Acute inflammatory disorders of the pharynx are pathological conditions caused by the activation of pathogens on the pharyngeal mucosa. These disorders present with a combination of local and systemic symptoms that may significantly impact overall well-being.

The primary conditions classified under this category include:

• Acute tonsillitis — inflammation of the palatine tonsils.
• Acute pharyngitis — inflammation of the pharyngeal mucosa.

Classification

• Acute Tonsillitis:
  • Catarrhal
  • Lacunar
  • Follicular
• Atypical Forms of Acute Tonsillitis:
  • Herpangina
  • Intratonsillar abscess
  • Necrotizing ulcerative tonsillitis (Vincent’s angina)
  • Fungal tonsillitis
• Specific Forms of Acute Tonsillitis:
  • Associated with diphtheria
  • Associated with measles
  • Associated with scarlet fever
  • Associated with infectious mononucleosis
  • Associated with syphilis
• Acute Tonsillitis in Blood Disorders:
  • Associated with leukemia
  • Associated with agranulocytosis
• Acute Catarrhal Pharyngitis

Acute Tonsillitis

Etiology

Acute tonsillitis is predominantly caused by bacteria, with group A β-hemolytic streptococcus (Streptococcus pyogenes; GABHS) accounting for approximately 80 % of cases. Other bacterial pathogens may include various species of Streptococcus, Staphylococcus, Pneumococcus, Enterococcus, and Haemophilus influenzae.

The condition may also result from viral infections, particularly those caused by adenoviruses and herpesviruses. In individuals with compromised local immunity, inflammation may be triggered by opportunistic microorganisms of the oral cavity, such as Streptococcus viridans, Leptothrix, fusobacteria, and fungi. These are microorganisms that do not typically cause diseases in healthy individuals but can act as pathogens under certain circumstances.

Anatomic Pathology

Acute inflammation of the palatine tonsils is typically characterized by swelling and redness, which often extend to the adjacent structures, including the uvula, the soft palate, and the posterior pharyngeal wall. The tongue is usually coated with a white film. These features are characteristic of catarrhal tonsillitis.

In follicular tonsillitis, in addition to the above-mentioned signs, small white or yellowish spots resembling millet seeds appear within the tonsillar follicles, forming a distinctive clinical pattern.

Lacunar tonsillitis, by contrast, is marked by extensive patches of exudate covering the inflamed and swollen tonsils. This exudate originates from the lacunae (crypts) and, in some cases, may merge to form larger deposits. These plaques represent microabscesses within the tonsillar parenchyma.

Clinical Manifestations

Acute tonsillitis is characterized by a sudden onset of symptoms. Patients typically experience a severe sore throat, which intensifies when swallowing and may radiate to the ear or neck. As the palatine tonsils become swollen and tender, patients may experience difficulty opening their mouth. Other common symptoms include nasal speech and halitosis (bad breath). A distinctive feature is tonsillar exudates, which can be easily removed with a spatula without causing bleeding.

Systemic symptoms are also prominent and include high-grade fever (38–40 °C), chills, headache, and significantly enlarged regional lymph nodes that are generally tender.

The disease typically lasts 5–7 days. However, complications are fairly common and can be classified as local or systemic. Local complications include peritonsillitis, peritonsillar abscess, and cervical lymphadenitis. Systemic complications may involve rheumatic fever, glomerulonephritis, arthritis, or even sepsis.

Diagnosis

The diagnosis of acute tonsillitis is primarily based on its characteristic clinical presentation and pharyngoscopy findings. To confirm the diagnosis and identify the causative pathogen, laboratory tests are often performed. These may include:

• Complete blood count (CBC);
• C-reactive protein (CRP) and rheumatoid factor;
• Urinalysis;
• Bacteriological examination of tonsillar exudate;
• Rapid streptococcal antigen test (rapid strep test, RST) for quick detection of group A β-hemolytic streptococcus (GABHS).

Treatment

The standard treatment for acute tonsillitis involves a 10-day course of penicillin antibiotics. For patients with penicillin allergies, cephalosporins or macrolides serve as effective alternatives.

Symptomatic management focuses on relieving pain and fever with nonsteroidal anti-inflammatory drugs (NSAIDs). Additionally, local therapy includes gargling with antiseptic solutions to reduce inflammation and lower the risk of secondary infections.

To facilitate recovery, patients are advised to follow a high-calorie, soft diet that minimizes throat irritation. Bed rest during the acute phase is also recommended.

Atypical Forms of Acute Tonsillitis

Herpangina

Etiology

Herpangina is primarily observed in children and is caused by Coxsackie viruses, retroviruses, echoviruses, and adenoviruses. The condition gets its name from the vesicular eruptions that resemble herpes simplex virus (HSV) lesions, although it is not related to HSV.

Anatomic Pathology

The hallmark of herpangina is the appearance of small vesicles on the soft palate and palatine arches against a background of pharyngeal erythema. The palatine tonsils may be mildly hyperemic and swollen. In some cases, whitish vesicles may also be present.

Clinical Manifestations

Unlike other pharyngeal infections, herpangina is primarily characterized by systemic symptoms rather than local manifestations. Patients typically present with high-grade fever, severe headache, and muscle pain. Despite its pronounced symptoms, the disease is self-limiting and usually resolves within 3–4 days.

Diagnosis

Diagnosis is based on clinical manifestation, as herpangina has distinct features. However, in some cases, laboratory tests may be used for confirmation. These include:

• Serological testing for IgM antibodies to detect a viral infection;
• Polymerase chain reaction (PCR) testing of a throat swab to identify viral RNA;
• Complete blood count (CBC) to assess the inflammatory response;
• C-reactive protein (CRP) to evaluate systemic involvement.

Treatment

There is no specific antiviral therapy for herpangina, so treatment focuses on symptom relief. Antipyretics are used to reduce fever, while regular rinsing with antiseptic solutions helps alleviate discomfort and prevent secondary infections.

Intratonsillar Abscess

Etiology

The pathogens causing intratonsillar abscess are similar to those responsible for nonspecific acute tonsillitis. The most common causative agent is group A β-hemolytic streptococcus (GABHS).

Anatomic Pathology

Intratonsillar abscess develops as a complication of classic acute tonsillitis. This condition is characterized by purulent destruction (liquefaction) of tissue within the palatine tonsil. It is usually unilateral, with the affected tonsil appearing infiltrated, hyperemic, tense, and bulging. A central purulent focus forms within the tonsillar parenchyma, and in some cases, pus may spontaneously drain through the tonsillar crypts. The surrounding oropharyngeal tissues are markedly inflamed, leading to oropharyngeal asymmetry. Additionally, the regional lymph nodes on the affected side become significantly enlarged and tender.

Clinical Manifestations

A distinctive feature of intratonsillar abscess is the second fever spike, which occurs 3–4 days after the illness onset. The body temperature surges rapidly to 39–41°C, accompanied by severe throat pain that worsens while swallowing, speaking, or moving the tongue. Other symptoms include foul breath (halitosis), excessive salivation, difficulty swallowing, and impaired speech. Many patients also experience difficulty opening their mouth.

Diagnosis

The diagnostic approach is similar to that of typical tonsillitis. For both therapeutic and diagnostic purposes, aspiration of the affected tonsil may be performed to evacuate pus and confirm the presence of an abscess.

Treatment

The primary treatment involves surgical incision and drainage of the abscess, followed by regular wound examination over the next several days.

Conservative therapy includes a 10-day course of penicillin antibiotics. In cases of penicillin allergy, cephalosporins or macrolides are used as alternatives. To control symptoms, nonsteroidal anti-inflammatory drugs (NSAIDs) are prescribed, and antiseptic gargles are recommended to reduce inflammation and prevent secondary infection.

Necrotizing Ulcerative Tonsillitis (Vincent’s Angina)

Etiology

Necrotizing ulcerative tonsillitis, also known as Vincent's angina or Simanovsky–Plaut–Vincent angina, is a rare form of tonsillitis caused by a mixed infection involving fusobacteria and spirochetes.

Anatomic Pathology

The condition is typically unilateral, with a deep necrotic lesion at the superior pole of one of the palatine tonsils. The affected area is covered with a whitish exudate that can be easily removed. In some cases, the necrotic process may extend to the soft palate, cheek, and gums.

Clinical Manifestations

Unlike other forms of tonsillitis, Vincent’s angina is notable for its mild systemic symptoms. Fever is not typical, setting it apart from more common bacterial infections. Patients may experience mild discomfort or localized throat pain on the affected side, often accompanied by foul breath. Additionally, the regional lymph nodes along the sternocleidomastoid muscle tend to be enlarged and tender.

Diagnosis

The diagnosis is based on characteristic clinical presentation and pharyngoscopy findings. To confirm the causative agents and guide the decision-making process regarding medical treatment, a throat swab culture is performed, including antibiotic susceptibility testing.

Treatment

The standard treatment includes a 7–10-day course of penicillins or cephalosporins. In addition, regular antiseptic rinses of the oral mucosa are recommended.

Fungal Tonsillitis

Etiology

Fungal tonsillitis, also known as tonsillomycosis, is caused by yeasts of the Candida genus, most commonly Candida albicans. Less frequently, other species such as C. tropicalis, C. krusei, and C. glabrata may be involved. In rare cases, molds like Geotrichum, Aspergillus, and Penicillium can act as causative agents.

Anatomic Pathology

The acute phase of tonsillomycosis is characterized by white or grayish curd-like plaques covering enlarged and hyperemic palatine tonsils. These plaques often extend to the oral mucosa. When removed, they expose intensely red, glossy areas that may bleed.

Clinical Manifestations

Fungal tonsillitis primarily presents with local symptoms such as itching, burning, dryness in the mouth, and an unpleasant odor. Pain, if present, is usually mild to moderate and most noticeable when eating. Unlike bacterial or viral tonsillitis, fungal infections tend to become chronic.

The condition is most frequently observed in young children, the elderly, and individuals with weakened immune systems. Those at higher risk include patients receiving long-term antibiotic or corticosteroid therapy (including topical and inhaled forms), individuals with diabetes mellitus, oncology patients undergoing chemotherapy, and HIV-positive individuals.

Diagnosis

A definitive diagnosis is established through microbiological culture of oral mucosal samples, which allows for identification of the fungal pathogen.

Treatment

The standard treatment for fungal tonsillitis is topical antifungal therapy.

Specific Forms of Acute Tonsillitis

Acute Tonsillitis Associated with Diphtheria

Etiology

Diphtheria is a highly contagious bacterial infection with significant morbidity and mortality. It is caused by Corynebacterium diphtheriae (Klebs-Löffler bacillus), a gram-positive bacterium.

Anatomic Pathology

Once Corynebacterium diphtheriae enters the body, it induces localized changes in the oropharyngeal mucosa and exerts systemic effects through a diphtheria exotoxin. The disease progresses in stages, with varying degrees of tissue involvement.

Initially, the infection affects the palatine tonsils, where firm, grayish-white fibrinous membranes form on their surface. As the process advances, the membranes may spread to the uvula, palatine arches, and soft palate. In the oropharynx, these membranes are tightly adherent and difficult to remove, leaving a bleeding, inflamed surface beneath.

In more severe cases, the infection may spread beyond the oropharynx, affecting the larynx, trachea, and bronchi. Unlike in the oropharynx, the membranes in the larynx detach easily into the airway, increasing the risk of life-threatening asphyxiation.

The tonsils appear erythematous and significantly swollen due to inflammatory infiltration. Significant enlargement of regional lymph nodes is also observed.

If the exotoxin enters the bloodstream, it may cause damage to the heart, peripheral nervous system, and kidneys.

Clinical Manifestations

Diphtheria typically presents with a high fever (39–40 °C), tachycardia, profuse sweating, and headache. Patients experience severe throat pain, which worsens while swallowing, often accompanied by halitosis and the characteristic diphtheritic plaques. Severe cervical lymphadenopathy leads to pronounced neck swelling, commonly referred to as a “bull neck”.

Diagnosis

The diagnosis is primarily clinical, based on characteristic pharyngoscopy findings. Laboratory tests help confirm the diagnosis and assess the severity of systemic involvement. These include:

• Complete blood count (CBC) to evaluate leukocyte levels,
• C-reactive protein (CRP) and rheumatoid factor,
• Urinalysis,
• Bacterial culture of a throat swab to confirm Corynebacterium diphtheriae,
• Rapid streptococcal antigen test (RST) to rule out Group A Streptococcus.

Treatment

Diphtheria requires immediate hospitalization and urgent administration of a diphtheria antitoxin to neutralize the circulating exotoxin. At the same time, a 7–10-day course of penicillin antibiotics is initiated to eliminate the bacterial infection. In severe cases, systemic corticosteroids may be indicated. Local treatment involves regular gargling with antiseptic solutions.

Vaccination remains the most effective measure in preventing diphtheria and controlling outbreaks.

Acute Tonsillitis Associated with Measles

Etiology

Measles is a highly contagious viral infection with a significant mortality rate. It is caused by a paramyxovirus belonging to the Morbillivirus genus.

Anatomic Pathology

Oropharyngeal inflammation is one of the earliest manifestations of measles. The pharynx becomes intensely erythematous, with large, bright red spots appearing on the soft palate. These spots often merge into a diffuse erythematous whole. As the infection progresses, tonsillar exudates may develop, resembling those seen in lacunar tonsillitis. The oropharyngeal tissues become moderately infiltrated, and the entire Waldeyer’s ring (lymphoepithelial tissue of the pharynx) undergoes noticeable hypertrophy.

A hallmark feature of measles is Koplik spots, also known as Belsky–Filatov–Koplik spots, on the buccal mucosa. These small, white papules with a bright red border appear on the buccal mucosa and measure approximately 2–3 mm in diameter. Unlike other enanthems, they remain discrete, making them a key diagnostic marker.

Clinical Manifestations

Measles typically begins with symptoms of oropharyngeal inflammation, conjunctivitis, and rhinitis, followed by a sudden high fever (39–40 °C), body aches, photophobia, and general malaise.

On the fourth or fifth day from the onset of symptoms, a characteristic maculopapular rash appears. This rash spreads in a descending pattern:

• Day 1: Begins on the face and neck.
• Day 2: Extends to the trunk.
• Day 3: Reaches the extremities

As the rash fades, it undergoes pigmentary changes in the same order.

Enlargement of lymphoid tissue in the pharynx increases the risk of complications such as otitis media and sinusitis.

Diagnosis

The diagnosis of measles is confirmed through serological testing, which detects measles-specific IgM antibodies in blood and saliva. These antibodies typically appear within 72 hours to 4 days after the symptom onset. Additionally, PCR testing of oropharyngeal swabs can confirm measles virus RNA, providing a definitive diagnosis.

Treatment

There is no specific antiviral therapy for measles; treatment is primarily symptomatic.

Vaccination is the most effective way to prevent measles, which significantly reduces its morbidity and mortality.

Acute Tonsillitis Associated with Scarlet Fever

Etiology

Scarlet fever is an infectious disease caused by Group A β-hemolytic Streptococcus (GABHS).

Anatomic Pathology

Tonsillitis in scarlet fever presents with classic signs of inflammation, including pronounced swelling and erythema of the palatine tonsils. The tonsillar exudate varies in severity, ranging from follicular deposits to extensive membranous coatings. In severe cases, ulceration of the mucosa may occur.

In addition to these typical changes, scarlet fever presents with distinctive features unique to the disease. A sharply demarcated pharyngeal erythema is observed, usually ending at the hard palate. The tongue is initially coated with a thick white layer, which disappears within 2–3 days, revealing a bright red, glossy surface with enlarged papillae, a hallmark known as the “strawberry tongue”.

Clinical Manifestations

Scarlet fever is characterized by systemic intoxication, a high fever (38–40 °C), and enlargement of regional lymph nodes. Some patients may also experience nausea, vomiting, and diarrhea.

A fine, punctate rash develops against a background of generalized skin erythema. It spreads in a descending pattern, starting from the upper body and progressing downward. The rash tends to merge into one big spot and intensify in natural skin folds (elbows, knees, and groin), a phenomenon known as Pastia’s lines. A distinctive diagnostic feature is the unaffected perioral (nasolabial) triangle, which remains pale against the flushed red face (Filatov’s sign).

During recovery, the exudative pharyngeal changes and rash gradually resolve. However, sheet-like desquamation of the skin on the palms and soles appears as a characteristic sign of convalescence.

Diagnosis

The diagnosis is based on clinical presentation, patient history, and epidemiological data. Laboratory confirmation includes microbiological culture of a throat swab to identify the pathogen and determine its antibiotic susceptibility. A rapid strep test may also be used for quick diagnosis.

Treatment

The primary treatment for scarlet fever is a 7–10-day course of systemic penicillin antibiotics. Proper oral hygiene is essential, and regular gargling with antiseptic solutions is recommended. Patients are advised to rest and follow a high-calorie diet to support recovery.

Acute Tonsillitis Associated with Infectious Mononucleosis

Etiology

Infectious mononucleosis is caused by the Epstein-Barr virus (EBV), also known as human herpesvirus 4. It predominantly affects children and young adults.

Anatomic Pathology

EBV induces significant changes in the oropharynx. The palatine tonsils and posterior pharyngeal wall become markedly erythematous and swollen. Their surfaces are covered with dense fibrinous exudates. Additionally, lymphoid follicles on the posterior pharyngeal wall become hypertrophic, forming prominent granules.

Clinical Manifestations

The disease typically begins with a high fever, reaching up to 41°C, accompanied by a headache and profound fatigue, which can persist for weeks. Severe sore throat and painful swallowing develop due to a pronounced oropharyngeal inflammation.

One of the hallmark features is symmetrical lymphadenopathy, primarily affecting the cervical lymph nodes. The nodes are enlarged but moderately tender. Other systemic signs include hepatosplenomegaly. In severe cases, splenic rupture may occur. The hepatobiliary system is also affected, leading to transient elevations in liver transaminases.

A distinctive feature of EBV infection is a maculopapular rash when penicillin-class antibiotics are mistakenly prescribed. This rash is not allergic but represents a pseudoallergic reaction.

Diagnosis

The diagnosis is primarily clinical, supported by laboratory findings. A complete blood count (CBC) reveals a characteristic shift: initial leukopenia, followed by progressive leukocytosis. Atypical mononuclear cells (mononuclears) can account for as much as 50 % of the total leukocyte count.

Serological tests confirm the presence of EBV-specific antibodies in the blood.

Treatment

There is no specific antiviral therapy for infectious mononucleosis. Treatment is symptomatic, including anti-inflammatory agents and supportive care. In severe cases, corticosteroids may be indicated.

Acute Tonsillitis Associated with Syphilis

Etiology

Syphilis is caused by the spirochete Treponema pallidum. The microorganism enters the body through direct contact with mucous membranes or skin, subsequently spreading via the lymphatic system to multiple organs.

Anatomic Pathology

Syphilis progresses through three distinct stages, each characterized by specific changes in the oropharynx.

1. Primary syphilis is marked by the formation of a chancre on the palatine tonsil, soft palate, inner cheek surface, or uvula. Initially, it appears as a papule, which then ulcerates. The chancre is a painless ulcer with a moist surface, exuding a fluid rich in spirochetes. The base of the chancre is lacquered, shiny, and bright red, while palpation reveals a firm, indurated, and non-tender lesion. Its size may vary from a few millimeters to 1.5 cm. When located on the tonsil, it leads to unilateral tonsillar enlargement, induration, and intense erythema.
2. Secondary syphilis affects the oropharynx with dull, pale spots surrounded by an erythematous halo. These spots primarily appear on the soft palate, tonsils, and uvula, while the hard palate remains unaffected. The lesions later evolve into dark-red papules, which may coalesce into one, giving rise to a condition known as syphilitic tonsillitis.
3. Tertiary syphilis can lead to the formation of gummas in the oropharynx, typically found on the soft or hard palate and posterior pharyngeal wall. Gummas appear as dense, large nodules within the tissue, which subsequently break down, discharging a thick, clear exudate through a narrow fistulous tract. The healing process results in fibrotic scarring, which may distort surrounding structures.

Clinical Manifestations

Primary syphilis lesions develop at the site of initial T. pallidum contact. Approximately 3–4 weeks after infection, a chancre forms, serving as the primary source of further transmission. Mild localized throat pain may be present that worsens while swallowing. Regional lymph nodes enlarge but remain painless. Fever is generally absent. The chancre spontaneously heals within 1–3 months, leading to a prolonged latent phase.

Secondary syphilis emerges 3–4 months after the chancre appears. This stage is characterized by persistent fever, fatigue, headaches, generalized lymphadenopathy, and a polymorphic rash. Oropharyngeal involvement includes syphilitic tonsillitis, as described above. Another latent period follows.

Tertiary syphilis, developing 3–15 years after initial infection, is now extremely rare. It can affect multiple systems, including the bones, cardiovascular system, and central nervous system (neurosyphilis). Neurosyphilis presents with vascular inflammation, meningeal involvement, and degeneration of brain or spinal cord tissue, often leading to severe neurological impairment.

Diagnosis

Screening involves rapid serological testing of blood or cerebrospinal fluid (CSF) using non-treponemal tests such as the rapid plasma reagin (RPR) test, venereal disease research laboratory (VDRL) test, and Wassermann reaction. These detect antibodies that react with cardiolipin, a lipid antigen derived from bovine heart tissue. However, false-positive results can occur, necessitating confirmatory treponemal tests.

Treponemal tests detect specific anti-T. pallidum antibodies in blood or CSF. These include:

• Enzyme-linked immunosorbent assay (ELISA)
• Treponema pallidum hemagglutination assay (TPHA)
• Microhemagglutination assay for Treponema pallidum antibodies (MHA-TP)
• Fluorescent treponemal antibody-absorption (FTA-ABS) test
• It is important to note the seronegative window, a period of 3–6 weeks post-infection when no diagnostic method is able to detect syphilis.

Treatment

Patients receive benzathine benzylpenicillin as systemic therapy for 2 weeks. Partner treatment is mandatory to prevent reinfection and further disease transmission.

Acute Tonsillitis in Blood Disorders

Acute Tonsillitis Associated with Leukemia

Etiology

Leukemia is a malignant blood disorder characterized by the production of immature or atypical blood cells. Tonsillitis in leukemia is not an isolated disease but rather an early manifestation of the underlying hematologic malignancy. It is more frequently observed in acute leukemia (commonly affecting younger individuals) but can also occur in chronic leukemia (more typical in elderly patients).

In leukemia, a bone marrow dysfunction disrupts the production of immune cells, leading to the release of immature, undifferentiated cells called blasts into the bloodstream. These cells are unable to provide proper immune defense, and even minor mucosal injuries may become an entry point for opportunistic infections.

Anatomic Pathology

Severe immunosuppression in leukemia patients allows for rapid proliferation of pathogenic microflora in the oropharynx. The tonsils become inflamed, with the infection progressing through all stages (catarrhal, lacunar, follicular), ultimately leading to necrotic changes. The tonsils appear hypertrophic, deeply infiltrated, and covered with a dense fibrinous exudate that is difficult to remove. In advanced cases, necrosis extends beyond the tonsils, affecting the gingival mucosa and soft palate.

Clinical Manifestations

The initial symptoms of leukemia are often non-specific, including fatigue, low-grade fever, and generalized body aches. A hemorrhagic syndrome frequently develops, characterized by:

• Petechial rash on the skin and mucous membranes
• Epistaxis (nosebleeds)
• Prolonged bleeding from minor wounds, posing a life-threatening risk

Oropharyngeal changes appear within 3–5 days after the disease onset. Tonsillitis progresses rapidly, often culminating in necrotizing ulcerative tonsillitis. Patients experience severe throat pain, which intensifies while swallowing and may radiate to the ear. The necrotic involvement of the tonsils is often accompanied by high-grade fever (39–40 °C), sweating, and chills. Regional lymph nodes become enlarged, and in some cases, generalized lymphadenopathy is observed, along with hepatosplenomegaly. In necrotic forms, a foul-smelling breath develops, and the patient's overall condition rapidly deteriorates. In the most severe cases, the disease follows a malignant course, leading to sepsis and multi-organ failure, which can be fatal if not treated promptly.

Diagnosis

Initial evaluation includes a general examination and oropharyngoscopy. While oropharyngoscopy may reveal characteristic necrotic tonsillar changes, diagnosing leukemia based on clinical presentation alone is challenging. A complete blood count (CBC) is essential and typically shows:

• Profound pancytopenia (reduction of all blood cell lines) except for leukocytes
• Marked leukocytosis, with an excessive number of immature blast cells
• In leukopenic forms, a significant decrease in total leukocyte count

A bone marrow biopsy is the definitive diagnostic tool, confirming the presence of malignant blast cells and suppression of normal hematopoiesis. Consultation with an oncologist-hematologist is required for further evaluation.

Treatment

Empiric broad-spectrum antibiotic therapy is initiated early to prevent severe infectious complications. Specific leukemia treatment is managed by oncologist-hematologists and includes chemotherapy, radiation therapy, and bone marrow transplantation. Blood transfusions are administered to compensate for deficiencies in blood cell components.

Acute Tonsillitis Associated with Agranulocytosis

Etiology

Agranulocytosis is not an independent diagnosis but rather a clinical and hematological syndrome characterized by a critical reduction in white blood cells called neutrophils (< 0.5 × 10⁹/L), which may reach complete absence. It is more commonly observed in women over 40.

Depending on the underlying cause, agranulocytosis may be myelotoxic, immune, and autoimmune. The myelotoxic form (such as in acute radiation sickness) develops due to exposure to ionizing radiation, cytostatic drugs, or certain medications (e.g., chloramphenicol, streptomycin, gentamicin, penicillin). Immune agranulocytosis may result from drug interactions (e.g., sulfonamides, NSAIDs, medications for diabetes and tuberculosis) or from infectious diseases such as influenza, infectious mononucleosis, poliomyelitis, and viral hepatitis. Autoimmune agranulocytosis is associated with autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus, and autoimmune thyroiditis.

Regardless of its cause, agranulocytosis leads to profound immune suppression, leaving patients highly vulnerable to infections. Even minor mucosal injuries or exposure to pathogens can trigger serious, rapidly progressing infections, particularly in the oropharynx. As a result, acute tonsillitis is one of the most characteristic clinical features of agranulocytosis.

Anatomic Pathology

The myelotoxic form of agranulocytosis develops due to the suppression of bone marrow progenitor cells involved in myelopoiesis, leading to a simultaneous decrease in lymphocytes, reticulocytes, and platelets. In immune agranulocytosis, drug-protein immune complexes mistakenly target and destroy leukocytes. In autoimmune agranulocytosis, the body produces antineutrophil antibodies that attack and eliminate neutrophils.

As neutrophil counts drop to critical levels, even minor trauma to the mucosa allows pathogenic bacteria to penetrate and colonize the tonsillar tissue. This process leads to the rapid development of acute tonsillitis. In milder cases, catarrhal tonsillitis manifests, marked by tonsillar swelling, infiltration, and hyperemia. However, in severe cases, necrotizing ulcerative tonsillitis may develop, progressively damaging the mucosa and deeper tissues, sometimes extending into the bone. As necrotic tissue sloughs off, deep ulcerations form, leaving large, poorly healing defects. Microscopically, necrotic areas are devoid of neutrophils, highlighting the extent of immune suppression.

Clinical Manifestations

The onset of agranulocytosis is typically abrupt and severe. Patients present with high fever (≥ 40 °C), chills, excessive sweating, and generalized body aches. Simultaneously, the oropharynx develops pathological lesions. Throat pain becomes intense and persistent, often accompanied by dysphagia, excessive salivation, and a foul-smelling breath. As a result, many patients refuse to eat. Regional lymph nodes, the liver, and the spleen become enlarged, reflecting systemic involvement. The fever remains prolonged and resistant to conventional antipyretic therapy. As the disease progresses, arthralgia may develop.

In cases of myelotoxic agranulocytosis, a hemorrhagic syndrome often emerges, leading to gingival bleeding, recurrent epistaxis, spontaneous bruising and hematomas, and hematuria. The most life-threatening complications include soft palate perforation, sepsis, and mediastinitis, any of which may prove fatal if not treated promptly.

Diagnosis

A comprehensive medical history is essential, with a particular focus on recent medication use and underlying conditions. A thorough physical examination and pharyngoscopy should be performed.

A complete blood count (CBC) typically reveals severe leukopenia (< 1.0 × 10⁹/L) due to a marked decrease in neutrophils (< 0.5 × 10⁹/L), often with relative lymphocytosis and monocytosis. In myelotoxic agranulocytosis, additional findings include anemia (reduced red blood cell count) and thrombocytopenia (reduced platelet counts).

A bone marrow biopsy is necessary to assess the extent of leukopoiesis suppression. In suspected autoimmune agranulocytosis, serological testing for antineutrophil antibodies is required. All patients should be evaluated by a hematologist to guide further management.

Treatment

The first and most crucial treatment step is to discontinue any medication that could have triggered agranulocytosis immediately. Patients must be admitted to a hematology unit for close monitoring and therapy.

Management strategies include:

• Blood transfusions to correct anemia and thrombocytopenia
• Colony-stimulating factors (CSFs) to stimulate leukopoiesis
• Empiric broad-spectrum antibiotic therapy
• Antifungal therapy due to the high risk of opportunistic fungal infections

Frequent oropharyngeal debridement is necessary, when necrotic tissues are removed and the oropharynx is irrigated with antiseptic solutions.

In immune agranulocytosis, treatment requires high-dose glucocorticoids to suppress abnormal immune activity. If excess immune complexes are present, plasmapheresis may be indicated.

Nutritional support is also critical. A high-calorie diet that includes easy-to-digest foods should be provided, and parenteral nutrition may be required if severe dysphagia prevents oral intake. Strict infection control measures must be implemented to reduce the risk of secondary infections.

Despite intensive treatment, the prognosis remains poor, particularly in severe or complicated cases.

Acute Catarrhal Pharyngitis

Etiology

Acute pharyngitis is most commonly caused by viruses, which account for approximately 70 % of cases. Among viral pathogens, the most frequent culprits include adenoviruses, respiratory syncytial viruses, rhinoviruses, herpes viruses, influenza and parainfluenza viruses, Coxsackie viruses, and coronaviruses.

Bacterial infections are responsible for about 30 % of cases. Among bacterial pathogens, group A beta-hemolytic streptococcus is the most common. Less frequently, the condition may be caused by Streptococcus pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, or Staphylococcus aureus.

In addition to infections, acute pharyngitis can also develop due to non-infectious irritants. Mechanical factors such as throat injuries, burns, exposure to corrosive substances, or allergens can damage the pharyngeal mucosa, leading to inflammation.

Anatomic Pathology

The inflammation results in pronounced hyperemia and swelling of the posterior pharyngeal wall, uvula, and palatine arches. The lymphoid follicles on the posterior pharyngeal wall become enlarged, giving them the appearance of numerous small yellowish nodules. In some cases, a scant amount of mucus may be present on the pharyngeal surface.

Clinical Manifestations

In acute pharyngitis, local symptoms are more prominent than systemic ones. Patients often experience throat dryness, irritation, and a persistent scratchy sensation in the throat, which may trigger a hacking cough. Many describe the discomfort as a sharp throat pain or a foreign body sensation.

General symptoms are usually mild. In some cases, a low-grade fever (37–37.5 °C) may persist for 2–3 days, accompanied by body aches and fatigue. Regional lymph nodes may become slightly enlarged and tender.

A distinctive feature of bacterial pharyngitis is a more prolonged fever, which can last 5–7 days and tends to be higher than in viral infections.

Diagnosis

A clinical examination and pharyngoscopy are the primary diagnostic methods. If a bacterial infection is suspected, further testing is necessary, including a complete blood count (CBC) and microscopic analysis of a throat swab to identify the specific pathogen to rule out streptococcal infection, in particular.

Treatment

For viral pharyngitis, treatment is symptomatic. Patients are advised to gargle with antiseptic solutions and use lozenges with a combination of soothing ingredients to relieve throat irritation.

If a bacterial infection is suspected, systemic broad-spectrum antibiotics are prescribed. In both viral and bacterial cases, anti-inflammatory medications are often recommended to reduce swelling and discomfort.

To relieve throat pain, lozenges containing lidocaine, menthol, or essential oils have been found to be highly effective.

Additional supportive measures include humidifying air in the room, staying well-hydrated, and avoiding irritants such as smoke or strong chemicals.