Diphtheria and pertussis (whooping cough)

A primer on diphtheria and pertussis infections

1. Diphtheria & Pertussis Dr. S. A. Rizwan, M.D., Assistant Professor, Dept. of Community Medicine, VMCHRI, Madurai.

2. Learning objectives At the end of this lecture you sh be able to Describe the epidemiological determinants of Diphtheria and Pertussis Describe their prevention and control measures Understand their current public health importance in India and the world 2

3. Introduction Two of the targets of DPT / PentaVac Similar in many aspects Rare but unacceptable Indicators of immunization effectiveness Potential for outbreaks 3

4. DIPHTHERIA Greek diphtérite ‘leather or hide’ - describes the coating in the throat 4

5. History 5 th century BC - recognized by Hippocrates 6 th century AD - epidemics described 1883 - C . diphtheriae described by Klebs 1920s - Toxoid developed Known ‘ Strangling Angel of Children ’ 5

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7. Agent Gram positive rod No invasive power Powerful exotoxin 4 types : gravis, mitis , belfanti , intermedius Beta phage Sensitive to penicillin/heat/chemical agents Toxin mediated disease 7

8. Agent (contd.) 8

9. Agent (contd.) Infective material : nasopharyngeal secretion, skin lesion Period of infectivity : 14 to 28 days from onset Mode of transmission : droplet, direct Portal of entry : respiratory & non-respiratory Incubation period : 2 – 6 days 9

10. Host Children aged 1 to 5 shift in age due to immunisation Both sexes are affected Immunity : maternal antibodies, inapparent infection Resistance to disease : depends on neutralizing antitoxin 10

11. Environment Winter favours spread Occurs in all seasons 11

12. Clinical features 12

13. Pharngotonsillar type 13

14. Pharngotonsillar type Sore throat, difficulty in swallowing , low grade fever. Mild erythema, localised exudate , pseudo membrane. Severe forms : “ Bull necked” appearance 14

15. Laryngotracheal type Most severe form Hoarseness of voice Croupy cough Obstruction by membrane leading to prostration and dyspnoea 15

16. Nasal type Mildest form Localised to septum / turbinates Nasal carriers are dangerous than throat carriers 16

17. Other forms Skin : on fingers & back of the hands, punched out ulcers Ocular : conjunctival, corneal damage Intestinal : Dysphagia & bloody diarrhoea Genital 17

18. Cutaneous type 18

19. Distant effects of toxin Necrosis in heart muscle, liver, kidneys, and adrenals Nerve damage, paralysis of the soft palate, eye muscles, or extremities Recovery is complete if cured 19

20. Diagnosis Clinical examination Direct microscopy using Albert’s stain Culture ( Loeffler’s serum slope ) Flourescent Ab technique Toxigenicity testing by Elek’s gel ppt Diagnosis of susceptibility by Shick test 20

21. Treatment Isolation Neutralization of free circulating toxin by administration of Antitoxin Antibiotics to eliminate bacteria Supportive and symptomatic therapy Management of complications 21

22. Isolation All cases should be promptly isolated for at least 14 days or until proved free of infection At least 2 consecutive samples taken from sites of lesions taken 24 hr apart should be negative before terminating isolation 22

23. Antitoxin Antitoxin interferes with the action of toxin and modifies the attack Dosage depends on severity of lesions 20,000 to 1,20,000 units 23

24. Antibiotics To terminate toxin production To limit proliferation of bacteria To prevent spread of organism to contacts To prevent development of carrier state Penicillin, erythromycin 24

25. Supportive therapy Bed rest for 2-3 weeks Avoid sudden exertion Observe the pt. closely for changes in rate & rhythm of heart Antipyretics & sedatives may be given if required Easily digestible high calorie diet should be advised 25

26. Treatment of contacts Based on immunity status Contacts should be placed under medical surveillance & examined daily for evidence of diphtheria for atleast a week after exposure 26

27. Treatment of carriers The carriers should be treated with 10 day course of oral erythromycin 27

28. Prevention Four key strategies: E nsuring high population immunity S trengthened surveillance Early diagnosis and case management Rapid investigation and management of contacts 28

29. DPT vaccine R oute: deep im injection S ite: lateral aspect of thigh D ose: 0.5 ml I nterval of doses: 4 weeks Schedule: DPT 1, 2, 3: 6, 10, 14 weeks (recently, Pentavalent vaccine ) Booster 1: 18-24 months Booster 2: 5-6 years Additional boosters ( dT ) every 10 years 29

30. PERTUSSIS / Whooping cough Latin   per ‘ extremely ’ +   tussis   ‘cough ’ 30

31. History 1578 - First epidemic (by Guillaume de Baillou ) 1906 - Bordet and Gengou isolated 1930-40s - Vaccine development started ‘ Whoop ’ loud crowing inspiration Hundred day cough – Chinese 31

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33. How does a ‘whoop’ sound? 33

34. Agent Bordetella Pertussis Gram negative Small, ovoid, coco-bacillus Non-motile , Non- sporing Survival in environment – very short Produce exotoxins and endotoxins, toxin-mediated disease 34

35. Agent Reservoir – human are only known reservoir Source of Infection – cases Infective Material – nasopharyngeal secretions Mode of transmission - droplet Period of Communicability – 1 week after exposure to 3 weeks after the onset of cough Incubation period : 7 – 14 days 35

36. Host Females > Male Age Incidence Post vaccination introduction - in s chool going children ( 5–10 years) Immunity Maternal antibodies offer no protection Secondary attack 8 0% 36

37. Environment Endemic disease with epidemic potential Epidemics during winter season 37

38. Pathogensis 38

39. Clinical features Three stages: catarrhal, paroxysmal, convalescent 1. Catarrhal stage Insidious onset of coryza Sneezing Low grade fever Occasional cough Maximum infectivity Duration - 1-2 weeks ( Approx. 10 days) 39

40. Clinical features 2. 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 Lasts for 2-4 weeks 3. Convalescence stage Period of gradual recovery even up to 6 months 40

41. 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 ) 41

42. Diagnosis Suspected on the basis of history and clinical examination Confirmed by culture, genomics or serology Blood investigations Elevated WBC count with lymphocytosis. The absolute lymphocyte count of ≥20,000 is highly suggestive Direct fluorescent antibody testing IgA antibodies in nasal secretions IgM antibodies against toxin 42

43. Diagnosis Culture and Microscopy Gold standard specially in the catarrhal stage A saline nasal swab Swab from the nasopharynx Direct plate method PCR most sensitive can be done even after antibiotic exposure 43

44. Treatment Avoidance of irritants, smoke and other cough promoting factors Antibiotics : Erythromycin orally for 2 weeks or Azithromycin orally for 5 days or Clarithromycin orally for 7 days or Supportive treatment: Supplemental oxygen, hydration, cough mixtures, bronchodilator 44

45. Prevention Cases and contacts Early detection, isolation, treatment of cases Isolation until the case is considered non-infectious For contacts, prophylactic antibiotics 45

46. Prevention: Active immunisation Route : deep im injection Site: lateral aspect of thigh Dose: 0.5 ml Interval of doses: 4 weeks Schedule: DPT 1, 2, 3: 6, 10, 14 weeks (recently, Pentavalent vaccine ) Booster 1: 18-24 months Booster 2: 5-6 years 46

47. Comparative study - 1 Feature Diphtheria Pertussis Disease Acute infection, capable of outbreaks Acute infection, capable of outbreaks Burden In thousands In lakhs Agent Corynebacterium diphtheriae Bordetella pertussis SOI Case or carrier Subclinical cases exist Case, no carrier state , No subclinical infection Infective material Nasopharyngeal secretions, Skin lesions Nasopharyngeal secretions Period of inf. 4 weeks from onset 3 weeks from paroxysmal stage Pathogenesis Not invasive, toxin mediated Not invasive, toxin mediated Age group Children Children Environmental All seasons All seasons, esp. winter MOT Droplet infection, direct contact, fomites Droplet infection, direct contact, 47

48. Comparative study - 2 Feature Diphtheria Pertussis Incubation 2-6 days 7-14 days Clinical features 3 types Pahryngotonsillar , laryngotracheal , nasal (Also, cutaneous, conjuctival ) Pseudomembrane , bullneck , suffocation, punched ulcer 3 stages Catarrhal, Paroxysmal, convalescent Complications Distant multi-organ toxic damage, paralysis, myocarditis, Deaths 5-10% Bronchitis, bronchopneumonia, bronchiectasis, haemorrhages , convulsions, coma, Death 1% 48

49. Comparative study - 3 Feature Diphtheria Pertussis Control Cases Carriers Contacts Community Cases Contacts Community For cases, carriers Early detection Isolation – 14 days till culture - ve Treatment: cases - antitoxin, erythromycin Carriers - erythromycin For cases Early detection Isolation – till non-infectious Treatment: cases – erythromycin For contacts Recently immunised – no action Not recently immunised - active immunization + prop. erythromycin Surveillance For contacts prop. Erythromycin 10 days For community Active immunisation For community Active immunisation 49

50. Comparative study - 4 Feature Diphtheria Pertussis Vaccination Active immunization Active immunization Vaccine is only a toxoid Only prevents the disease not infection, no herd immunity. So immunization coverage needs to be high Acellular or whole cell components May decrease pharyngeal colonisation Pentavalent vaccine Primary doses – 6, 10, 14 weeks DPT vaccine Booster 1 – 16-24 months Booster 2 – 5-6 years Pentavalent vaccine Primary doses – 6, 10, 14 weeks DPT vaccine Booster 1 – 16-24 months Booster 2 – 5-6 years Passive immunization Diphtheria antitoxin – horse serum Not effective so far 50

51. Review 51

52. Review 1 True about diphtheria are all except Carriers are commoner SOI than cases IB is 2-6 days 25 Lf of diphtheria toxoid is present in 1ml of DPT vaccine Diphtheria is endemic in India 52

53. Review 2 Positive Schick test indicates Immunity to diphtheria Susceptibility to diphtheria Infection with diphtheria Hypersensitivity to diphtheria 53

54. Review 3 The level of herd immunity required to prevent epidemics of diphtheria is 50% 55% 60 % 65% 70% 54

55. Review 4 Treatment of choice for diphtheria carriers Erythromycin Tetracycline Penicillin DPT 55

56. Review 5 Schick test does not indicate Immunity to diphtheria Susceptibility to diphtheria Carrier of diphtheria Hypersensitivity to diphtheria 56

57. Review 6 Diphtheria carrier is diagnosed by Throat culture Gram staining Albert’s staining Schick test 57

58. Review 7 A negative Schick test indicates Immunity to diphtheria Susceptibility to diphtheria Immunity to Pertussis Immunity to Mumps 58

59. Review 8 Usual incubation period of pertussis 7-14 days 2-6 days Less than 10 days Less than 3 weeks 59

60. Review 9 True regarding pertussis is Neurological complication of DPT is 1 in 50,000 Vaccine efficacy is >95% Erythromycin prevents the spread of disease Leucocytosis correlates with severity of cough 60

61. Review 10 True regarding pertussis is all except Associated with inspiratory whoop Droplet infection Parapertussis is more severe than pertussis Pneumonia is the commonest complication 61

62. Review 11 Treatment of pertussis contacts is Prophylactic oral antibiotics for 10 days Parenteral antibiotics for 10 days DPT vaccination Diphtheria antitoxin Pertussis antitoxin 62

63. Review 12 Pertussis case should be isolated for 1-2 weeks 3-4 weeks 4-5 weeks Till the patient is considered non infectious 63

64. Review 13 True about Pertussis is Secondary attack rate 90% Has cross immunity with parapertussis Most infectious during paroxysmal stage Affects humans, animals and insects 64

65. Thank you 65