Kharkiv National Medical UniversityDepartment of infectious diseases

DYPHTERIADYPHTERIAANGINAANGINA

Associate professor D.V. Katsapov

Angina – acute infection disease caused by streptococci and/or staphylococci, characterized by intoxication, fever, inflammatory process in lymphatic tissues of oropharynx (pharyngeal cycle of Pirogov - Valdeer). Tonsillitis – specific (diphtheria, Epstein-Barr mononucleosis, syphilis, tularemia, leucosis) inflammation of tonsils and regional lymph nodes, often with chronic course.

DIPHTHERIA. DEFINITION

Diphtheria is a contagious acute localized infection of mucous membranes or skin caused by Corynebacterium diphtheriae. Respiratory diphtheria characterized by sore throat, fever, an adherent membrane (a pseudomembrane) and exudation thrown out on the mucous of tonsils, pharynx, larynx and nasal cavity.

DIPHTHERIA. Hystory

5th century BC - the disease was described in the by Hippocrates

6th century AD - epidemics were described in the by Aetius

1826 - Bretano – described clinical picture

1883-1884 - Klebs, Leffler – dyscovered and cultivated the pathogen

1923 - Ramon - introdused immunisation of diphteria anatoxin

DIPHTHERIA. Etiology

Causative agent – Corinеbacterium diphtheriae.

3 cultural and biological species: gravis intermedius mitisExotoxin – protein with antigenic

properties. Two fragments:- A – termostable, biosynthesis inhibition- B – termolabile, adhesion.

DIPHTHERIA. Epidemiology

• Human carriers are the main reservoir of infection

• Transmission - via respiratory droplets, nasopharyngeal secretions, and rarely fomites.

• In the case of cutaneous disease, contact with wound exudates.

• Season – autumn, winter

• Immunity – specific, antitoxic.

DIPHTHERIA. Pathogenesis

Inoculation of the pathogen Colonization of mucosal layers, fixation on

cellular membranes Action of a toxin (A and B fragments) localized inflammatory reaction followed by

tissue destruction and necrosis Production of pseudomembranes Regional edema

General reactions Affection of distant organs: Myocardium, Kidneys, Nervous system

DIPHTHERIA. Clinical classification

By form: Subclinical Mild Moderate Severe Hypertoxic Bacteriocarrier By spread: Localized Diffused (in one anatomical region) Combined (in different regions)

DIPHTHERIA. Clinical classification

By localization: Tonsillopharyngeal Nasal Laryngeal Tracheal and bronchial By character of process: Catarrhal Islet Membranous

DIPHTHERIA. Clinical manifestations

Incubation period - 2 to 5 days (1-10 days) Gradual onset, moderate intoxication Moderate pharyngeal pain White pseudomembranes (greyish) Local edema Paresis of soft palate Affection of miocardium

DIPHTHERIA. Diffused form with hemorrhagic impregnation

DIPHTHERIA. Toxic edema of a neck

Predictors of gravity of clinical course

Expressed intoxication Affection of CNS (delirium, cramps) Affection of CVS (hemodynamic

disturbances, collapse) Hemorrhagic syndrome (bleedings) Edema of cellular tissue of a neck Lymphadenopathy Complications

DIPHTHERIA. Complications

Diphtheric croup Myocarditis (early and late) Polyneuritis and neuropathies Toxic nephritis Acute renal insufficiency Secondary pneumonia

Diphtheritic croupCLINICAL FORMS DESCRIPTION

a) Localized croup(I – III stage)

- Larynx is affected (membranes, edema)- Severity is determined by the stage of croup

a) Diffuse croup(I – III stage)

- Other parts are involved besides the larynx (trachea, bronchus)- Severity is determined by the stage of croup

THE CROUP STAGES

I stagecatarrhal

- Edema and hyperemia of laryngeal mucous under laryngoscopy- Mild pyrexia- Productive cough → barking cough → hoarse voice

II stagestenotic

- Grey membranes on the laryngeal mucous- Intoxication, hypoxemia- Aphonia → soundless cough → noisy heavy respiration, breath is extended- Anxiety

III stageasphyctic

- Hypoxemia, cyanosis- Somnolence, adynamy- Thready pulse, arrhythmia- Forced position- Stop of breathing

DIPHTHERIA. Diagnosis

Clinical presentation, epidemiological data Microscopy Bacteriological 24-48 hrs- preliminary answer 48-72 hrs – toxigenic properties Indirect agglutination reaction PCR ESG Clinical tests

DIPHTHERIA. Treatment

Antitoxin Desintoxication Antibiotics Glucocorticosteroids Supportive treatment

DIPHTHERIA. Treatment antitoxin doses for adults

Clinical form1st dose

(IU)Dosing regimen

Course dose(IU)

Comment

Subclinical - - - -

Mild 30.000-40.000 1 30.000-40.000In bacteriocarriers with

catarrhal process– 20.000 IU

Moderate 50.000-70.000 1-2 50.000-90.000Repeatedly injected in the absence of the 1st

dose effect

Severe 100.000-120.0002-3

(every 12-24 hours)

250.000-300.000

During the first 2 days of treatment all dose is injected. 2 and 3 doses

make up ¾ of the 1st dose.

Hypertoxic 130.000-150.0002-3

(every 12 hours)300.000-400.000

All doses are injected during first two days. 2 and 3 doses make up ¾

of the 1st dose.

Clinical classification of angina By etiology:

Streptococcus Strepto-staphylococcus Staphylococcus Fusospirochetal

By localization of pathological process: palatine tonsils (tonsilla palatina) pharyngeal tonsil (tonsilla pharyngealis) lingual tonsil (tonsilla lingualis) tonsils of torus tubaris (tonsilla tubaris) tororum levatorium lymphoid formations of pharynx posterior wall lymphoid formations of larynx

Clinical classification of angina

By character of inflammatory process: catarrhal lacunar follicular necrotic By severity: mild moderate severe By rate: primary recurrent By complications: uncomplicated complicated

Clinical manifestation of angina

Course of angina: Incubation period (1-2 days) Initial period (few hours - to 1 day) Climax period Convalescence (early and late) Criteria of angina severity: Degree and duration of fever Level of intoxication Character of inflammatory process Functional disorders of nervous, cardiovascular and other

systems and organs. Presence of early or late complications.

Clinical manifestation of angina

Complications of angina: tonsillar abscess paratonsillar abscess parapharyngeal phlegmon mediastinitis cervical lymphadenitis retropharyngeal abscess tonsillar sepsis myocarditis rheumatism glomerulonephritis

PLAUT-VINCENT ANGINA

Plaut-Vincent angina (trench mouth, acute necrotizing ulcerative gingivitis) is a polymicrobial progressive infection of the throat characterized by ulcerations, necrosis of the mucous membranes, bleeding, and foul breath.

Etyology:-gram-positive Peptostreptococcus spp.,

-gram-negative bacilli from Bacteroidales order

-spirochetes (Borrelia spp. and Treponema spp.)

Infectious mononucleosis

Moderate onset with prodromal phase Moderate tonsillitis with necrotic

detritus on surface Generalized lymphadenopathy Enlargement lever and spleen Polymorphic rash In blood test: atypical mononuclears Specific antibodies Ig G (ЕА) + Ig M

(VCA); PCR

Infectious mononucleosis. Lymphadenopathy