Definition

• Is an infectious diseases cause by corynebacteruim

diphtheria, characterized by the formation of
pseudomembrane, commonly in the faucial area and
tonsils, and the elotoration of powerful exotoxin affecting
the important viscera of the heart and kidneys and the
peripheral nervous system.
• Diphtheria causes the progressive deterioration of myelin
sheaths in the central and peripheral nervous system
leading to degenerating motor control and loss of
sensation. Diphtheria is a contagious disease spread by
direct physical contact or breathing the aerosolized
secretions of infected individuals.
• Acute febrile infection of the tonsils, throat, nose, larynx or
a wound marked by a patches of grayish membrane from
which bacilli is readily cultured.
 Etiology
• Corynebacteruim diphtheriae (Klebs-
loeffler bacillus)
• Is typically a slender, curved and slightly tapered clubbed
organism which gram + to variable, facultatively aerobic
 Mode of transmission
• Contact with a patient, carrier,
articles soiled with discharged of
infected person
• Source: discharged from nose
pharynx, eyes or lesion on other
parts of body of infected person.
 Period of communicability
• Variable until virulent bacilli has
disappeared from secretions and
lesions: usually 2 weeks and
seldom more than 4 weeks.
 Sign and symptoms
• Fatigue
• Dysphagia
• Nausea/vomiting
• Chills
• High fever
• Neck swelling
• Bull neck
• Toxaema (except in nasal type): apathy, malaise,
weakness and pulse disproportionately rapid to
temperature.
 Pathogenesis
• The typical pseudomembrane is formed by leukocytes,
fibrin, necrotic tissue and micro organism; which is
adherent to the underlying tissues and leaves a raw
bleeding area when detached.
• The toxin elaborated by the organism initiates and
contributes to the further growth of lesion and formation
of more toxins which attacks the myocardium, kidneys,
liver, cranial and peripheral nerves producing foci of
necrosis and degeneration.
• The site of membrane formation influence the clinical
features, produced more toxins absorbed from the upper
respiratory tract than lower respiratory.
 Pathophysiology
• the damage to body is a results of
liberation of soluble toxins in the local
lesion.
• Size of membrane reflects the amount
of toxins being produce.
• The larger the membrane the more
toxins present in blood.
• Toxin-tissue union in many body ports
but special affinity appears to exist in
certain parts, heart and peripheral
nerves.
 Diagnostic test
• Nose and throat swab
• Virulence test
• Shick test
• Moloney test
• Differential diagnosis
 Nose and throat swab
• Culture of both nose and
throat in all types ( swab
are streak on fresh pais
loeefler serum apgar, blood
tellurite or tisdale media
and examine 8- 24 hours of
incubation.
• Negative results do not rule
out diphtheria.
 Virulence test
• Direct smear property stained
will appear typical gram (+)
organism but although having an
advantage of being simple delay
is not entirely reliable.
 Schick test
• Intradermal injection of dilute
diphtheria toxins ( 0.1cc)
• (+) to individual w/o immunity,
hence susceptible to diphtheria
• After 48-72 hours (+) reaction
reveals itself as local
circumscribed area of redness 1-
3 cm in diameter, but
occasionally larger.
 Moloney test
• Test to determined hypersensitivity
to diphtheria toxoid
• Performed by injecting 1.0cc fluid
toxoid intradermally.
• If (+) an area erythema will
developed in 24 hours.
 Medication
• Serum therapy
• antibiotic
 Serum therapy ( diphtheria
antitoxin)
• Early administration aim to
neutralizing the toxins present in
general circulation before it absorbed
by the tissues.
• Skin testing is required before
administration of antitoxin for
allergic reaction.
One must be guided with some several
factor:
a. The day of disease which patient is
first observed
b. Apparent severity of the lesion,
namely the extent of membrane.
c. Evidence of toxemia.
Dosage and route in administration
of antitoxin
Type Dose Route

Anterior nasal 10,000-20,000 Intramuscular

units
Faucial 15,000-25,000 IM/IV
units
Pharyngeal/lary 20,000-40,000 IV
ngeal units
Combined, late 40,000-80,000 IV
cases units
 Antibiotics
Effective for sensitive strain
a. Penicillin G potassium,
100,000 mg/kg/day in 4
doses, IM or IV.

b. Erythromycin, 40mg/kg in
4 doses, oral, for 7-10
days
 Prophylaxis
• Active immunization
• Passive immunization
 Active immunization
• Based on principle that the small
doses of toxins stimulates the
production of antitoxin in the body.
• Most desirable period is between 6-
12 months of age, preferably 9
months.
 Method of active
immunization
a. toxin-antitoxin – is a preparation in w/c
the active immunizing substance, the
toxin has been buffered or attenuated,
with suitable amount of antitoxins.
-has been replace by toxoid w/c is prepared
by addition of 1.4% formalin, thus
attenuating the toxin.
The dose is 0.5cc subQ for 3 doses interval
of 3 months
Toxoid
• As in routine of DPT immunization program of infancy
and childhood and provide protection about 10
years.
• Booster doses is given at suitable interval until
adulthood.
• Protection may not absolute, but disease become
milder and minimum of complication.
• Given subQ or IM by large gauge needle coz danger
of blockage by particles of precipitate.
 Passive immunization
• For susceptible person who has been
directly exposed to an unquestioned
case of the disease.
• Advisable to protect them at once by
injection of 10,000 units of antitoxins,
IM and last about 3-4 weeks.
• Antitoxin prevent development of the
disease.
Nursing management
• Rest
• Care of nose and
throat
• Ice collar
• Diet
 Rest
• Patient should be confined to bed
at least 2 weeks, not permitted
to feed himself, bathe, or to
make exertion.
• Patient is restless, especially
when dyspneic of laryngeal
diphtheria, therefore warm, fresh
air must be ensured.
• In severe cases even making bed
is omitted to conserved energy.
• Vomiting is exhausting, therefore no
procedure that might nauseate the
patient should be used.
• This means small, frequent feeding,
rather than larger ones at longer
intervals.
• Another important point in rest is to
prevent straining at defecation
 Care of nose and throat
• Nose, throat, mouth should be kept clean.
• Gentle swabbing must be done to prevent
bleeding.
• Liquid albolene is soothing to mucous
membrane after cleansing and it prevent
dryness and excoriation caused by the
discharges from the lesions.
• The whole room must be moist atmosphere,
with humidity carefully regulated, in order to
lessen irritability to nose and throat.
 Ice collar
• Sometimes ice collar is more
effective than warm
application in relieving pain of
the sore throat.
• Kept aroud the neck as
intended.
• Rubber collar must be placed
in cloth or gauge to protect
patient skin and prevent
wetting patient clothing.
 Diet
• When throat is very sore, soft
foods.
• Small amounts given frequently.
• Fruit juices help to maintain
alkalinity of blood, citrus may
comfort when in sore throat.
• Creamed soups, purees, soft eggs,
jellies, custards, broth and
buttermilk should provide a
balanced ration if a sufficient
amount can be swallowed.
 complication
• Toxemia
• Neuritis
• Difficulty swallowing and breathing
• Pneumonia
• Kidney failure
• Death
 Toxemia
• Due to toxemia
a. Toxic myocarditis- Myocarditis is inflammation of the
heart muscle that can cause an irregular heartbeat
and lead to heart failure. It often is fatal.
b. Due to action of toxins in the heart muscles.
c. Usually during the first 10-14 days.
d. Diminution in intensity of first heart sound.
e. Arrhythmia
f. E.C.G elevation of S-T segment prolongation of P-R
interval evidence of heart block.
Abdominal pain due to enlargement of
the liver caused by cardiac failure, so
called “ chronic passive congestion”.
 Neuritis
• Caused by absorption of toxin in the nerves.
• May appear early o late may affect the:
a. Palate (paralysis of soft palate); nasal twang
and regurgitation occurring the 3rd week na
last 1-2 weeks.
b. Extra ocular muscles (ocular palsy) bilateral
paralysis of ocular muscles of accommodation
causing blurring of vision during 5th week,
strabismus.
c. Diaphragm (paralysis) occurs 6th-10th week;
simulating guillain-barre
d. Motor and skeletal muscle (motor and
sensory paralysis)) respiratory difficulty limb
or trunk weakness.
e. Toxic nephritis with albuminuria, cast an
edema may also occur
 Difficulty swallowing and
breathing
• Soft-palate paralysis prevents normal
swallowing and can lead to choking or
aspiration of food into the lungs, causing
aspiration pneumonia.
• Paralysis of the diaphragm can lead to
difficulty breathing, pneumonia, and even
respiratory failure and death. In addition, the
membrane at the back of the throat or in the
voice box can partially or completely block
the airway, resulting in suffocation.
 Pneumonia

• Pneumonia can result from the

infection itself, or it can be secondary
to the swallowing and breathing
difficulties
 Kidney failure
• The toxin produced by
Corynebacteruim diphtheriae can
cause kidney failure directly, or
kidney failure can develop
secondarily as a complication of
heart failure.
 Death

• The mortality rate is about 5 to 10

percent, although it can climb as
high as 20 percent in children under
the age of five years. In recent years,
the mortality rate in diphtheria
epidemics in the independent states
of the former Soviet Union has
ranged from 3 to 23 percent.
 Types of diphtheria(2)
• Respiratory diphtheria
• Non respiratory diphtheria
 Respiratory diphtheria
Faucial and pharyngeal (tonsilar, uvular,
palatar).
• Low grade fever, malaise, H/A, sore throat.
• w/in 24 hours, small yellowish spot appear in
tonsils w/c coalesce to form the adherent
pseudomembrane, w/c extends to the rest of
fauces and nasopharynx.
• Cervical nodes enlarged
• Dysphagia and noisy breathing with nasal
voice, regurgitation of fluids due to palatal
weakness
• Very toxic infection, the bullneck appearance
–due to massive enlargement of lymph
glands.
• Death may occur due to bronchopneumonia
or toxic myocarditis.
Laryngotracheal diphtheria (tracheal, bronchial)
• More commonly in infants
• Hoarseness with barking cough and noisy breathing
(croupy cough, braze-metallic cough)
• Inspiratory stridor, aphonia, dyspnea with
subclavicular and suprasternal retractions.
• In severe cases with progressive obstruction leads to
suffocation, cyanosis, cardiac failure and death.
Nasal (anterior, posterior)
• Occurs mostly at 1st three years of life.
• Persistent serous nasal discharged later
become bloody and foul smelling.
• Discharges: serous –serosanguinous –
mucopurulent –(excoriating anterior nares
and upper lips) – impetiginous appearance.
(Lateral or bilateral.)
 Non respiratory diphtheria
• Ocular (conjucntival)
reddened
• Ears (aural) purulent
discharged
• Wound and ulcer in the
skin
• Genito urinary tract –
external genitalis,
ulcerative lesions on
vulva and vagina.
• Umbilical of the newborn.
 Epidemiology
• Incidence
• December to February –higher prevalence
occurring at cooler months.
• Mainly disease of childhood, peak
incidence between 2 to 5 years.
• Rare below 6 months due to transplacental
transmission of immunity acquired from
mother who presumably developed active
immunity from inapparent infection.
 Prognosis
• The prognosis depends on the size
and location of the membrane and
on early treatment with antitoxin; the
longer the delay, the higher the
death rate. The most vulnerable
patients are children under age 15
and those who develop pneumonia or
myocarditis. Nasal and cutaneous
diphtheria are rarely fatal.