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