Follicular and lacunar angina

In its general and local clinical course, the follicular and lacunar angina are, as it were, two phases of a single infectious process.

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What causes lacunar angina?

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

Pathological changes in lacunar angina compared with catarrhal angina are more pronounced, since they are not limited to the lesion of only the mucous membrane and its superficial submucosal layers, but also the parenchyma of the palatine tonsils. Streptococcus primarily attacks the lymphadenoid tissue of the palatine tonsils, but even in tonsillectomized patients it can affect lateral ridges, lingual and nasopharyngeal tonsils.

With follicular angina in the parenchyma of the tonsils, powerful infiltrates are formed, festering follicles, sometimes merging into microabscesses. With a significant amount of these abscesses, they are called "tonsillar abscesses". Particularly significant changes undergo the crypt (lacunae), the violation of the integrity of which is due to the massive release through it into the lacunae of leukocytes and fibrin. The latter covers the surface of the lacuna with a fibrinous film that prolapses from the lacuna to the surface of the amygdala, and gives the disease a form of lacunar angina. Sometimes these raids merge, covering most of the surface of the amygdala, sometimes even leaving it (the so-called draining lacunar angina). With special toxic forms of follicular and lacunar angina, thrombosis of small tonsillar veins is detected.

Symptoms of lacunar angina

Streptococcal follicular and lacunar angina may occur in several clinical forms. A typical form is characterized by a rapid onset with the appearance of chills, high body temperature (39-40 ° C), a sharp deterioration in general condition, low back pain and calf muscles, children may experience confusion, delirium, cramps, and meningism. In the blood, as a rule, leukocytosis is observed (20-25) × ^{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 throat there are sharp hyperemia and infiltration of the pharynx, swelling of the palatine tonsils. With follicular angina, small yellowish-white vesicles appear on their surface-infectious follicles, reminiscent of the image of the "starry sky" in the words of BS Preobrazhensky. These bubbles, merging with each other, form a grayish-whitish fibrinous plaque, easily removed by a cotton bud from the surface of the tonsils.

With lacunar angina, grayish-whitish or yellowish raids are observed in the depth and along the edges of the crypts, which, growing and spreading over the surface of the tonsil, merge with each other, forming a purulent-caseous cover throughout the surface of the amygdala. As B.S. Preobrazhensky (1954) notes, the division of angina into follicular and lacunar angina, based only on a visual assessment of the pathoanatomical picture of the visible part of the amygdala, has no practical significance. Sometimes on one tonsil there is a picture of lacunar angina, on the other - a follicular sore throat. In some cases, careful examination of the surface of the amygdala, not completely covered with lacunar coating, can reveal elements of follicular angina. We consider follicular and lacunar angina as a single systemic disease, manifested in varying degrees in superficially located follicles and deep lacunae in the bowels. With follicular and lacunar angina, the regional lymph nodes are enlarged and sharply painful.

The severe form of lacunar angina is characterized by a sudden onset, a lightening increase in the symptoms described above, the severity of which exceeds those in a typical course of angina. With this form of angina, the lesion of follicles, both on the surface of the tonsil and in the depth of the lacunae, is of a massive nature, as a result of which the resulting grayish-yellow coating quickly covers the entire surface of the amygdala and extends beyond the second day of the disease. The soft palate and tongue are sharply hyperemic and swollen to such an extent that they hang in the larynx, creating obstacles for eating and phonation. There is abundant salivation, however, swallowing movements due to sharp pains in the throat are rare, as a result of which saliva spontaneously expires from the oral cavity (in the patient's co-morbid state) or the patient wipes it with a towel.

The general condition of the patient sharply suffers. At the height of the disease, he often falls into oblivion, raves, and children develop involuntary movements in the limbs, convulsions, often the phenomena of opisthotonus and meningism. Heart sounds are muffled, the pulse is threadlike, frequent, breathing frequent, superficial, lips, hands and feet are cyanotic, in the urine - protein. During this period, patients complain of severe headache, nausea, spontaneous pain along the spine, soreness of the eyeballs during their movement and pressure on them. 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 an average of about 10 days, but often there are protracted and recurrent forms, in which the disease acquires a torpid character. These forms are most often observed with insufficiently timely and ineffective treatment, as well as high virulence of the microbiota, its high resistance to antibiotics used, and weakened immunity.

Lacunar angina in a mild form is much less common and is characterized by a worn out symptom, a shortened clinical period of the disease, a significant effectiveness of the treatment used. Probably, the precedent for the existence of such a form should be used in the scientific plan to elucidate the reasons behind these reasons and use them to increase the body's resistance to infection and the effectiveness of therapeutic measures.