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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
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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
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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
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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
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By form:
Subclinical
Mild
Moderate
Severe
Hypertoxic
Bacteriocarrier
By spread:
Localized
Diffused (in one anatomical region)
Combined (in different regions)
DIPHTHERIA. Clinical classification
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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
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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
CLINICAL FORMS
DESCRIPTION
a) Localized croup
(I – III stage)
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Larynx is affected (membranes, edema)
Severity is determined by the stage of croup
a) Diffuse croup
(I – III stage)
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Other parts are involved besides the larynx (trachea, bronchus)
Severity is determined by the stage of croup
THE CROUP STAGES
I stage
catarrhal
II stage
stenotic
III stage
asphyctic
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Edema and hyperemia of laryngeal mucous under laryngoscopy
Mild pyrexia
Productive cough → barking cough → hoarse voice
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Grey membranes on the laryngeal mucous
Intoxication, hypoxemia
Aphonia → soundless cough → noisy heavy respiration, breath is extended
Anxiety
Hypoxemia, cyanosis
Somnolence, adynamy
Thready pulse, arrhythmia
Forced position
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
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DIPHTHERIA. Treatment
Antitoxin
 Desintoxication
 Antibiotics
 Glucocorticosteroids
 Supportive treatment
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DIPHTHERIA. Treatment
antitoxin doses for adults
Clinical form
1st dose
(IU)
Dosing regimen
Course dose
(IU)
Comment
Subclinical
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30.000-40.000
In bacteriocarriers with
catarrhal process
– 20.000 IU
50.000-90.000
Repeatedly injected in
the absence of the 1st
dose effect
Mild
Moderate
30.000-40.000
50.000-70.000
1
1-2
Severe
100.000-120.000
2-3
(every 12-24
hours)
Hypertoxic
130.000-150.000
2-3
(every 12 hours)
250.000-300.000
300.000-400.000
During the first 2 days
of treatment all dose is
injected. 2 and 3 doses
make up ¾ of the 1st
dose.
All doses are injected
during first two days. 2
and 3 doses make up ¾
of the 1st dose.
Clinical classification of angina
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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
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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
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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
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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.,
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-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