis

Herpetic sore throat

Etiology of herpetic sore throat

Herpetic sore throat (herpangina) is caused by coxsackieviruses, retroviruses, echoviruses and adenoviruses. The name herpetic sore throat is consonant with the herpes virus because of the similar vesicular rashes that characterize the disease. Herpetic sore throat occurs most often in children.

Anatomy of herpetic sore throat

In herpangina, vesicular rashes are found on the soft palate and palatine g lands against a background of hyperemic pharynx. The palatine tonsils are slightly hyperemic and edematous, occasionally also covered with whitish vesicles.

Clinical picture of herpetic sore throat

Herpangina is characterized by the predominance of general symptoms over local symptoms. There is a pronounced fever with high fever, headache and muscle pain. The disease usually resolves on its own in 3-4 days. Throat pain is mild, and children may refuse to eat.

Diagnosis of herpetic sore throat

The diagnosis is made on the basis of a typical clinical picture. For laboratory diagnosis, blood is tested for antibodies(IgM) or an oropharyngeal swab for RNA detection by PCR. It is recommended to prescribe a general blood test to assess the degree of intoxication and determine the level of C-reactive protein.

Treatment of herpetic sore throat

When treating herpangina, symptomatic therapy is used: use antipyretics and regularly rinse the oral cavity with antiseptic agents.

Phlegmonous tonsillitis (intratonsillar abscess)

Etiology of phlegmonous tonsillitis

The causative agents of phlegmonous tonsillitis are similar to those of the typical form of acute tonsillitis (see the article «Acute inflammatory diseases of the pharynx: classification, clinical manifestations, treatment»). Beta-hemolytic streptococcus group A (BHSA) is the most common.

Anatomy of phlegmonous tonsillitis

In phlegmonous tonsillitis, there is purulent melting of tissue inside the palatine tonsil. The disease develops against the background of classic acute tonsillitis and usually affects one tonsil. The tonsil is infiltrated, hyperemic, tense and bulging. In the center is formed purulent foci of melting, which can drain independently through the lacunae of the tonsils. Surrounding tissues of oropharynx are markedly hyperemic. Asymmetry of the pharynx is noted. Regional lymph nodes on the side of the lesion are enlarged.

Clinical picture of phlegmonous tonsillitis

Данная форма заболевания характеризуется наличием второй волны лихорадки, которая развивается через 3–4 дня после начала заболевания. Температура тела повышается до 39–41°C. Отмечается выраженная боль в горле, усиливающаяся при глотании, разговорах и движении языком. Наблюдается неприятный запах изо рта,гиперсаливация, а также затруднение глотания и речи. Больному трудно открыть рот.

Diagnosis of phlegmonous tonsillitis

Diagnosis is similar to that of the usual form of tonsillitis. For therapeutic and diagnostic purposes, puncture of the affected tonsil is performed.

Treatment of phlegmonous tonsillitis

Patients have the intratonsillar abscess opened and drained. Over the next few days, the abscess is revisited. For conservative treatment, antibacterial drugs of the penicillin series are used for 10 days; in case of allergy – cephalosporins or macrolides. In addition to antibiotics, non-steroidal anti-inflammatory drugs are prescribed, and local rinsing with antiseptic solutions.

Ulcerative plaque sore throat (Simanowsky-Venson’s sore throat)

Etiology of ulcerative plaque sore throat

The causative agent of ulcerative-film sore throat (Simanowsky-Plaut-Vensan sore throat) is a symbiosis of fusobacteria and spirochetes.

The anatomy of ulcerative plaque sore throat

For ulcerative-film sore throat is characterized by a unilateral lesion of the palatine tonsil, which manifests itself as a zone of deep necrosis at the upper pole with a whitish plaque, which is easily separated from the tissue. The process can spread to the soft palate, cheek and gingiva.

Clinical picture of ulcerative plaque sore throat

Simanowsky-Plaut-Vensan angina is characterized by unilateral lesions of the palatine tonsils and the absence of general symptoms. Patients note discomfort and slight pain in the throat on the affected side, as well as bad breath. Lymph nodes located along the sternoclavicular-papillary muscle are enlarged. Fever is not characteristic.

Diagnosis of ulcerative plaque sore throat

Diagnosis is established on the basis of a typical clinical picture and the results of pharyngoscopy. Bacteriologic examination of oropharyngeal secretion with determination of sensitivity to antibiotics is obligatory.

Treatment of ulcerative plaque sore throat

For treatment, antibacterial drugs of penicillin series or cephalosporins are used for 7-10 days. The oral mucosa is also treated with antiseptic solutions.

Fungal tonsillitis

Etiology of the fungal form of tonsillitis

The fungal form of tonsillitis (tonsillomycosis) is caused by yeast fungi of the genus Candida (in most cases C.albicans, less frequently C.tropicalis, C.krusei, C.glabrata). In rare cases, mold fungi of the genus Geotrichum, Aspergillus, Penicillium can be found.

Tonsillomycosis occurs in young children, the elderly, long-term users of antibacterial or hormonal drugs (including topical or aerosolized), immunodeficient patients (including often HIV-infected patients), diabetics, and cancer patients receiving chemotherapy.

Anatomy of the fungal form of tonsillitis

In tonsillomycosis in the acute phase of the process is characterized by the presence of white-gray curdy plaques on enlarged, hyperemic palatine tonsils. Often these plaques spread to the mucous membrane of the oral cavity. When the plaques are removed, bleeding foci remain, the affected mucosa is brightly hyperemic and has a varnished appearance.

Clinical picture of the fungal form of tonsillitis

Fungal tonsillitis has only local manifestations, such as itching, burning and dry mouth, bad breath. There may be soreness when eating, but it is expressed moderately. The process is often chronic.

Diagnosis of the fungal form of tonsillitis

A microbiological study of the oral mucosal secretion for fungal infection is performed.

Treatment of the fungal form of tonsillitis

Standard therapy of tonsillomycosis includes treatment of the oral cavity with antifungal drugs.

Specific forms of acute tonsillitis

Diphtheria

Etiology

Diphtheria is a highly contagious anthroponotic disease with high contagiousness and lethality. It is caused by gram-positive bacteria. Corynebacterium diphtheriae (Leffler’s bacillus).

Anatomic Pathology

Entering the body, diphtheria bacillus causes local changes in the oropharyngeal mucosa and a general effect on the body through diphtheria exotoxin. Depending on the severity (stage) of the process, the palatine tonsils, larynx, trachea, bronchi are affected.

In the localized form, white-gray dense fibrin films form on the surface of the tonsils . In the widespread form, they spreadto the uvula, palatine and larynx. The films are difficult to separate and leave a bleeding surface. However, films spreading into the larynx are easily detached into its lumen and cause asphyxia. The palatine tonsils are hyperemic and infiltrated. There is a reaction from the regional lymph nodes, which sharply increase in size. Penetration of exotoxin into the general bloodstream leads to damage to target organs (heart, peripheral nervous system, kidneys).

Clinical Manifestations

In diphtheria, there is a pronounced fever, a rise in temperature to 39-40°C, tachycardia, heavy sweats and headache. Against the background of general symptomatology, there is pain in the throat, intensified by swallowing, bad breath and plaque on the tonsils. Enlarged lymph nodes in the neck become sharply painful and the neck may swell significantly (“bull neck”).

Diagnosis

The examination is similar to that in acute tonsillitis. The diagnosis is established on the basis of the characteristic clinical picture, the results of pharyngoscopy. Determination of the level of leukocytes, C-reactive protein and rheumatoid factor in the blood, urinalysis, as well as bacteriological examination of the discharge or strepto-test for the diagnosis of BHSA is performed.

Treatment

Treatment of diphtheria is carried out strictly in a hospital. Immediately administered anti-diphtheria serum, which neutralizes diphtheria toxin. Simultaneously with the serum administered antibacterial drugs (penicillin series), a course of 7-10 days. In some cases, the introduction of systemic corticosteroids is indicated. Topical rinsing with antiseptic solutions is recommended. Vaccination against diphtheria is of great importance for prophylaxis.

Measles

Etiology

Measles belongs to a group of highly contagious diseases with a high degree of lethality and is caused by a paramyxovirus of the genus Morbillivirus.

Anatomic Pathology

In measles infection, even in the prodromal period, a pronounced hyperemia of the pharynx is characteristic. Large red spots appear on the soft palate, which may merge together. Later, plaques appear on the palatine tonsils, as in lacunar tonsillitis, and the oropharyngeal tissues are moderately infiltrated. There is hypertrophy of the entire lymphoepithelial pharyngeal ring. A distinctive feature of measles is the appearance of characteristic Belsky-Filatov-Koplik spots on the mucosa of the cheek area (whitish spots with a bright red outline, 2-3 mm in diameter, not merging with each other).

Clinical Manifestations

Measles infection usually manifests with local changes in the oropharynx, conjunctivitis, rhinitis. Then body temperature rises to high values (39-40°C), body aches, photophobia, general intoxication are observed. On the 4th-5th day from the onset of the disease, a pathognomonic patchy-papular rash appears, which spreads from top to bottom and tends to coalesce. The rash is seen on the face and neck on the first day, on the body on the 2nd day, and reaches the extremities by the third day. After emergence, the rash is pigmented and diminishes in the same order. Due to the increase in lymphoid tissue of the pharynx, complications such as otitis media and sinusitis are common.

Diagnosis

To diagnose measles, blood is tested for IgM antibodies, as well as for these antibodies in saliva. It should be noted that measles antibodies do not appear in the blood immediately, but in the range from 72 hours to 4 days from the onset of the disease. It is possible to detect measles virus RNA by PCR in oropharyngeal swabs.

Treatment

There is currently nospecific therapy for measles; only symptomatic treatment is used. Vaccination remains the most important aspect of measles prevention.

Scarlatina

Etiology

The causative agent of scarlatina is group A beta-hemolytic streptococcus (BHSA).

Anatomic Pathology

In scarlatina there is the development of classical tonsillitis: swelling and hyperemia of the palatine tonsils, plaque from follicular to filmy, and in severe cases may be ulceration of the oral mucosa. In addition, there are special changes that are characteristic only for scarlet fever. These include sharply delineated hyperemia of the pharynx, which ends, as a rule, on the hard palate. Dense white plaques are formed on the tongue, which after 2-3 days disappear, and the tongue becomes bright red, varnished with protruding papillae and is called “crimson“.

Clinical Manifestations

This infectious disease is characterized by general intoxication, fever up to 38-40°C, enlargement of regional lymph nodes, and there may be vomiting and diarrhea. Against the background of local changes in the oropharynx, the patient has a small-pointed rash on hyperemic skin. The rash spreads from top to bottom, tends to merge and intensify in places of natural folds (folds of arms and legs, groin area). A distinctive feature is the uninvolved nasolabial triangle, which remains white against the background of a bright red face. During the recovery period, changes in the oropharynx, plaque and rash disappear, but lamellar desquamation appears on the palms of the hands and feet.

Diagnosis

Diagnosis is established on the basis of typical clinical picture, anamnesis data and epidemiologic situation. Laboratory microbiological examination of oropharyngeal secretion is performed to determine the causative agent and sensitivity to antibacterial drugs. Strepto-test may be used.

Treatment

Penicillin antibiotics are used systemically for a course of 7-10 days. Careful care of the oral cavity is important, rinsing with antiseptic solutions is recommended. Bed rest and a high-calorie diet are prescribed for rapid recovery.

Infectious mononucleosis

Etiology

It is caused by the herpes virus type 4 (Epstein-Barr virus, VEB). Most often affects children.

Anatomic Pathology

The Epstein-Barr virus causes pronounced changes in the oropharynx. The palatine tonsils and the back of the pharynx become brightly hyperemic and swollen. Their surface is covered with dense fibrinous plaques. Lymphoid granules increase along the posterior pharyngeal wall.

Clinical Manifestations

As in other infectious diseases, infectious mononucleosis manifests itself with an increase in body temperature to febrile values, up to 41 °C. Against the background of hyperthermia there is a headache, severe fatigue, which persists for up to a month. Local changes in the oropharynx are accompanied by pronounced pain in the throat and difficulty swallowing. Increase symmetrically different groups of lymph nodes, more often cervical localization, moderately painful. Hepatosplenomegaly is noted , in severe cases with rupture of the spleen capsule. On the part of the hepatobiliary system, transient hypertransaminasemia is observed. In case of incorrect prescription of penicillin antibiotics, a pseudoallergic rash of patchy-papular character appears on the body.

Diagnosis

The diagnosis is established on the basis of a typical clinical picture. The general blood count has characteristic features: initially leukopenia is noted, and then leukocytosis increases. About half of the leukocytes are represented by atypical mononuclear cells. Blood is also tested for the presence of antibodies to VEB.

Treatment

There is no specific treatment for infectious mononucleosis. Symptomatic therapy is prescribed, including anti-inflammatory drugs. In severe cases, the prescription of corticosteroids is justified.

Syphilis

Etiology

The causative agent of this disease is the spirochete pale treponema (Treponema pallidum). The microorganism enters the body by contact through mucous membranes or skin, then penetrates the lymphatic system and spreads throughout the body.

Anatomic Pathology

Syphilis progresses through 3 successive stages, and each stage has specific changes in the oropharynx. The first stage is characterized by the formation of a hard chancre on the palatine tonsil, soft palate, inner cheek or uvula. Initially, this formation is represented by a papule, which then ulcerates. Syphiloma, or hard chancre, is a painless ulcer with a wet surface from which a fluid containing a large number of spirochetes oozes. The bottom of the chancre is varnished, shiny, bright red, dense and painless on palpation. The size can vary from a few millimeters to 1.5 centimeters. When the chancre is located on the tonsil, it changes, becoming bright red, enlarged and dense.

The secondary stage of syphilis in the oropharynx is characterized by matte-pale spots surrounded by a wreath of hyperemia on the bright red mucosa of the soft palate, tonsils, uvula, while the hard palate remains intact. Then the spots change into dark-red papules, which tend to merge, forming the so-called papular sore throat.

In tertiary syphilis, gummas may form in the oropharynx. They are most often found on the soft or hard palate and the back of the pharynx. These formations are dense large nodules located in the thickness of the tissue, which eventually disintegrate. After disintegration through a narrow fistulous passage in the oropharynx, a clear thick content is released into the oropharynx. After healing, dense scars remain, which constrict the surrounding tissue.

Clinical Manifestations

Pathologic changes of the first stage of syphilis develop at the site of primary contact of the treponema with the mucous membrane. In 3-4 weeks after penetration of the pathogen into the body, a hard chancre is formed, through which further infection of others usually occurs. There may be a localized pain in the throat, intensified by swallowing. Increased regional lymph nodes, they are usually painless. Fever is not characteristic. Within 1-3 months, the chancre heals, and there is a long latency period.

After 3-4 months from the appearance of the chancre begins the second stage, which is characterized by persistent fever, weakness, headache, spilt rash on the body of different character, enlarged lymph nodes. There are also local changes in the oropharynx. Then the latent stage occurs again.

Tertiary syphilis develops 3-15 years after the onset of the disease and affects various systems, but it is now extremely rare. When syphilitic gummas form in the oropharynx, complaints of throat discomfort, swallowing disorders, speech changes, and breathing difficulties are noted. The most severe outcome is seen in neurosyphilis, in which the vessels or membranes of the brain, as well as the substance of the brain or spinal cord itself, become inflamed.

Diagnosis

A rapid blood or CSF (cerebrospinal fluid) test for syphilis (serologic reagin test, anticardiolipin test, Wasserman reaction) is used for screening. In this test, antibodies to syphilis that are produced in the patient’s body bind to lipid antigens (bovine cardiolipin). However, this test can produce false positives and is not highly specific. If the reagin test is positive, treponemal tests are performed, which determine the qualitative presence of antibodies in the blood or CSF. Such tests include enzyme immunoassay, passive hemagglutination reaction, microhemagglutination reaction for antibodies, fluorescence analysis for absorption of treponemal antibodies. It should be noted that there is a seronegative window of 3-6 weeks from infection in which syphilis will not be diagnosed by any method.

Treatment

The patient is prescribed benzathine benzylpenicillin systemically for 2 weeks. It is obligatory to treat sexual partners.