This document discusses diphtheria, an infectious disease caused by the bacteria Corynebacterium diphtheriae. It produces an exotoxin that can cause local infection in the throat and airways and lead to complications affecting the heart, kidneys and nerves if the toxin spreads systemically. Clinical manifestations depend on the site of infection and may include pseudomembrane formation. Diagnosis involves culture, microscopy and toxin testing. Treatment is with antitoxin to neutralize the toxin as well as antibiotics. Active immunization with diphtheria, tetanus and pertussis vaccine (DwPT or TdaP) provides protection.

1. 100 days Cough
Dr Deepak UpadhyayDr Deepak Upadhyay
Assistant Professor
Department of Community Medicine

2. Agent factors
• Bacteria – Bordetelle Pertussis
• Gram negative
• Small, ovoid, coco-bacillus
• Non motile, Non sporing
• Survival in environment – very short
• Produce Exotoxins (Toxin mediated
disease)

3. Agent factors (cont.)
 Reservoir – Human are only known reservoir
 Source of Infection – Cases (Clinical + Subclinical)
 Infective Material – Nasopharyngeal secretions
 Mode of transmission - Airborne droplets
 Period of Communicability – In the catarrhal stage and 3 weeks
after the onset of cough

4. Host Factors
 Females > Male
 Age Incidence
 Pre vaccination era - children birth to 5 years
of age (Preschool Children)
 Post vaccination introduction - in School going
children (5 - 10 yr)
 Immunity –
 Maternal antibodies – no role / no protection
 One attack – 90% immunity
 Secondary attack – 10% cases

5. Environmental factors
 Endemic disease with epidemic potential
 Epidemics during winter season.
 Incubation period – 7 – 14 days

6. PATHOGENESIS

7. Clinical Manifestations
 Three stages
 Catarrhal stage
 Paroxysmal stage
 Convalescent stage
 Catarrhal stage
 Insidious onset of coryza
 Sneezing
 Low grade fever
 Occasional cough
 Maximum infectivity
 Duration - 1-2 weeks (Appr. 10 days)

8. Clinical Manifestations (cont.)
 Paroxysmal cough stage
 Cough increases – distinctive bouts
 Violent spasms of continuous coughing (Paroxysm)
 At the end of paroxysm - long inspiratory effort (whoop)
 Whoop end with vomiting and occasional aspiration
 During episode of cough - Cyanosis followed by vomiting,
exhaustion and seizures

9. Clinical Manifestations (cont.)
 In between episodes child look well
 Cough increase for next 2-3 weeks and decreases over next 10
weeks
 Paroxysmal cough>2 weeks with or without whoop and/or post-
tussive vomiting is the hallmark feature of pertussis
Convalescence stage
period of gradual recovery even up to 6 months

10. Complications
 Due to increase intra abdominal pressure
 Hernias (inguinal / umbilical)
 Rectal prolapse
 Sub-conjuctival hemorrhage
 Subcutaneous emphysema
 Bronchopneumonia
 Atelectasis
 Neurological complications (due to the toxin or hypoxia or cerebral
hemorrhage)
 Seizures (1 in 100)
 Encephalopathy (1 in 300)

11. DIAGNOSIS
Suspected on the basis of history and clinical examination
Confirmed by culture, genomics or serology
1.Blood investigations
Elevated WBC count with lymphocytosis.
The absolute lymphocyte count of ≥20,000 is highly suggestive
1.Direct fluorescent antibody testing
IgA antibodies in nasal secretions
IgM antibodies against toxin

12. DIAGNOSIS
3. Culture and Microscopy:
 Gold standard specially in the
catarrhal stage.
 A saline nasal swab
 Swab from the nasopharynx
 Direct plate method
4. PCR:
 most sensitive
 can be done even after antibiotic
exposure.

13. TREATMENT
1. Avoidance of irritants, smoke and other cough promoting factors
2.2. Antibiotics:Antibiotics:
Erythromycin orally for 2 weeks
or
Azithromycin orally for 5 days
or
Clarithromycin orally for 7 days
3.3. Supportive treatmentSupportive treatment -Supplemental oxygen, hydration, cough
mixtures and bronchodilators (in individual cases)

14.  Active Prevention
 Children < 7 years
 DwPT (whole cell pertussis)
 Children > 7 years
 TdaP (acellular pertussis)
 Passive prevention
 By immunoglobulin
 Chemoprophylaxis
 Erythromycin

15. Dr Deepak UpadhyayDr Deepak Upadhyay
Assistant Professor
Department of Community Medicine

16. Agent factors
• Bacteria – Corynebacterium diptheriae (Klebs-
Loefflers bacilli)
• Gram positive
• Pleomorphic appearance (various shaps)
• Appear in pair ( Chinese letter )
• Contain metachromatic granules
• Survive in dust, freezing & drying
• Produce Exotoxins (Toxin mediated disease)
• 3 serotypes (Gravis, Intermedius & Mitis)

17. Agent factors (cont.)
 Reservoir – Human are only
known reservoir
 Source of Infection – Cases
(Clinical) + Carriers
 Infective Material
 Nasopharyngeal secretions
 Discharge from cutaneous
lesions
 Mode of transmission –
 Airborne droplets
 Direct contact to skin lesion
 Fomites
 Period of Communicability
 Cases – during clinical disease
 Carrier – remain infectious
up to 1 year

18. Host Factors
 Females > Male
 Age Incidence
 Pre vaccination era - children 6 months to 5 years of age
(Preschool Children)
 Post vaccination introduction - in School going children (5 -
10 yr)
 Immunity –
 Maternal antibodies – through milk
 70 % children develop immunity through subclinical
infection

19. Environmental factors
 Endemic disease with epidemic potential
 Epidemics during winter season.
 Incubation period – 7 – 14 days

20. PATHOGENESIS

21.  Local effect of diphtheritic toxin:
Paralysis of the palate and hypopharynx
Pneumonia
 Systemic effects (Toxin absorption ):
kidney tubule necrosis
myocarditis and/or demyelination of nerves
 Myocarditis:10-14 days
 Demyelination of nerves: 3-7 weeks

22. Clinical Manifestations
 Classification ( depend upon location):
 Nasal
 Pharyngeal (Faucial Diptheria)
 tonsilar
 laryngeal or laryngo-tracheal
 skin, eye or genitalia

23. Nasal Diphtheria
 Infection of the anterior nares
 More common among infants,
 Causes serosanguineous, purulent, erosive rhinitis with membrane
formation
 Shallow ulceration of the external nares and upper lip is
characteristic
 Unilateral nasal discharge is quite pathognomic of nasal diphtheria

24. Pharyngeal & Tonsilar diptheria
Sore throat is the universal early symptom
 Only half of patients have fever
 Dysphagia, hoarseness, malaise, or headache
 On examination
 Foul smell
 A yellowish membrane (Pseudomemdrane) on tonsils / pharyngeal
wall may extend to uvula, soft palate, posterior oropharynx,
hypopharynx, or glottic areas
 Erythema in adjacent areas
 Enlarged cervical lymph nodes: bull-neck appearance

26. Pseudo membrane

27.  Laryngeal diphtheria:
 Restless child with hoarseness of voice, cyanosis
(Fear of death)
 At significant risk for suffocation because of
local soft tissue edema and airway obstruction by
the diphtheritic membrane
 Classic cutaneous diphtheria is an indolent, non
progressive infection characterized by a
superficial, ecthymic, non healing ulcer with a
gray-brown membrane

28. COMPLICATIONS
1.1. Respiratory tract obstructionRespiratory tract obstruction by pseudomembranes
1.1. Toxic CardiomyopathyToxic Cardiomyopathy:
1. In 10-25% of patients
2. Responsible for 50-60% of deaths
3. Tachycardia out of proportion to fever
4. Prolonged PR interval and changes in the ST-T wave
5. Elevation of the serum aspartate aminotransferase
concentration closely parallels the severity of myonecrosis

29. 3.3. Toxic NeuropathyToxic Neuropathy:
 Hypoesthesia and soft palate paralysis
 Afterwards weakness of the posterior pharyngeal, laryngeal, and
facial nerves : a nasal quality in the voice, difficulty in swallowing and
risk for aspiration
 Cranial neuropathies (5th wk): oculomotor and ciliary paralysis-
strabismus, blurred vision, or difficulty with accommodation
 Symmetric polyneuropathy (10 days to 3 mo): motor deficits with
diminished deep tendon reflexes
 Monitoring for paralysis of the diaphragm muscle
Recovery from the neuritis is often slow but usually complete.
Corticosteroids are not recommended.

30. DIAGNOSIS
Suspected on the basis of history and clinical examination
Confirmed by culture, toxigenicity
1.Blood investigations
Elevated WBC count with lymphocytosis.
1.Toxigenicity testing
•Elek s Gel precipitation testing
•Shick test

31. Microscopy & Culture
 Specimen – throat swab
 Smear microscopic examinations
Gram s staining
Albert's stain
Immunoflorescent methods
 Cultures on
 Loeffers serum slope
 Tellurite Blood agar

32. TREATMENT
1. Antitoxin:
 Mainstay of therapy
 Neutralizes only free toxin, efficacy diminishes with elapsed
time
2. Antimicrobial therapy
 Halt toxin production, treat localized infection and prevent
transmission of the organism to contacts
Erythromycin
Or
aqueous crystalline penicillin G / procaine penicillin

33.  Active Prevention
 Children < 7 years
 DwPT (whole cell pertussis)
 Children > 7 years
 TdaP (acellular pertussis)
 Passive prevention
 By immunoglobulin
 Chemoprophylaxis
 Erythromycin (all contact)

34. DwPT
 Dose – 0.5 ml
 Route – Intramuscular
 Site – anterolateral thigh / deltoid region
 Schedule –
 Three primary doses – at 6, 10, 14 weeks
 Two booster doses – at 18 months & 5 years
 Side effects – Local pain, fever, swelling
 Diphtheria – Toxoid
 Tetanus – Toxoid
 Pertussis – Live whole
cell vaccine
 Adjuvant – Aluminum
Phosphate
 Preservative –
Thiomersal

35. TdaP
 Dose – 0.5 ml
 Route – Intramuscular
 Site – anterolateral thigh / deltoid region
 Schedule –
 Two primary doses – at 0 and 1 month
 Booster dose – at 6 month
 Side effects – Local pain, fever, swelling
 Diphtheria – Toxoid
 Tetanus – Toxoid
 Pertussis – acellular
pertussis (Killed)