Follicular and lacunar sore throat

In terms of their general and local clinical course, follicular and lacunar tonsillitis are, as it were, two phases of a single infectious process.

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What causes lacunar tonsillitis?

Lacunar tonsillitis, unlike catarrhal tonsillitis, which occurs on the basis of adenovirus infection with subsequent activation of saprophytic microbiota, firstly, is much less contagious, and secondly, most often initially caused by streptococcal infection, in particular hemolytic streptococcus (type A) or pathogenic streptococcus (type B, usually of alimentary origin). Often these forms of tonsillitis occur as a result of infection with type D streptococcus (enterococcus, according to the old nomenclature). In rare cases, lacunar tonsillitis can occur as a result of infection with other types of pathogenic microorganisms - pneumococci (in second place after streptococci ), staphylococci, Friedlander's bacillus, infection of which occurs gradually, proceeds more favorably, and the microorganism itself is highly sensitive to antibiotics. Angina caused by Pfeiffer's bacillus is most often observed in children and is often complicated by swelling of the larynx, requiring emergency measures to combat asphyxia, including tracheal intubation or tracheotomy.

Pathological changes in lacunar tonsillitis are more pronounced than in catarrhal tonsillitis, since they are not limited to damage of the mucous membrane and its superficial submucous layers, but also to the parenchyma of the palatine tonsils. Streptococcus primarily attacks the lymphadenoid tissue of the palatine tonsils, but even in tonsillectomy patients it can affect the lateral ridges, lingual and nasopharyngeal tonsils.

In follicular tonsillitis, powerful infiltrates, suppurating follicles, sometimes merging into microabscesses, are formed in the parenchyma of the palatine tonsils. If these abscesses are large, they are called "tonsillar abscesses". The crypt (lacunae) cover undergoes particularly significant changes, the integrity of which is disrupted by the massive release of leukocytes and fibrin through it into the lumen of the lacuna. The latter covers the surface of the lacuna with a fibrinous film, which prolapses from the lacuna onto the surface of the tonsil, giving the disease the form of lacunar tonsillitis. Sometimes these deposits merge with each other, covering most of the surface of the tonsil, sometimes even going beyond it (the so-called confluent lacunar tonsillitis). In special toxic forms of follicular and lacunar tonsillitis, thrombosis of small tonsillar veins is detected.

Symptoms of lacunar tonsillitis

Streptococcal follicular and lacunar tonsillitis can occur in several clinical forms. The typical form is characterized by a rapid onset with the appearance of chills, high body temperature (39-40 ° C), a sharp deterioration in the general condition, pain in the lower back and calf muscles, in children there may be clouding of consciousness, delirium, convulsions, meningism. In the blood, as a rule, leukocytosis is observed - (20-25) x 10 ⁹ /l with a shift in the leukocyte formula to the left, young forms and toxic granularity of leukocytes, high ESR (40-50 mm / h).

In the pharynx, there is a sharp hyperemia and infiltration of the pharynx, swelling of the palatine tonsils. In follicular tonsillitis, small yellowish-white bubbles are found on their surface - follicles affected by infection, reminiscent, in the words of B.S. Preobrazhensky, of a picture of the "starry sky". These bubbles, merging with each other, form a grayish-whitish fibrinous plaque, easily removed with a cotton swab from the surface of the tonsils.

In lacunar tonsillitis, grayish-whitish or yellowish plaques are observed in the depths and along the edges of the crypts, which, increasing and spreading over the surface of the tonsil, merge with each other, forming a purulent-caseous cover over the entire surface of the tonsil. As B.S. Preobrazhensky (1954) notes, the division of tonsillitis into follicular and lacunar tonsillitis, based only on a visual assessment of the pathological picture of the visible part of the tonsil, has no practical significance. Sometimes a picture of lacunar tonsillitis is observed on one tonsil, and follicular tonsillitis on the other. In some cases, upon careful examination of the surface of the tonsil, not completely covered with lacunar plaque, elements of follicular tonsillitis can be detected. We consider follicular and lacunar tonsillitis as a single systemic disease, manifested to varying degrees in superficially located follicles and deep-lying lacunae. In follicular and lacunar tonsillitis, regional lymph nodes are enlarged and sharply painful.

A severe form of lacunar tonsillitis is characterized by a sudden onset, a lightning-fast increase in the symptoms described above, the severity of which exceeds those in the typical course of tonsillitis. In this form of tonsillitis, the defeat of the follicles both on the surface of the tonsil and in the depth of the lacunae is of a mass nature, as a result of which the resulting grayish-yellow plaque quickly, by the 2nd day of the disease, covers the entire surface of the tonsil and goes beyond it. The soft palate and uvula are sharply hyperemic and edematous to such an extent that they hang down into the laryngopharynx, creating obstacles to food intake and phonation. Profuse salivation appears, but swallowing movements are rare due to sharp pains in the throat, as a result of which saliva spontaneously flows out of the oral cavity (in the soporous state of the patient) or the patient wipes it with a towel.

The general condition of the patient suffers sharply. At the height of the disease, he often falls into oblivion, delirium, and in children, involuntary movements in the limbs, convulsions, often phenomena of opisthotonus and meningism occur. The heart sounds are muffled, the pulse is thready, rapid, breathing is rapid, shallow, the lips, hands and feet are cyanotic, there is protein in the urine. During this period, patients complain of severe headache, nausea, spontaneous pain along the spine, soreness of the eyeballs when they move and when pressed. It is these forms of angina that give the most serious local and distant complications.

In the absence of the latter, the entire cycle of the clinical course of the disease lasts on average about 10 days, but protracted and recurrent forms are often observed, in which the disease acquires a torpid character. These forms are most often observed with insufficiently timely and ineffective treatment, as well as with high virulence of the microbiota, its high resistance to the antibiotics used, and weakened immunity.

Lacunar tonsillitis in a mild form is much less common and is characterized by the erasure of symptoms, a shortened clinical period of the disease, and significant effectiveness of the treatment applied. Probably, the precedent of the presence of such a form should be used scientifically to clarify the causes that caused it and use them to increase the body's resistance to infection and the effectiveness of therapeutic measures.