Acute Inflammatory Diseases of Pharynx: Classification, Clinical Manifestations, and Treatment

Acute inflammatory diseases of the pharynx are pathologic conditions that result from the activation of pathogenic microorganisms on the pharyngeal mucosa. They present with both local and systemic symptoms.

These include:

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

Classification of Acute Inflammatory Diseases of Pharynx

1. Acute Tonsillitis (Nonspecific):

• catarrhal form;
• follicular form;
• lacunar form.

2. Acute Tonsillitis Associated With Hematologic Disorders:

• associated with leukemia;
• associated with agranulocytosis.

3. Acute Catarrhal Pharyngitis.

Acute Tonsillitis

Etiology

Pathogenic bacteria are responsible for most cases of acute tonsillitis. Group A β-hemolytic streptococcus (Streptococcus pyogenes; GABHS) accounts for approximately 80% of cases. Other potential bacterial pathogens include streptococci, staphylococci, pneumococci, enterococci, and Haemophilus influenzae. Viral causes include various viruses, particularly adenoviruses and herpesviruses. When local immunity is compromised, opportunistic microorganisms that normally inhabit the oral cavity (Streptococcus viridans, Leptothrix, fusobacteria, and fungi) can also trigger inflammation. These microorganisms do not typically cause disease in healthy individuals but may become pathogenic under certain circumstances.

Anatomic Pathology

Acute inflammation of the palatine tonsils is characterized by swelling and erythema. Similar inflammatory changes can also involve adjacent structures, including the uvula, soft palate, and posterior pharyngeal wall. The tongue is usually coated with a white film. Together, these findings are characteristic of catarrhal tonsillitis.

In follicular tonsillitis, the changes described above are accompanied by small yellowish-white spots resembling millet seeds within the tonsillar follicles.

By contrast, lacunar tonsillitis is characterized by extensive patches of exudate that spread from the lacunae over the erythematous, swollen tonsils. In some cases, these patches may coalesce. These exudates represent microabscesses within the tonsillar parenchyma.

Clinical Manifestations

Acute tonsillitis often begins abruptly. Patients may develop a severe sore throat that worsens with swallowing and can radiate to the ear or neck. As the palatine tonsils become swollen and tender, patients may have difficulty opening the mouth. A nasal quality to the voice and halitosis (bad breath) may also occur. Exudates on the tonsils can be easily removed with a spatula, and the underlying surface does not bleed. Systemic symptoms are also prominent and include fever of 38–40°C, chills, and headache. Regional lymph nodes are enlarged and markedly tender. The illness generally lasts 5–7 days.

Complications, however, are common. Local complications include peritonsillar cellulitis, peritonsillar abscess, and cervical lymphadenitis. Systemic complications may include rheumatic fever, glomerulonephritis, arthritis, sepsis, and endocarditis.

Diagnosis

Diagnosis is based on the characteristic clinical presentation and pharyngoscopic findings. Laboratory evaluation includes a white blood cell count, C-reactive protein and rheumatoid factor testing, and urinalysis. Bacteriologic testing is performed using a throat culture or a rapid streptococcal antigen test (rapid strep test) for GABHS.

If neither a throat culture nor a rapid strep test can be performed, the Centor–McIsaac score can be used to estimate the likelihood of a bacterial infection. A total score of 3 or higher suggests a bacterial etiology, in which case antibiotic therapy is prescribed.

Centor–McIsaac Score

Treatment

The standard treatment for acute bacterial tonsillitis is a 10-day course of a penicillin antibiotic. For patients with a penicillin allergy, cephalosporins or macrolides are used as alternatives. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also prescribed to relieve pain and fever. To support recovery, patients are advised to follow a high-calorie, soft diet that minimizes throat irritation. Bed rest is also recommended.

Acute Tonsillitis Associated with Hematologic Disorders

Acute Tonsillitis Associated with Leukemia

Etiology

Leukemia is a malignant hematologic disorder characterized by the production of immature or atypical blood cells. Tonsillitis in leukemia is not a separate disease but may be one of the presenting manifestations of the underlying hematologic malignancy. It is more often seen in acute leukemia, particularly in younger patients, but may also occur in chronic forms of leukemia, which are more common in older adults.

In leukemia, abnormal hematopoiesis in the bone marrow disrupts normal immune cell production, allowing immature, undifferentiated cells known as blasts to enter the bloodstream. These immature cells are unable to provide an adequate immune defense. As a result, even a minor disruption of the oropharyngeal mucosa can provide an entry point for pathogenic microorganisms and trigger an infectious process.

Anatomy

A marked decline in both local and systemic immunity predisposes the tonsils to pathologic changes. Pathogenic microorganisms can then proliferate unchecked throughout the oropharynx, leading to inflammation of the tonsils. Tonsillitis may progress rapidly through the catarrhal, lacunar, and follicular stages, ultimately leading to necrotic changes in the tonsils. The oropharyngeal mucosa becomes infiltrated, while the palatine tonsils enlarge and become covered with a dense fibrinous exudate that is difficult to remove. As the process advances, necrosis may extend to the gingival mucosa and soft palate.

Clinical presentation

Early manifestations of leukemia may include generalized weakness, low-grade fever, and body aches. A hemorrhagic syndrome is also characteristic, with a widespread petechial rash on the skin and mucous membranes, epistaxis (nosebleeds), and prolonged bleeding from even minor wounds, which can become life-threatening. Oropharyngeal changes usually develop within 3–5 days after disease onset. Tonsillitis may progress through successive stages and eventually culminate in ulcerative-necrotizing tonsillitis. Patients develop severe throat pain that worsens with swallowing and may radiate to the ear. These tonsillar changes are often accompanied by high fever (39–40°C), sweating, and chills. Regional lymph nodes enlarge, and some patients develop generalized lymphadenopathy as well as enlargement of the liver and spleen. Once necrosis develops, foul-smelling breath may appear and the patient’s overall condition can deteriorate rapidly, with the disease taking on a fulminant course. As the process progresses, sepsis and multiorgan failure may develop and can be fatal.

Diagnosis

Initial evaluation includes a general physical examination and oropharyngoscopy. However, leukemia can be difficult to suspect on clinical grounds alone. A complete blood count (CBC) is essential and typically shows reduced levels of the other formed elements of blood, apart from leukocytes. The leukocyte count may increase several-fold because of the large number of immature blast cells. In the leukopenic form, however, the total leukocyte count may be markedly reduced. Bone marrow aspiration is performed to establish the definitive diagnosis. Bone marrow findings in leukemia are characterized by suppression of normal hematopoietic lineages and a large number of blast cells. Consultation with a hematologist-oncologist is recommended.

Treatment

Empiric broad-spectrum antibiotic therapy is started early to reduce the risk of severe infectious complications. Definitive treatment of leukemia is managed by hematologist-oncologists. Specific treatment may include chemotherapy, radiation therapy, and bone marrow transplantation. Transfusion support is provided to correct deficiencies in blood cell components.

Acute Tonsillitis Associated with Agranulocytosis

Etiology

Agranulocytosis is not a disease in its own right but rather a clinical and hematologic syndrome. It is characterized by a marked reduction in neutrophil granulocytes to <0.5 × 10⁹/L, sometimes progressing to their complete absence. The condition is more common in women over 40 years of age.

Depending on the underlying cause, agranulocytosis is classified as myelotoxic, immune, or autoimmune.

• Myelotoxic agranulocytosis (e.g., in acute radiation sickness) may develop after exposure to ionizing radiation, cytotoxic agents, or certain medications, including chloramphenicol, streptomycin, gentamicin, and penicillin.
• Immune agranulocytosis may develop as an immune-mediated reaction to certain medications, including sulfonamides, NSAIDs, and drugs used to treat diabetes or tuberculosis. It may also occur in association with infections such as influenza, infectious mononucleosis, poliomyelitis, and viral hepatitis.
• Autoimmune agranulocytosis is associated with a range of autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus, and autoimmune thyroiditis.

Regardless of the underlying form, infections can develop at sites of tissue injury or exposure to large numbers of pathogenic microorganisms. Acute tonsillitis is one such manifestation. Tonsillar involvement is a characteristic feature of agranulocytosis.

Anatomy

In myelotoxic agranulocytosis, suppression of myeloid progenitor cell production in the bone marrow is accompanied by reductions in lymphocytes, reticulocytes, and platelets.

In immune agranulocytosis, drug–protein complexes can induce the formation of antibodies directed against leukocytes.

In autoimmune agranulocytosis, the body produces antineutrophil antibodies that lead to neutrophil destruction.

As the leukocyte count falls, even minor microbial penetration through damaged tonsillar mucosa can initiate a pathologic process that leads to acute tonsillitis. In mild cases, the process is limited to catarrhal tonsillitis, characterized by infiltration and erythema of the palatine tonsils. In severe disease, however, ulcerative-necrotizing tonsillitis may develop. The mucosa and underlying tissues become involved, and the process can extend as deep as the bone. As the necrotic tissue sloughs away, deep ulcers remain. Microscopically, neutrophils are absent from areas of necrosis.

Clinical presentation

The disease often begins abruptly with high fever of up to 40°C, chills, sweating, and generalized body aches.

At the same time, pathologic changes develop in the oropharynx alongside the systemic symptoms. Patients develop severe throat pain with difficulty swallowing, excessive salivation (hypersalivation), and foul-smelling breath. These symptoms may become severe enough that patients refuse food. Regional lymph nodes enlarge, along with the liver and spleen. The high fever may persist for a prolonged period, with arthralgia developing later in the course of the disease.

Myelotoxic agranulocytosis may also be accompanied by a hemorrhagic syndrome, with gingival bleeding, epistaxis, bruising, hematomas, and hematuria.

Serious complications include soft palate perforation, sepsis, and potentially fatal mediastinitis.

Diagnosis

A thorough medical history should be obtained, with particular attention to the patient’s current medications and any underlying medical conditions.

Evaluation also includes a general physical examination and pharyngoscopy. A complete blood count (CBC) is essential and typically shows leukopenia due to a marked reduction in neutrophils. The total leukocyte count is <1.0 × 10⁹/L, with the neutrophil count falling below 0.5 × 10⁹/L. Relative lymphocytosis and monocytosis may also be present. In myelotoxic agranulocytosis, red blood cell and platelet counts are also reduced. Bone marrow examination is then performed and demonstrates impaired leukopoiesis. If autoimmune agranulocytosis is suspected, blood testing for antineutrophil antibodies is performed. Consultation with a hematologist is required in all cases.

Treatment

The first step is to discontinue all medications that may have contributed to the development of agranulocytosis. Patients are treated in a hematology unit, where management may include transfusion support, agents that stimulate leukopoiesis, broad-spectrum antibiotic therapy, and antifungal treatment.

Regular oropharyngeal debridement is required, with removal of necrotic tissue followed by treatment with antiseptic solutions. In immune-mediated agranulocytosis, high-dose glucocorticoids are administered. If large amounts of circulating immune complexes are present, plasmapheresis is indicated. A high-calorie, soft diet that minimizes irritation is recommended. If oral nutrition is inadequate, parenteral nutrition may be required. Careful prevention of infectious complications is essential throughout treatment. Overall, the prognosis is poor.

Acute Catarrhal Pharyngitis

Etiology

Infectious inflammation of the pharynx is most often viral, accounting for approximately 70% of cases, while bacterial causes account for about 30%.

The most common viral pathogens include:

• adenoviruses;
• respiratory syncytial virus (RSV);
• rhinoviruses;
• herpesviruses;
• influenza and parainfluenza viruses;
• coxsackieviruses and coronaviruses.

Among bacterial pathogens, group A β-hemolytic streptococcus (Streptococcus pyogenes) is the most common. Pneumococci, mycoplasmas, Haemophilus influenzae, and Staphylococcus aureus are identified less frequently.

Noninfectious mechanical factors should also be considered among the causes of acute pharyngitis. These include trauma, burns, and irritation from corrosive substances or allergens.

Anatomic Pathology

Pronounced erythema and edema are seen in the posterior pharyngeal wall, uvula, and palatine arches. Lymphoid follicles on the posterior pharyngeal wall become enlarged and appear as multiple small, yellow, millet seed–like nodules. In some cases, a scant amount of mucous discharge may also be present.

Clinical Manifestations of Acute Catarrhal Pharyngitis

In acute pharyngitis, local symptoms tend to predominate over systemic complaints. Patients often report dryness and a scratchy sensation in the throat, which may trigger a hacking cough. Severe throat pain and a foreign-body sensation may also occur. Systemic symptoms are generally mild. A low-grade fever of 37–37.5°C may persist for 2–3 days, accompanied by body aches and weakness. Regional lymph nodes may become enlarged and moderately tender. A more prolonged fever, lasting up to 5–7 days, is a distinguishing feature of bacterial infection.

Diagnosis

At presentation, patients undergo a general physical examination and pharyngoscopy. To help characterize the inflammation, a complete blood count (CBC) is obtained along with microscopic examination of a swab from the posterior pharyngeal wall. When a bacterial infection is suspected, particularly a streptococcal infection, the swab is examined to identify the causative organism.

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Treatment

For viral pharyngitis, which is the most common form, treatment is symptomatic. Patients are advised to gargle with antiseptic solutions and use combination lozenges.

If a bacterial infection is suspected, systemic broad-spectrum antibiotic therapy is prescribed.

Anti-inflammatory medications are indicated in both viral and bacterial pharyngitis. For throat pain, lozenges containing lidocaine, menthol, or essential oils are commonly used and can provide effective symptomatic relief. Additional supportive measures include humidifying indoor air and maintaining adequate fluid intake.