1) Diphtheria, pertussis, and tetanus are acute infectious diseases caused by Corynebacterium diphtheriae, Bordetella pertussis/parapertussis, and Clostridium tetani respectively. 2) They present with respiratory symptoms like sore throat and cough and neurological symptoms like muscle spasms. Diagnosis involves identification of bacteria and supportive lab tests. 3) Treatment involves antitoxins, antibiotics, wound care and supportive measures. Immunization provides effective prevention against these diseases.

1. DIPTHERIA
PERTUSIS
TETANUS
Dr M.Sanjeevappa
Designated Associate Professor
Dept of Paediatrics
GMC ,Anantapur

2. DIPTHERIA
 Diphtheria is a potentially acute disease caused by
exotoxin producing Corynebacterium diphtheriae, a
Gram-positive bacillus.

3. DIPTHERIA
Epidemiology :
 Humans are the only natural reservoir of C.
diphtheriae.
 Spread occurs in close-contact settings through
respiratory droplets or direct contact with
respiratory secretions or skin lesions.
 Diphtheria immunization protects against disease
but does not prevent carriage.
 Vaccine-induced immunity to diphtheria wanes with
time.

4. DIPTHERIA
Continued….
 In 2005, India contributed 5,826 (71%) of
the 8,229 diphtheria cases reported
globally.
 In 2010, a total of 3,129 cases of
diphtheria were reported in India.

5. DIPTHERIA
Pathogenesis :
 Corynebacterium diphtheriae is a nonmotile, non
capsulated, club-shaped, gram-positive bacillus.
 Toxigenic strains are lysogenic for one of a family of
corynebacteriophages that carry the structural gene
for diphtheria toxin.
 Corynebacterium diphtheriae is classified into
biotypes (mitis, intermedius, and gravis) according
to colony morphology on tellurite containing media

6. DIPTHERIA
Pathogenesis :
 Corynebacterium diphtheriae colonizes the mucosal surface
of the nasopharynx and multiplies locally without blood
stream invasion.
 Released toxin causes local tissue necrosis with the formation
of a tough, adherent pseudomembrane composed of a
mixture of fibrin, dead cells, and bacteria.
 Toxin absorption can lead to systemic manifestations:
kidney tubule necrosis, thrombocytopenia,
cardiomyopathy, and demyelination of nerves.

7. DIPTHERIA
Clinical Manifestations :
 RespiratoryTractDiphtheria :
 averageincubationperiod is 2-4 days(range 1-10
days).
 anterior Nasal diphtheria.
 Pharyngeal and Tonsillar diphtheria .
sore throat
Malaise
mild-to-moderate fever
grayish membrane

8. DIPTHERIA
Continued….
 Cervical adenopathy and soft tissue edema result in
the typical bull neck appearance and stridor.
 Laryngeal diphtheria :manifested as hoarseness,
stridor and dyspnea.

9. DIPTHERIA
 Cutaneous diphtheria :
 Classic cutaneous diphtheria is an indolent,
nonprogressive infection characterized by a
superficial , non healing ulcer with a gray-brown
membrane.

10. DIPTHERIA
Diagnosis :
 Specimens for culture should be obtained from the nose
and throat and any other mucocutaneous lesion.
 Gram stain is used to accurately identify the organism.
 special stain like Albert’s stain, Ponders stain to detect
metachromatic granular structure.
 selective media like tellurite agar or specially enriched
Loeffler, Tinsdale medium.

11. DIPTHERIA
Differential diagnosis :
 streptococcal and viral tonsillopharyngitis,
 infectious mononucleosis,
 Vincent’s angina,
 candidiasis
 acute epiglottitis.

12. DIPTHERIA
Management :
 The goals of treatment :
- neutralize the toxin rapidly.
- eliminate the infecting organism.
- provide supportive care.
- prevent further transmission.

13. DIPTHERIA
Management :
 The mainstay of therapy is equine diphtheria
antitoxin.
 A single dose ranging in quantity from 20,000 units for
localized tonsillar diphtheria up to 100,000 units is
given for extensive disease with severe toxicity.
 Route of administration :intramuscularly or
intravenously.

14. DIPTHERIA
Management :
Antimicrobial therapy :
 Erythromycin (40-50 mg/kg/day divided every 6 hr
by mouth [PO] or intravenously [IV]; maximum 2
g/day).
 Aqueous crystalline penicillin G (100,000-150,000
units/kg/day divided every 6 hr IV or intramuscularly
[IM]).
 Procaine penicillin (300,000units every 12 hr IM for
those ≤10 kg in weight; 600,000 units every 12 hr IM
for those >10 kg in weight) for14 days.
 Once oral medications are tolerated, oral
penicillin V (250 mg four times daily)may be used.

15. DIPTHERIA
Complications :
 Myocarditis.
 Conduction disturbances like ST-T wave
abnormalities, arrhythmias, and heart block .
 Neurologic complications : cranial nerve palsies and
polyneuritis , Palatal or pharyngeal paralysis.

16. DIPTHERIA
Prognosis : depends on
The virulence of the organism.
Patient age.
Immunization status.
Site of infection.
Speed of administration of the antitoxin.

17. DIPTHERIA
Prevention :
 immunization.
 minimum protective level for diphtheria antitoxin is
0.01-0.10 IU/mL.
 Asymptomatic Case Contacts :
All household contacts and people who have had
intimate respiratory or habitual physical contact with
a patient are closely monitored for illness for
7 days.
 a single injectionof benzathine penicillinG(600,000
units IM forpatients <6 yr old, or 1,200,000 units IM
forpatients >6 yr old) or
 erythromycin (40-50 mg/kg/day divided qid PO for
10 days.

18. PERTUSSIS
 Pertussis is an infection of the respiratory tract characterized
by a paroxysmal cough.
 Bordetella pertussis and Bordetella parapertussis cause
whooping cough.
 Bacteria spread via aerosolized droplets from coughing of
infected individuals.
 The global incidence is 48.5 million cases and 295,000 deaths
annually.
 The case-fatality rate among infants in low-income countries
is 4%.
 Neither natural infection, nor vaccination provides lifelong
immunity.

19. PERTUSSIS
Pathogenesis :
 Bordetella organisms are small, fastidious, gram-
negative coccobacilli that colonize only ciliated
epithelium.
 B. pertussis expresses pertussis toxin (PT), the
major virulence protein.
 Tracheal cytotoxin, dermonecrotic factor, and
adenylate cyclase are responsible for the local
epithelial damage that produces respiratory
symptoms and facilitates absorption of PT.

20. PERTUSSIS
Clinical Manifestations :
 Incubation period 3-12 days (up to 21 days)
 Insidious onset, similar to minor upper respiratory
infection with nonspecific cough
 Fever usually minimal throughout course
 Apnea & Cyanosis in infant

21. PERTUSSIS
Clinical Manifestations :
STAGES :
 1st Stage- Catarrhal Stage
1 to 2 weeks ,URI, very contagious
 2nd Stage- Paroxysmal Stage
1to 6 weeks , worsening cough ,post –tussive emesis,
inspiratory whooping ,cyanosis, exhaustion.
 3rd Stage- Covalescent Stage
2 to 3weeks, cough decreases, symptoms may return
or woren.

22. PERTUSSIS
Diagnosis :
 A pure or predominant complaint of cough.
 Cough of ≥14 days’ duration with at least 1
associated symptomof paroxysms, whoop, or post
tussive vomiting has sensitivity of 81% and
specificity of 58%.
 Pertussis should be suspected in older children
whose cough illness is escalating at 7-10 days
and whose coughing comes in bursts.
 Pertussis should be suspected in infants <3 months
old with gagging, gasping, apnea, cyanosis,or an
apparentlife-threatening event.

23. PERTUSSIS
Diagnosis :
 Leuckocytosis (Lymphocytosis)
 Thrombocytosis
 Culture(Nasopharengeal swab)
 Direct Flurocent Antibody.
 PCR (Nasopharengeal)
 CXR :Perihilar Infiltration’…signs of segmental lung
atelectasis .

24. PERTUSSIS
Indications for hospitalization :
 Respiratory distress, including tachypnea,
retractions, nasal flaring, grunting, and the use of
accessory muscles
 Evidence of pneumonia
 Inability to feed
 Cyanosis or apnea, with or without coughing
 Seizures
 Age <4 months

25. PERTUSSIS
Isolation :
 Droplet precautions (mask within 3 feet), are
recommended for children with pertussis who are
admitted to the hospital .
 These precautions should be in effect until five days of
effective therapy.
 three weeks after the onset of symptoms in untreated
patients.

26. PERTUSSIS
Antimicrobial therapy :
Indications :
 cultures or positive PCR within three weeks of cough onset
(individuals >1 year) or six weeks of cough onset (individuals
<1 year)
 infants and children with a clinical diagnosis of pertussis
(with or without laboratory confirmation) who have had
symptoms <21 days
 have had >21 days of symptoms, particularly those who are
likely to be in contact with high-risk individuals

27. PERTUSSIS

28. PERTUSSIS
Complications :
 hypoxia, apnea, pneumonia, seizures,
encephalopathy, and malnutrition
 The most frequent complication is pneumonia
 Atelectasis may develop secondary to mucous
plugs.
 The force of the paroxysm may rupture alveoli and
produce pneumomediastinum pneumothorax, or
interstitial or subcutaneous emphysema
 epistaxis; hernias; and retinal and subconjunctival
hemorrhages.

29. PERTUSSIS
Post exposure prophylaxis :
 Antibiotic prophylaxis has traditionally been used
to prevent transmission to personal contacts of
patients with pertussis
 Azithromycin is the preferred agent for
prophylaxis

30. TETANUS
Definition :
 Tetanus is a neurologic disorder, characterized by
increased muscle tone and spasms, that is caused
by tetanospasmin, a powerful protein toxin
produced by Clostridium tetani.
 Types ( generalized, neonatal, and localized).

31. TETANUS
 Tetanus was well known to ancient people who recognized
the relationship between wounds and fatal muscle spasms.
 In 1884, Arthur Nicolaier isolated the strychnine-like toxin of
tetanus from free-living, anaerobic soil bacteria.
 In 1891, C. tetani was isolated from a human victim by
Kitasato Shibasaburō
 In 1897, Edmond Nocard showed that tetanus antitoxin
induced passive immunity in humans, and could be used for
prophylaxis and treatment.

32. TETANUS
ETIOLOGIC AGENT :
 C. tetani is an anaerobic, motile, gram-positive rod that
forms an oval, colorless, terminal spore and thus assumes
a shape resembling a tennis racket or drumstick.
 They can survive autoclaving at 121°C for 10–15 minutes.
EPIDEMIOLOGY :
 Occurs sporadically and almost always affect
1-unimmunized persons;
2-partially immunized persons
3- fully immunized individuals who fail to maintain
adequate immunity with booster doses of vaccine ).

33. TETANUS
EPIDEMIOLOGY :
 Approximately 57,000 deaths were caused by
tetanus globally in 2015.Of these, approximately
20,000 deaths occurred in neonates and 37,000
in older children and adults.

34. TETANUS
Pathogenesis :
 Tetanus toxin binds at the neuromuscular junction
and enters the motor nerve by endocytosis.
 It undergoes retrograde axonal transport to the
cytoplasm of the α-motoneuron.
 The toxin exits the motoneuron in the spinal cord
and enters adjacent spinal inhibitory interneurons,
where it prevents release of the neurotransmitters
glycine and γ aminobutyric acid (GABA).
 Thus blocks the normal inhibition of antagonistic
muscles on which voluntary coordinated movement
depends.
 As a consequence, affected muscles sustain maximal
contraction and cannot relax.

35. TETANUS
CLINICAL MANIFESTATIONS :
 The incubation period of tetanus is around 10
days (range 3–30 days).
Three forms of tetanus
 generalized tetanus (80%)
 Localized tetanus
 Cephalic tetanus - rare form seen in children with
otitis media.

36. TETANUS
Generalized tetanus :
 present with a descending pattern.
 The first sign most of the time is trismus or lockjaw.
 Headache, restlessness and irritability may be early
symptoms.
 stiffness of the neck, difficulty in swallowing and rigidity
of abdominal muscles.
 The rigidity of facial muscles leads to the sardonic smile
of tetanus.
 Rigidity and spasm of back and abdominal muscles causes
arching (opisthotonus).

38. TETANUS
Generalized tetanus :
 Laryngeal and respiratory muscle spasm can lead to
airway obstruction and asphyxia.
 Constipation and retention of urine may also occur.
 Hyperpyrexia, hypertension, excessive sweating,
tachycardia and cardiac arrhythmia can occur due
to sympathetic nerve involvement.
 Paralysis is evident in the first week, stabilizes in
second week and ameliorates in the next 1–4 weeks.

39. TETANUS
NEONATAL TETANUS :
 This typically occurs when the umbilical cord is cut
with an unsterilized instrument and manifests within
3–12 days of birth.
 It is generalized tetanus and often fatal.
 Progressive difficulty in feeding with associated
hunger and crying.
 stiffness to touch, spasms with or without
opisthotonos posturing.

40. TETANUS
Diagnosis :
 Mainly clinical.
 The typical setting is an injured unimmunized patient
or baby born to an unimmunized mother presenting
within 2 weeks with trismus, rigid muscles and clear
sensorium.
 The organism can be isolated from wound or ear
discharge.

41. TETANUS
Management :
 wound debridement.
 immunoglobulin administration.
 Antibiotics.
 supportive care.
 The aim of therapy is to neutralize all toxins, eradication of C.
tetani.
 Human tetanus immunoglobulin (TIG) 3,000–6,000 units IM is to
be given immediately.
 TIG has no effect on toxin which is already fixed to the neural
tissue and does not penetrate the blood-CSF barrier.
 It can neutralize circulating tetanospasmin.
 If TIG is not available, human IVIG can be used.

42. TETANUS
 Penicillin G 200,000 units/kg body weight can be given
intravenously in four divided doses for 10–14 days.
 Local wound, discharging ears, umbilical cord should be
cleaned and debrided.
 Diazepam is used formuscle relaxation and seizure
control.
 Initial dose is 0.1–0.2 mg/kg every 3–6 hours given
intravenously. Midazolam, baclofen can also be used.
 The best survival rates with generalized tetanus are
achieved with neuromuscular blocking agents like
vecuronium and pancuronium.
 Meticulous nursing care is needed. The patient should be
kept in a quiet, dark environment with minimum auditory
or visual stimuli.

43. TETANUS
Prevention :
 Tetanus is an entirely preventable disease.
 Active immunization is the best method to prevent
tetanus.
 All children should be immunized with three doses of
DPT at 6, 10 and 14 weeks followed by booster doses
at 18 months and 5 years of age. Boosters should be
given at 10 years and then every 10 years. Td or Tdap
is the vaccine of choice above 7 years of age.

44. THANK YOU