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Kharkiv National Medical University Department of infectious diseases DYPHTERIAANGINA Associate professor D.V. Katsapov.

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Presentation on theme: "Kharkiv National Medical University Department of infectious diseases DYPHTERIAANGINA Associate professor D.V. Katsapov."— Presentation transcript:

1 Kharkiv National Medical University Department of infectious diseases DYPHTERIAANGINA Associate professor D.V. Katsapov

2 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.

3 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.

4 DIPHTHERIA. Hystory  5th century BC - the disease was described in the by Hippocrates  6th century AD - epidemics were described in the by Aetius  Bretano – described clinical picture  Klebs, Leffler – dyscovered and cultivated the pathogen  Ramon - introdused immunisation of diphteria anatoxin

5 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.

6 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.

7 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

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

9 DIPHTHERIA. Clinical classification By localization: Tonsillopharyngeal Nasal Laryngeal Tracheal and bronchial By character of process: Catarrhal Islet Membranous

10 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

11 DIPHTHERIA. Diffused form with hemorrhagic impregnation

12 DIPHTHERIA. Toxic edema of a neck

13 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

14 DIPHTHERIA. Complications  Diphtheric croup  Myocarditis (early and late)  Polyneuritis and neuropathies  Toxic nephritis  Acute renal insufficiency  Secondary pneumonia

15 Diphtheritic croup CLINICAL FORMSDESCRIPTION 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 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

16 DIPHTHERIA. Diagnosis Clinical presentation, epidemiological data Microscopy Bacteriological hrs- preliminary answer hrs – toxigenic properties Indirect agglutination reaction PCR ESG Clinical tests

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

18 DIPHTHERIA. Treatment antitoxin doses for adults Clinical form 1 st dose (IU) Dosing regimen Course dose (IU) Comment Subclinical--- - Mild In bacteriocarriers with catarrhal process – IU Moderate Repeatedly injected in the absence of the 1 st dose effect Severe (every hours) During the first 2 days of treatment all dose is injected. 2 and 3 doses make up ¾ of the 1 st dose. Hypertoxic (every 12 hours) All doses are injected during first two days. 2 and 3 doses make up ¾ of the 1 st dose.

19 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

20 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

21 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.

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

23 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 orderBacteroidales -spirochetes (Borrelia spp. and Treponema spp.)

24 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

25 Infectious mononucleosis. Lymphadenopathy


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