Diptheria & pertussis
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Transcript of Diptheria & pertussis
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100 days Cough
Dr Deepak UpadhyayDr Deepak UpadhyayAssistant Professor
Department of Community Medicine
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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)
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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
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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 protectionOne attack – 90% immunitySecondary attack – 10% cases
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Environmental factors Endemic disease with epidemic potential
Epidemics during winter season.
Incubation period – 7 – 14 days
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PATHOGENESIS
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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)
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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
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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
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Complications Due to increase intra abdominal pressure
Hernias (inguinal / umbilical)Rectal prolapseSub-conjuctival hemorrhageSubcutaneous emphysema
Bronchopneumonia Atelectasis Neurological complications (due to the toxin or hypoxia or
cerebral hemorrhage)Seizures (1 in 100) Encephalopathy (1 in 300)
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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
2.Direct fluorescent antibody testing IgA antibodies in nasal secretionsIgM antibodies against toxin
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DIAGNOSIS3. 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.
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TREATMENT1. Avoidance of irritants, smoke and other cough promoting
factors2.2. Antibiotics: Antibiotics:
Erythromycin orally for 2 weeksor
Azithromycin orally for 5 daysor
Clarithromycin orally for 7 days
3.3. Supportive treatment Supportive treatment -Supplemental oxygen, hydration, cough mixtures and bronchodilators (in individual cases)
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Active Prevention Children < 7 years
DwPT (whole cell pertussis)
Children > 7 yearsTdaP (acellular pertussis)
Passive prevention By immunoglobulin
Chemoprophylaxis Erythromycin
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Dr Deepak UpadhyayDr Deepak UpadhyayAssistant Professor
Department of Community Medicine
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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)
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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
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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
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Environmental factors Endemic disease with epidemic potential
Epidemics during winter season.
Incubation period – 7 – 14 days
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PATHOGENESIS
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Local effect of diphtheritic toxin:Paralysis of the palate and hypopharynxPneumonia
Systemic effects (Toxin absorption ): kidney tubule necrosismyocarditis and/or demyelination of nerves
Myocarditis:10-14 days Demyelination of nerves: 3-7 weeks
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Clinical Manifestations
Classification ( depend upon location): Nasal Pharyngeal (Faucial Diptheria) tonsilar laryngeal or laryngo-tracheal skin, eye or genitalia
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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
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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
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Pseudo membrane
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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
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COMPLICATIONS
1.1. Respiratory tract obstruction Respiratory tract obstruction by pseudomembranes
1.1. Toxic CardiomyopathyToxic Cardiomyopathy: 1. In 10-25% of patients2. Responsible for 50-60% of deaths3. Tachycardia out of proportion to fever4. Prolonged PR interval and changes in the ST-T wave5. Elevation of the serum aspartate aminotransferase
concentration closely parallels the severity of myonecrosis
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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 muscleRecovery from the neuritis is often slow but usually complete.
Corticosteroids are not recommended.
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DIAGNOSIS
Suspected on the basis of history and clinical examination
Confirmed by culture, toxigenicity
1.Blood investigations Elevated WBC count with lymphocytosis.
2.Toxigenicity testing•Elek s Gel precipitation testing•Shick test
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Microscopy & Culture
Specimen – throat swab
Smear microscopic examinations Gram s stainingAlbert's stainImmunoflorescent methods
Cultures on Loeffers serum slope Tellurite Blood agar
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TREATMENT
1. Antitoxin: Mainstay of therapy Neutralizes only free toxin, efficacy diminishes with
elapsed time2. Antimicrobial therapy
Halt toxin production, treat localized infection and prevent transmission of the organism to contacts
ErythromycinOr
aqueous crystalline penicillin G / procaine penicillin
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Active Prevention Children < 7 years
DwPT (whole cell pertussis)
Children > 7 yearsTdaP (acellular pertussis)
Passive prevention By immunoglobulin
Chemoprophylaxis Erythromycin (all contact)
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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
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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)