3 . 4 . 1  -  Acute catarrhal angina (or erythematous angina)

Elles sont le plus souvent d’origine virale, peuvent inaugurer ou accompagner une maladie infectieuse spécifique : oreillons, grippe, rougeole, rubéole, varicelle, poliomyélite…

Enfin, une angine rouge peut constituer le premier signe d’une scarlatine, maladie infectieuse d’origine microbienne. Une température à 40 °C avec vomissements, l’aspect rouge vif du pharynx, des deux amygdales et des bords de la langue, l’absence de catarrhe rhinopharyngé doivent faire rechercher un début de rash scarlatineux aux plis de flexion et pratiquer un frottis amygdalien pour mettre en évidence un streptocoque β-hémolytique A.

Fig 5.

3 . 4 . 2  -  Angina with purulent exudate (or erythemato-pultaceous angina)

These forms often succeed the previous one and are characterized by the presence of bright-red tonsils with purulent exudate: of yellowish gray, with spots or streaks, thin and brittle, easily dissociated, and not exceeding the tonsillar area. Functional symptoms are generally more noticeable. In addition to viruses and GAS angina, the causal agent may be hemolytic streptococcus other than Group A, staphylococcus, pneumococcus, Pasteurella tularensis (tularemia), or Toxoplasma gondii (toxoplasmosis).

Fig 6.

3 . 4 . 3  -  Pseudomembranous angina (or false-membrane angina)

Examination of the pharynx shows false membranes with a pearly sheen that can extend beyond the tonsil region onto the cion (uvula palatinae), soft palate, and its arcus palatini.

It is necessary to think particularly of infectious mononucleosis (Epstein-Barr virus) when angina is prolonged and associated with diffuse adenopathies, splenomegaly, marked asthenia, and purpura of the soft palate. A complete blood count (hyperleukocytosis with hyperbasophilic mononuclear cells) and infectious mononucleosis serology testing confirm the diagnosis.  Treatment is symptomatic.

Diphtheria, formerly a classic etiology, has become rare in France ever since compulsory vaccination. However, one must always keep this etiology in mind when confronted with rapidly extensive pseudomembranous angina, associated with unusual pallor and fatigue. The false membranes are sticky and non-severable. With a growing population of transplant patients, two factors guide the diagnosis, notably the lack of vaccination as well as return visits to an endemic area. Isolation (for 1 month), diphtheria serotherapy (10,000-20,000 U in children; 30,000-50,000 U in adults), and screening for Corynebacterium diphteriae must be implemented immediately in order to avoid malignant forms, previously of very poor prognosis. Antibiotic therapy must be used in combination.

Other possible but rare causes include staphylococcus, streptococcus, pneumococcus, or other mononuclear syndromes (CMV and HIV).

If in doubt, a diphtheria serotherapy and antibiotics are instituted immediately.

Fig 7.

3 . 4 . 4  -  Ulcerative and necrotic angina

Ulceration, usually unilateral, is deeper and covered by a necrotic coating.

Vincent's disease starts develops insidiously in a teenager or young adult in a generally poor state (fatigue, overworked during examination times, etc.)

  • general and functional signs are minor: sub-febrile state, mild unilateral dysphagia, followed by bad breath;
  • examination reveals a grayish-white purulent coating on the tonsil that is crumbly, covering a slow developing ulceration with irregular and raised edges, which is non-indurated to the touch. Lymph node reaction is minimal;
  • throat swab shows a fusospirochetal association. The blood count result is normal;
  • there is often an oral starting point (gingivitis, dental caries, or lower wisdom tooth pericoronitis);
  • evolution is benign in 8-10 days. The main differential diagnosis is tonsil cancer;
  • treatment with penicillin (after having eliminated syphilis) is very efficient and results in a speedy recovery.
Syphilitic chancre sores on the tonsils have a very similar appearance, however:

  • ulceration of the tonsil is unilateral, on a telltale sign induration;
  • adenopathy is more pronounced, with a large central lymph node surrounded by smaller lymph nodes;
  • throat swab samples with ultramicroscopic examination reveal Treponema pallidum.
Moreover, the anamnesis is often delicate. Syphilitic serology testing confirms the diagnosis (initial testing and at Day 15): VDRL is positive 2-3 weeks following chancre, TPHA is positive 10 days after chancre, FTA is positive very early (7 to 8 days) and has excellent specificity, whereas the Nelson test is positive much later at 1 month. HIV serology testing is systematically proposed. Penicillin therapy is the standard treatment, such as Extencillin (2.4 MU at 8-day intervals) or Biclinocillin.

Fig 8.

3 . 4 . 5  -  Vesicular angina

Vesicular angina is characterized by exulceration of the epithelial layer, followed by an elusive vesicular rash on the tonsils and arcus palatini.

Herpes angina is a prime example, which is usually caused by Type 1 Herpes simplex virus:

  • onset is brutal with a temperature of 39-40°C, along with shivering and intensely painful dysphonia;
  • in the first few hours, small clusters of hyaline vesicles are seen on the bright-red tonsils, while later in the course of the disease,  white exudate spots arise surrounded by a red ring, converging into a false membrane of polycyclic contours. This exudate covers the superficial erosions with well-defined edges;
  • labial or nostril herpes is frequently associated;
  • the evolution is benign in 4 to 5 days, without complications or sequelae;
  • treatment is only symptomatic.
Herpes angina has a very similar symptomatology and is caused by Group A coxsackie viruses, occurring mainly in young children. Its evolution is also benign, and treatment is symptomatic.

Fig 9.

3 . 4 . 6  -  Gangrenous, necrotizing angina

This angina, caused by anaerobic germ infections, occurs in patients in a very fragile state: diabetes, kidney failure, and blood diseases. It is mainly of historical interest.