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Diptheria & pertussis

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Epidemiology of Diptheria & Pertussis, diagnostic investigations and control of these

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Diptheria & pertussis

  1. 1. 100 days Cough Dr Deepak UpadhyayDr Deepak Upadhyay Assistant Professor Department of Community Medicine
  2. 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. 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. 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. 5. Environmental factors  Endemic disease with epidemic potential  Epidemics during winter season.  Incubation period – 7 – 14 days
  6. 6. PATHOGENESIS
  7. 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. 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. 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. 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. 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. 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. 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. 14.  Active Prevention  Children < 7 years  DwPT (whole cell pertussis)  Children > 7 years  TdaP (acellular pertussis)  Passive prevention  By immunoglobulin  Chemoprophylaxis  Erythromycin
  15. 15. Dr Deepak UpadhyayDr Deepak Upadhyay Assistant Professor Department of Community Medicine
  16. 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. 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. 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. 19. Environmental factors  Endemic disease with epidemic potential  Epidemics during winter season.  Incubation period – 7 – 14 days
  20. 20. PATHOGENESIS
  21. 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. 22. Clinical Manifestations  Classification ( depend upon location):  Nasal  Pharyngeal (Faucial Diptheria)  tonsilar  laryngeal or laryngo-tracheal  skin, eye or genitalia
  23. 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. 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
  25. 25. Pseudo membrane
  26. 26.  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
  27. 27. 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
  28. 28. 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.
  29. 29. 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
  30. 30. Microscopy & Culture  Specimen – throat swab  Smear microscopic examinations Gram s staining Albert's stain Immunoflorescent methods  Cultures on  Loeffers serum slope  Tellurite Blood agar
  31. 31. 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
  32. 32.  Active Prevention  Children < 7 years  DwPT (whole cell pertussis)  Children > 7 years  TdaP (acellular pertussis)  Passive prevention  By immunoglobulin  Chemoprophylaxis  Erythromycin (all contact)
  33. 33. 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
  34. 34. 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)

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