Diptheria & pertussis

100 days Cough

Dr Deepak UpadhyayDr Deepak UpadhyayAssistant Professor

Department of Community Medicine

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)

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

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

Environmental factors Endemic disease with epidemic potential

Epidemics during winter season.

Incubation period – 7 – 14 days

PATHOGENESIS

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)

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

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

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)

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

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.

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)

Active Prevention Children < 7 years

DwPT (whole cell pertussis)

Children > 7 yearsTdaP (acellular pertussis)

Passive prevention By immunoglobulin

Chemoprophylaxis Erythromycin

Dr Deepak UpadhyayDr Deepak UpadhyayAssistant Professor

Department of Community Medicine

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)

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

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

Environmental factors Endemic disease with epidemic potential

Epidemics during winter season.

Incubation period – 7 – 14 days

PATHOGENESIS

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

Clinical Manifestations

Classification ( depend upon location): Nasal Pharyngeal (Faucial Diptheria) tonsilar laryngeal or laryngo-tracheal skin, eye or genitalia

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

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

Pseudo membrane

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

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

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.

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

Microscopy & Culture

Specimen – throat swab

Smear microscopic examinations Gram s stainingAlbert's stainImmunoflorescent methods

Cultures on Loeffers serum slope Tellurite Blood agar

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

Active Prevention Children < 7 years

DwPT (whole cell pertussis)

Children > 7 yearsTdaP (acellular pertussis)

Passive prevention By immunoglobulin

Chemoprophylaxis Erythromycin (all contact)

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

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)