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Diphtheria & Pertussis
Dr. S. A. Rizwan, M.D.,Assistant Professor,
Dept. of Community Medicine,VMCHRI, Madurai.
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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
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Introduction
• Two of the targets of DPT / PentaVac• Similar in many aspects• Rare but unacceptable• Indicators of immunization effectiveness• Potential for outbreaks
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DIPHTHERIAGreek diphtérite ‘leather or hide’ - describes the coating in the throat
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History
• 5th century BC - recognized by Hippocrates • 6th century AD - epidemics described • 1883 - C. diphtheriae described by Klebs • 1920s - Toxoid developed
• Known ‘Strangling Angel of Children’
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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
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Agent (contd.)
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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
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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
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Environment
• Winter favours spread• Occurs in all seasons
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Clinical features
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Pharngotonsillar type
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Pharngotonsillar type
• Sore throat, difficulty in swallowing , low grade fever.
• Mild erythema, localised exudate , pseudo membrane.
• Severe forms : “Bull necked” appearance
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Laryngotracheal type
• Most severe form• Hoarseness of voice • Croupy cough• Obstruction by
membrane leading to prostration and dyspnoea
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Nasal type
• Mildest form• Localised to septum / turbinates• Nasal carriers are dangerous than throat
carriers
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Other forms
• Skin: on fingers & back of the hands, punched out ulcers
• Ocular: conjunctival, corneal damage• Intestinal: Dysphagia & bloody diarrhoea• Genital
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Cutaneous type
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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
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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
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Treatment
• Isolation • Neutralization of free circulating toxin by
administration of Antitoxin• Antibiotics to eliminate bacteria• Supportive and symptomatic therapy• Management of complications
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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
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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
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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
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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
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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
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Treatment of carriers
• The carriers should be treated with 10 day course of oral erythromycin
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Prevention
Four key strategies:1. Ensuring high population immunity2. Strengthened surveillance3. Early diagnosis and case management4. Rapid investigation and management of
contacts
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DPT vaccine• 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
– Additional boosters (dT) every 10 years
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PERTUSSIS / WHOOPING COUGHLatin per ‘extremely’ + tussis ‘cough’
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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
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How does a ‘whoop’ sound?
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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
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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
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Host
• Females > Male• Age Incidence
– Post vaccination introduction - in school going children (5–10 years)
• Immunity– Maternal antibodies offer no protection– Secondary attack 80%
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Environment
• Endemic disease with epidemic potential• Epidemics during winter season
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Pathogensis
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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)
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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
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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)
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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
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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
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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
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Prevention
• Cases and contacts– Early detection, isolation, treatment of cases– Isolation until the case is considered non-
infectious– For contacts, prophylactic antibiotics
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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
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Comparative study - 1Feature 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 carrierSubclinical 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,
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Comparative study - 2Feature Diphtheria Pertussis
Incubation 2-6 days 7-14 days
Clinical features 3 typesPahryngotonsillar, laryngotracheal, nasal(Also, cutaneous, conjuctival)
Pseudomembrane, bullneck, suffocation, punched ulcer
3 stagesCatarrhal, Paroxysmal, convalescent
Complications Distant multi-organ toxic damage, paralysis, myocarditis,
Deaths 5-10%
Bronchitis, bronchopneumonia, bronchiectasis, haemorrhages, convulsions, coma,Death 1%
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Comparative study - 3Feature Diphtheria Pertussis
Control Cases CarriersContactsCommunity
CasesContacts Community
For cases, carriersEarly detectionIsolation – 14 days till culture -veTreatment: cases - antitoxin, erythromycin Carriers - erythromycin
For casesEarly detectionIsolation – till non-infectiousTreatment: cases – erythromycin
For contactsRecently immunised – no action Not recently immunised - active immunization + prop. erythromycinSurveillance
For contactsprop. Erythromycin 10 days
For community Active immunisation
For community Active immunisation
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Comparative study - 4Feature Diphtheria Pertussis
Vaccination Active immunization Active immunization
Vaccine is only a toxoidOnly prevents the disease not infection, no herd immunity.So immunization coverage needs to be high
Acellular or whole cell componentsMay decrease pharyngeal colonisation
Pentavalent vaccinePrimary doses – 6, 10, 14 weeksDPT vaccine Booster 1 – 16-24 months Booster 2 – 5-6 years
Pentavalent vaccinePrimary doses – 6, 10, 14 weeksDPT vaccine Booster 1 – 16-24 months Booster 2 – 5-6 years
Passive immunizationDiphtheria antitoxin – horse serum
Not effective so far
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REVIEW
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Review 1
• True about diphtheria are all excepta) Carriers are commoner SOI than casesb) IB is 2-6 daysc) 25 Lf of diphtheria toxoid is present in 1ml of
DPT vaccined) Diphtheria is endemic in India
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Review 2
• Positive Schick test indicatesa) Immunity to diphtheriab) Susceptibility to diphtheriac) Infection with diphtheriad) Hypersensitivity to diphtheria
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Review 3
• The level of herd immunity required to prevent epidemics of diphtheria is a) 50%b) 55%c) 60%d) 65%e) 70%
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Review 4
• Treatment of choice for diphtheria carriersa) Erythromycinb) Tetracyclinec) Penicillind) DPT
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Review 5
• Schick test does not indicatea) Immunity to diphtheriab) Susceptibility to diphtheriac) Carrier of diphtheriad) Hypersensitivity to diphtheria
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Review 6
• Diphtheria carrier is diagnosed bya) Throat cultureb) Gram stainingc) Albert’s stainingd) Schick test
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Review 7
• A negative Schick test indicatesa) Immunity to diphtheriab) Susceptibility to diphtheriac) Immunity to Pertussisd) Immunity to Mumps
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Review 8
• Usual incubation period of pertussisa) 7-14 daysb) 2-6 daysc) Less than 10 daysd) Less than 3 weeks
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Review 9
• True regarding pertussis is a) Neurological complication of DPT is 1 in 50,000b) Vaccine efficacy is >95%c) Erythromycin prevents the spread of disease d) Leucocytosis correlates with severity of cough
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Review 10
• True regarding pertussis is all excepta) Associated with inspiratory whoopb) Droplet infectionc) Parapertussis is more severe than pertussisd) Pneumonia is the commonest complication
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Review 11
• Treatment of pertussis contacts is a) Prophylactic oral antibiotics for 10 daysb) Parenteral antibiotics for 10 daysc) DPT vaccinationd) Diphtheria antitoxine) Pertussis antitoxin
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Review 12
• Pertussis case should be isolated fora) 1-2 weeksb) 3-4 weeksc) 4-5 weeksd) Till the patient is considered non infectious
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Review 13
• True about Pertussis isa) Secondary attack rate 90%b) Has cross immunity with parapertussisc) Most infectious during paroxysmal staged) Affects humans, animals and insects
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THANK YOU
