1. Kharkiv National Medical University Department of infectious diseases
DYPHTERIA
ANGINA
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. i

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 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

16. 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

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

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