Kharkiv National Medical University Department of infectious diseases DYPHTERIA ANGINA 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 mitis Exotoxin – 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. i

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 croup THE CROUP STAGES CLINICAL FORMS DESCRIPTION Localized croup (I – III stage) Larynx is affected (membranes, edema) Severity is determined by the stage of croup Diffuse croup Other parts are involved besides the larynx (trachea, bronchus) THE CROUP STAGES I stage catarrhal Edema and hyperemia of laryngeal mucous under laryngoscopy Mild pyrexia Productive cough → barking cough → hoarse voice II stage stenotic Grey membranes on the laryngeal mucous Intoxication, hypoxemia Aphonia → soundless cough → noisy heavy respiration, breath is extended Anxiety III stage asphyctic 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

Glucocorticosteroids Supportive treatment DIPHTHERIA. Treatment Antitoxin Desintoxication Antibiotics Glucocorticosteroids Supportive treatment

DIPHTHERIA. Treatment antitoxin doses for adults Clinical form 1st dose (IU) Dosing regimen Course dose Comment Subclinical - Mild 30.000-40.000 1 In bacteriocarriers with catarrhal process – 20.000 IU Moderate 50.000-70.000 1-2 50.000-90.000 Repeatedly injected in the absence of the 1st dose effect Severe 100.000-120.000 2-3 (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 130.000-150.000 (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