Transcript upper respiratory tract infections

UPPER RESPIRATORY
TRACT INFECTIONS
The classification of upper respiratory
tract infections includes:
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The common cold
Pharyngitis
Epiglotitis
Acute laryngitis
Acute laryngotracheobronchitis
Sinusitis
Otitis externa, otitis media and mastoiditis
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The common cold
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Viruses associated with the common cold
are adenoviruses, parainfluenza virus,
influenza virus, rhinoviruses and
respiratory syncytial virus.
2. Pharyngitis
Table 1. Etiology of pharyngitis
Viral:
Bacterial:
-Rhinoviruses
-Adenoviruses
-Herpes simplex virus (type 1 and 2)
-Parainfluenza virus
-Influenza virus
-Coxsackievirus A
--Epstein Barr virus
-Cytomegalovirus
-HIV-1
-Streptococcus pyogenes (Group A and C
beta-hemolytic streptococcus)
-N. gonorrhoeae
-Corynebacterium diphteriae
-Yersinia enterocolitica
-Treponema
Chlamydia pneumoniae
Mycoplasma pneumoniae and hominis
Mixed anaerobic bacterial infection
(Vincent’s angina)
Clinical manifestations
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Streptococcal pharyngitis
Streptococcal pharyngitis - is characterized by:
 High fever
 Severe pharyngeal pain
 Odynophagia
 Headache, chills
 Edema and hyperemia of the tonsills/uvula
 A patchy, grayish-yellow exudate on the tonsils
 Tender, enlarged cervical lymph nodes.
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Complications of streptococcal
pharyngitis
Suppurative complications:
 Nonsuppurative complications: acute
rheumatic fever, acute glomerulonephritis.
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Anaerobic pharyngitis (Vincent’s angina)
The etiology is represented by mixture of anaerobic bacteria
(Fusobacterium necrophorum) and spirochetes.
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Pharyngoconjunctival fever
Adenoviruses are involved in etiology and the manifestations
include: malaise, myalgia, sore throat, headache, chills, dizziness,
conjunctivitis, erythema and inflammatory exudate. Evolution of
temperature is usually 5-6 days.
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Herpetic pharyngitis
It is characterized by the presence of:
- vesicle and shallow ulcers on the palate
- inflammation and inflammatory exudate
-cervical adenopahy.
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Herpangina
Herpangina is primarily seen in children. The etiologic
agent are coxsackieviruses.
Clinical features consist of:
-marked sore throat, dysphagia, anorexia
-small vesicles (1-2 mm) on the soft palate, uvula, and
anterior tonsilar pillars; after the rupture of vesicles,
small and white ulcers appear.
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Infection with Mycoplasma pneumoniae occurs
primarily in collectivities of children and young.
Differential diagnosis
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Infectious pharyngitis must be
distinguished from noninfectious
conditions:
Bullous pemphigoid
Systemic lupus erythematous
Behcet’s disease
Kawasaki disease
Laboratory diagnosis
Throat culture
 Rapid antigen detection tests in throat
swab
 Specific serologic tests for infectious
mononucleosis
 Serologic tests for My. pneumoniae,
herpes simplex, adenoviruses, etc.
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Treatment of sterptococcal pharyngitis:
1. The current recommended treatment for this infection is
penicillin V 25-50 mg/kg/day divided into a 4-dose-perday schedule for 10 days.
2. Benzathine penicillin (penicillin G) 50,000 u/kg
intramuscular
3. If a patient is penicillin-allergic: erythromycin 30
mg/kg/day or azithromycin (given once daily for 5
days only) or clarithromycin (twice daily for 10 days)
First-generation cephalosporins
 Second-generation cephalosporins
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3. Epiglottitis
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Acute epiglottitis is defined as a cellulitis of the epiglottis
and adjacent structures that may produces complete
airway obstruction.
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The most frequently etiologic pathogen is H. influenza
type B, and occasionally pneumococcus, staphylococcus,
streptococcus. H. influenzae epiglottitis may be
associated in a large proportion of cases with bacteremia
and sepsis, with different secondary location of infection.
Clinical manifestations
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Onset is abrupt, marked by fever,
irritability, dysphonia, dysphagia, followed
by respiratory distressLaryngoscopy
reveals a “cherry-red” epiglottis.
Laboratory features
Leukocytosis with neutrophilia
 Positive cultures of blood and epiglottis
 Radiograph of the lateral neck shows enlarged
 Differential diagnosis includes: croup, dyphteria,
angioneurotic edema, foreign body aspiration,
etc..
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Therapy:
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intravenous therapy with antibiotics such as: cefotaxime
(100-180mg/kg/day), ceftriaxone (80-100mg/kg/day) or
amocicillin-clavulanic acid(200mg of amoxicillin/kg/day)
for 7-10 days.
4. Acute laryngitis
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Etiology:
- viruses
- bacteria
- fungi
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Clinical manifestations: recent onset of hoarsness or episodes of
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Examination of larynx reveals hyperemia of vocal folds.
Differential diagnosis: croup, acute epiglottitis, supraglottitis,
bacterial tracheitis, voice abuse, gastroesophageal reflux disease,
laryngeal malignancy.
Antibiotics are not routinely recommended.
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aphonia.
5. Acute laryngotracheobronchitis (croup)
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Acute laryngotracheobronchitis is a viral infection that consists of
inflammation in the subglottic area.
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Etiology: parainfluenza viruses, influenza A, B viruses, respiratory syncitial
virus, adenovirus, rhinovirus, enterovirus, and rarely, Mycoplasma
pneumoniae.
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Clinical manifestations
The croup is preceded by an upper respiratory tract infection.
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Laboratory findings
Differential diagnosis
Non infectious causes of stridor:
 Bacterial epiglottitis
 Complications
 Therapy: humidification devices of the airway, good supportive care,
corticosteroids.
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6. Sinusitis
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The most common bacteria are: Streptococcus
pneumoniae, Haemophilus influenzae, Moraxella
catarrhalis, Streptococcus pyogenes, and Staphylococcus
aureus. Anaerobic bacteria ,Fungal sinusitis
Viruses may also cause sinusitis.
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Diagnostic modalities include fiberoptic nasal endoscopy,
CT scans, and plain x-rays.
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Amoxicillin-clavulanic acid,
trimethoprim/sulfametoxazole, amocillin
Azithromycin/Clarithromycin (if penicillin allergy);
Levofloxacin/moxifloxacin (when Penicillin-Resistant
Pneumococcus is suspected);
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7. Otitis Media
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Etiological agents the most frequently seen are: S.
pneumoniae, H. influenzae, M. catarrhalis, viruses
(respiratory syncitial virus, rhinoviruses)
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Diagnosis is suggested by:
Hearing loss
Ear pain
Fever
Delayed speech development in children
Therapy
-Amoxillin or amoxicillin-clavulanic acid
-Cefuroxime, ceftriaxone (50 mg/kg/day)
-Clindamycin (if failure of treatment after 3 days).
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INFLUENZA
The Orthomyxoviridae (influenza viruses)
Three immunologic types are known:
Type A;
Type B
Type C
Etiology
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The HA protein.
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The antigenicity of NA,
The standard nomenclature system for influenza virus isolates includes the following information:
-type,
-host of origin,
-geographic origin,
-strain number,
-year of isolation (example: A/Hong Kong/03/68(H3N2).
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So far, 14 subtypes of HA (H1-H14) and nine subtypes of NA (N1-N9) in many different
combinations have been recovered.
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Antigenic drift and antigenic shift
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Minor antigenic changes are termed antigenic drift;
Major antigenic changes in HA or NA, called antigenic shift
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Influenza virus replication
Epidemiology
The three types of influenza vary in their
epidemiologic patterns.
Influenza C is least significant: it causes mild,
sporadic respiratory disease, but not epidemic.
 Influenza B sometimes causes epidemics,
 Influenza type A can causes around the world
massive epidemics called pandemics
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Pathogenesis
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Influenza virus spreads from person to
person by airborne droplets or by contact
with contaminated hands or surfaces.
Clinical findings
 Uncomplicated Influenza
 Incubation period: 1-4 days.
 Symptoms usually appear abruptly and include:
- chills,
- headache,
- dry cough- respiratory symptoms typically last another
3-4 days. The cough and weakness may persist for 1-3
weeks.
- high fever- lasts 3 days
- generalised muscle aches,
- malaise and anorexia
 Complications
-Pneumonia
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Reye’s Syndrome :.
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Early signs:
-persistent/continuous vomiting
-loss of energy
-irritability
-fluctuating personality changes
-confusion
As the encephalopathy becomes more severe, extreme
irritability, agitation, delirium, convulsions, and coma
may develop.
Laboratory findings
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hyperammoniemia
elevated levels of alanin aminotransferase and
aspartat aminotransferase
prolonged prothrombin time
hypoglycemia
hyperlactatemia
acid-base disorders
CSF – with <8cells/mmc, and normal level of
protein and glucose
Treatment
Glucose administration
 Antiedematous drugs, diuretics
 Fresh frozen plasma/fresh blood (if
bleeding occurs)
 Corticosteroids
 The mortality rate is high (10-50%).
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Other complications: sinusites,
myocarditis, pericarditis, cardiac failure,
renal failure, neurological complications.
Immunity
Immunity to influenza is long-lived and
subtype-specific.
Laboratory Diagnosis
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Diagnosis of influenza relies on:
isolation of the virus;
identification of viral antigen or viral nucleic acid
in the patient’s cells, or
demonstration of a specific immunologic
response.
Other tests are: ELISA and RIA. Paired acute
and convalescent sera are necessary, because
normal individuals usually have influenza
antibodies. A fourfold or greater increased in
titer must occur to indicate influenza infection.
Treatment
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Amantadine and rimantadine,
Zanamivir and Oseltamivir
All people at risk in whom influenza develops
Persons with severe influenza
For persons who wish to shorten the duration of
illness.
Prevention
Inactivated viral vaccines
 The vaccine is usually a cocktail containing two influenza A subtypes
(H1N1, H3N2) and a type B virus of the strains isolated in the
previous winter’s outbreaks.
 Annual influenza vaccination is recommended for high-risk groups.:
• Persons >50 years old
• those with either chronic heart or lung disease,
• adult and children with asthma, or metabolic or renal disorders,
immunossuppression, hemoglobinopathy
•residents of nursing homes;
• persons who might transmit influenza to high-risk groups :
- medical personnel,
- employees in chronic care facilities,
- household members.
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MUMPS
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Mumps is an acute viral disease
characterized by nonsuppurative swelling
and tenderness of the salivary glands.
Etiology
Mumps virus belongs to paramyxoviridae
family.
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Epidemiology
The virus is spread by infectious saliva or by
urine. Neonates are protected by
transplacental maternal antibodies.
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Clinical manifestations
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Incubation period: 14-25 days.
Prodromal symptoms (3 days): fever, headache, malaise.
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Glandular involvement:
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The onset of parotitis:
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Submandibular/sublingual glands involvement (10% of
cases)
Epididymo-orchitis
Oophoritis –
Neurologic manifestations
1.CSF pleoocytosis
-Meningitis
2.Encephalitis
3.Other features in mumps are:
-Renal function abnormalities (>60%);
-ECG abnormalities (5-15%);
-Pancreatitis
-Thyroid inflammation:
Complications
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Myocarditis – is very rare
Arthritis.
Hemolytic anemia, trombocytopenia;
Deafness with uni, or bilateral involvement;
In pregnant women (with gestational viral
infection):
fetal death is common during the first trimester.
low birth weight
endocardial fibroelastosis
juvenile diabetes mellitus.
Laboratory features
 Diagnosis is based on: history of exposure, parotid
swelling and tenderness, constitutional symptoms.
 Differential diagnosis
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Parotid swelling must be differentiated by:
- Other infectious causes:
- Noninfectious causes:
- Extraparotid causes:
 Prognosis is generally good, except severe forms of
encephalitis, myocarditis, glotic edema. Lethality is
approximately 0,01%.
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Treatment
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Treatment is entirely symptomatic: analgesics for
orchitis or pancreatitis, drugs against vomiting,
etc. Patients should avoid acid food, the diet
must be light, with a good hydration.
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The vaccine contains a live mumps, virus and
may be administrated alone or in combination
with measles and rubella vaccines.
INFECTIOUS MONONUCLEOSIS
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Infectious mononucleosis is an acute
illness characterized by fever, pharyngitis,
lymphadenopathy, and mononuclear
leukocytosis with atypical lymphocytes.
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Etiology
The Epstein-Barr virus (EBV)
Pathogenesis
EBV infects B lymphocytes and epithelial cells in the oropharynx and
cervix.
During primary infection, EBV-infected B-cells undergo lytic
infection with production of virus or express the full complement of
latent viral proteins. The latter cells are kept in check by natural
killer and cytotoxic T cells, which may appear as “atypical
lymphocytes” on the peripheral blood smear.
Some latently infected cells undergo lytic replication in the
oropharynx, resulting in production of virus with shedding the virus
into the saliva.
Clinical manifestations
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Incubation period: 30-50 days.
Characteristic triad consists of: fever (75% of cases),
pharyngitis (84%), and lymphadenopathy (94%).
Other common signs and symptoms are: splenomegaly
(50%), hepatomegaly (10%), palatal petechiae (10%),
rash (10%), jaundice (10%) associated with sore throat,
headache, anorexia, abdominal pain, nausea, chills,
myalgia.
A morbilliform rash
As a result of congenital infection an embriopathy may
occasionally result:
Complications
Neurologic complications.
 Haematologic complication:
 Hepatitis, myocarditis, splenic rupture,
genital ulcers.
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Laboratory tests
a. Hemoleucogram shows a mononucleosis syndrome:
-Leukocytosis
- an absolute increase in the number of peripheral
mononuclear cells
-atypical lymphocytes (>10%) which are primary T cells
responding to the EBV-infected cells.
b. Elevated serum aminotransferase levels
c. Serological tests.
 The humoral immune response to EBV infection involves
both viral-specific and nonspecific antibodies.
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Nonspecific antibodies:
Paul-Bunnell-Davidson test –
 Three specific antibodies to EBV antigens
are diagnostically important, and the
antigens are:
• VCA – viral capsid antigen
• EA – early antigen
• EBNA – EBV nuclear antigen
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d. Isolation of the pathogen
-EBV culture is not a routine method
-demonstration of EBV genoma by PCR and
of EBV antigen by immunoblot techniques.
Other clinical syndromes produced by EBV infection
 Chronic active EBV infection - is a rare disorder
 X-Linked Lymphoproliferative Disease -.
 Cancers associated with EBV
1.Nasopharyngeal carcinoma –
3.Hodgkin’s disease.
4.Lymphoproliferative disease –
5.Other tumors:
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Treatment
No specific therapy is indicated for most patients with infectious
mononucleosis.
Corticosteroid therapy is recommended for patients with severe
complications:
Treatment
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No specific therapy is indicated for most
patients with infectious mononucleosis.
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Corticosteroid therapy is recommended for
patients with severe complications:
DIPHTHERIA
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Diphtheria is an acute disease manifested
by both local infection of the upper
respiratory tract and the systemic effects
of a toxin, which are most notable in the
heart and peripheral nerves.
Etiology
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The etiologic agent is the principal human
pathogen of the Corynebacterium group,
C. diphtheriae, an aerobic gram-positive
bacillus with irregular shape.
Pathology
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All human tissues may suffer by the toxin because all human cells
have receptor sites.
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The diphtheria bacilli within the membrane continue to produce
toxin actively. This is absorbed and leads to distant toxic damage,
particularly parenchymatous degeneration, fatty infiltration and
necrosis in heart muscle, liver, kidneys (tubular necrosis), adrenals,
sometimes accompanied by important hemorrhage. The toxin also
produces nerve damage (neuronal demyelination), resulting often in
paralysis of the soft palate, eye muscles, or extremities.
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There are 2 phases of diphtheria: the initial local presentation
as a severe pharyngitis with tough membranes that can cause
suffocation and a late systemic phase caused by the effects of the
circulating exotoxin on tissues of the host.
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Nondiptheria corynebacteria produce localized or systemic diseases
Clinical Findings
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Incubation period is usually less than 1 week.
Pharyngitis.
Laryngeal diphtheria.
Nasal diphteria
 Cutaneous infection
 Other organ involvement includes: ears,
conjunctiva, cornea.
Complications
1. Cardiovascular complications
 Myocarditis
 Late myocarditis
2. Neurologic complications
a.Palatal paralysis
b.Oculomotor paralysis
c.Peripheral polyneuritis
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Laboratory Tests
1.Isolation of C. diphteriae
2. Stained smears show beaded rods in
typical arrangement.
Diagnosis
Differential diagnosis
Other pharyngeal diseases:
 Retropharyngeal and peritonsillar
abscesses.
 A foreign body in the larynx, viral
laryngitis
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Treatment
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Note: specific treatment must never be delayed for laboratory
reports if the clinical picture is strongly suggestive of diphtheria.
1.The imperative in diphtheria treatment is to administer the antitoxin
as soon
 as possible, as it is the only mean to neutralize toxin that has not
already bound to cells. The mainstay of therapy is prompt
administration of equine diphtheria antitoxin: 20000-100000 IU,
i.v. the test for hypersensitivity consists of administration of one
drop of antitoxin diluted 1:10 in one eye.
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If the antitoxin is administrated in the first day of illness, the
mortality is less than 1%.
Antibiotics PENICILLIN or ERYTHROMYCIN
2. Supportive care and maintenance of an airway
3.Strict bed rest during the acute phase of diphteria.
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Prevention
Diphtheria was the first bacterial disease for which toxic
cause was demonstrated and the first to be treated
successfully with an antitoxin. In 1913 a vaccine was
created, composed of treated diphtheria toxin, called
anatoxin, later transformed in diphtheria toxoid. In 1940
a combined vaccine appeared: DTP = Diphtheria toxoid
+ Tetanus toxoid + Pertussis vaccine.
 Active immunization in childhood with diphtheria toxoid
 In the most developing countries, immunization with
diphteria and tetanus toxoids and pertussis vaccine was
introduced by the late 1970s; in countries with low
immunization coverage, diphteria continues to be
endemic.
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