192. Scarlet fever: etiology, pathogenesis, pathological anatomy of the first and second periods, complications, causes of death.

Scarlet fever is an acute infectious disease characterized by intoxication, a typical rash and inflammatory changes, mainly in the throat.

Etiology - B - hemolytic Strept gr. And, children from 3 to 10 years old are more often ill.

The source of the infection is a sick person.

Infection is an airborne pathway.

The pathogenesis of scarlet fever is determined by 3 factors in the relationship between macro- and microorganism: toxic, allergic and septic.

The disease occurs in 2 periods:

1 period - toxic-septic - 1 week.

Period 2 - allergic - 2-3 weeks of illness.

Period 1 is due to the presence of a local inflammatory process at the gates of infection (pharynx, pharynx), from where Strept penetrates lymphogenously, causes regional lymphadenitis, and then spreads hematogenously. Toxemia leads to damage to the central nervous system, internal organs, and skin. There is an immune restructuring with the production of a /m.

Period 2 is optional. It is associated with autoimmune processes. It is characterized by allergic processes in the skin, joints, kidneys, blood vessels, and heart.

According to the degree of severity, they are distinguished - light, medium, and heavy.

According to the localization of the local focus - scarlet fever of the throat and tonsils (buccal form), - wounds and genitals (extrabuccal form)

Pat anatomy.

The local focus of scarlet fever is called the primary scarlet fever affect, and in combination with regional lymphadenitis - the primary complex. The most common localization is the pharynx and tonsils. The mucous membrane is full-blooded, red (“flaming throat” and “crimson tongue”). The tonsils are bright red, juicy, enlarged - catarrhal angina develops, then necrotic, which in severe cases turns into fibrinous necrotic. Depending on the severity of the disease, necrosis can spread to the soft palate, pharynx, and middle ear. Cervical l/u are enlarged, full-blooded, with foci of necrosis.

General changes are associated with toxemia and are manifested by the formation of a small-point rash on hyperemic skin. The rash appears in the first

two days of illness and covers the entire surface of the body with the exception of the nasolabial triangle.

Microscopically, perivascular lymphohistiocytic infiltrates, vascular fullness, edema, and exudation are detected in the skin. In the surface layers of the epithelium - dystrophy, necrosis, parakeratosis (incomplete keratinization). After 3-4 weeks, the rash disappears and lamellar peeling develops in the form of rejection of the stratum corneum, especially where the stratum corneum is thick (palms).

Dystrophy and lymphohistiocytic infiltration are detected in internal organs (liver, kidneys, myocardium), and follicle hyperplasia in hematopoiesis organs.

There are toxic, septic, toxic-septic forms of the disease.

1. With a toxic form, toxicosis is pronounced, even hypertoxic forms are isolated (death on 1-2 days). Signs of toxicosis - agitation, depression, vomiting, drop in blood pressure, hyperthermia, rash.

2. With septic form, purulent complications prevail. Death is possible due to erosive bleeding from large vessels with neck phlegmon.

3. Toxic-septic form - complications of a mixed nature.

Complications of the 1st period are of a toxic and purulent nature.

- pharyngeal abscess,

- otitis media,

- osteomyelitis of the temporal bone,

- lymphadenitis,

- phlegmon of the neck,

- brain abscess,

- purulent meningitis.

The occurrence of period 2 cannot be foreseen, because it occurs regardless of the severity of period 1. At 2-3 weeks of illness, after a light interval, signs of a return of the disease appear: local and general changes without rash.

Complications of the 2nd period are allergic:

- acute or chronic glomerulonephritis,

- arthritis,

- warty endocarditis,

- vasculitis.

Death: previously from 1) toxemia 2) septic complications.

193. Meningococcal infection: forms, pathogenesis, morphological characteristics, complications, causes of death.

Meningococcal infection is an acute infectious disease characterized by damage to the mucous membrane of the nasopharynx, the membranes of the brain and septicemia; anthroponosis.

The causative agent of meningococcal infection is the gram-positive diplococcus Neisseria meningitidis. Meningococci are highly sensitive to various environmental factors and die outside the human body within 30 minutes. The range of clinical forms of meningococcal infection is very wide. There are localized forms of meningococcal infection (meningococcal carrier and acute nasopharyngitis) and generalized (meningococcemia, meningitis, meningoencephalitis, mixed forms).

Only people suffer from meningococcal infection. The source of infection is a patient or a bacterial carrier.

The transmission mechanism is airborne. Since meningococcus is unstable in the external environment, infection occurs more often with prolonged human contact, in cramped, poorly ventilated rooms, and in public places. Meningococcal infection occurs at any age, but children of the first three years of life are most often ill.

The entrance gates of infection are the mucous membranes of the nasopharynx and oropharynx. In most cases, no pathological changes occur at the site of meningococcal injection, and asymptomatic carriage develops. In 10-15% of cases, inflammation occurs in the area of the entrance gate (meningococcal nasopharyngitis). Recovery in meningococcal nasopharyngitis usually occurs 5-7 days after the onset of the disease, however, nasopharyngitis may precede the development of generalized forms. Only in 1-2% of cases, meningococcus enters the bloodstream and causes the development of meningococcal meningitis, or meningoencephalitis, or meningococcal sepsis (meningococcemia). In some cases, meningococcal sepsis occurs as a lightning-fast form, leading to death 12-24 hours after the onset of the disease. Clinical manifestations in generalized infection are mainly determined by the action of endotoxin, which leads to the development of DIC syndrome and endotoxic shock. The reasons for the significant variability in the course of the disease remain unclear.

Pathomorphology. Nasopharyngitis is characterized by catarrhal inflammation with pronounced hyperemia and hyperplasia of the lymphoid apparatus of the posterior pharyngeal wall. Usually the inflammation is serous or purulent in nature, only in rare cases fibrinous-purulent inflammation is observed. This form of meningococcal infection has no specific signs.

Meningococcemia (meningococcal sepsis) It is characterized by an acute onset and rapid development of symptoms. Morphological changes are mainly determined by the severity of DIC syndrome and endotoxic shock, due to the degree of bacteremia and the amount of endotoxin released during bacterial death. Hemorrhagic rash in the form of asterisks is detected on the skin, in the center of which necrosis foci are often detected. Histological examination of the skin shows foci of necrosis, diapedesis hemorrhages, fibrin thrombi can be found in the vessels of the dermis. Sometimes vessels of a fairly large caliber are affected, which leads to the development of gangrene of the phalanges of the fingers, auricles. Dystrophic changes and hemorrhagic syndrome are expressed everywhere, but the most important is the bilateral massive hemorrhage into the adrenal glands characteristic of meningococcemia with the development of acute adrenal insufficiency (Waterhouse—Friederiksen syndrome). Such changes in the adrenal glands are found in 60-100% of fatal cases.

Meningococcal meningitis is characterized most often by diffuse purulent inflammation of the soft meninges. In the absence of adequate treatment, starting from the 3rd-4th day of the disease, fibrin appears in the exudate, which leads to increased signs of intracranial hypertension. The immediate cause of death in meningitis patients is most often cerebral edema with the insertion of the tonsils of the cerebellum into the large occipital foramen. It is possible that the inflammatory process may spread to brain tissue with the development of meningoencephalitis.

The mixed form of meningococcal infection (a combination of meningococcemia and meningococcal meningitis) is the most common, and the prognosis for this form is more favorable than for ”pure” forms of meningococcemia or meningococcal meningitis.

Rare forms of meningococcal infection include arthritis, pneumonia, iridocyclitis, endocarditis, which can be observed as an isolated lesion, but more often develop in patients with meningococcemia.

Death can occur in the acute period from swelling of the brain with wedging of the tonsils of the cerebellum into the large occipital foramen and infringement of the medulla oblongata in it, or in subsequent periods from meningoencephalitis, purulent ependymitis, later from general cerebral cachexia due to hydrocephalus and atrophy of the cerebral hemispheres.

The death of patients with a lightning course occurs from bacterial shock, the severity of which is aggravated by hemorrhages in the adrenal glands, acute renal failure is less common (in adults). With a longer course, the fatal outcome is due to septicopyemia or purulent meningitis