Diphtheria, Pertussis, and Tetanus PDF

Diphtheria, Pertussis and Tetanus Presented by : DR. Omer Mohammed Dakeen Senior Pediatric specialist  DIPTHERIA Diphtheria is a potentially acute disease caused by exotoxin producing Corynebacterium diphtheriae, a Gram- positive bacillus. ...

Diphtheria, Pertussis and Tetanus Presented by : DR. Omer Mohammed Dakeen Senior Pediatric specialist  DIPTHERIA Diphtheria is a potentially acute disease caused by exotoxin producing Corynebacterium diphtheriae, a Gram- positive bacillus.  DIPTHERIA Epidemiology : Humans are the only natural reservoir of C. diphtheriae. Spread occurs in close-contact settings through respiratory droplets or direct contact with respiratory secretions or skin lesions. Diphtheria immunization protects against disease but does not prevent carriage. Vaccine-induced immunity to diphtheria wanes with time.  DIPTHERIA Pathogenesis : Corynebacterium diphtheriae is a nonmotile, non capsulated, club-shaped, gram-positive bacillus. Toxigenic strains are lysogenic for one of a family of corynebacteriophages that carry the structural gene for diphtheria toxin. Corynebacterium diphtheriae is classified into biotypes (mitis, intermedius, and gravis) according to colony morphology on tellurite containing media.  DIPTHERIA Pathogenesis : Corynebacterium diphtheriae colonizes the mucosal surface of the nasopharynx and multiplies locally without blood stream invasion. Released toxin causes local tissue necrosis with the formation of a tough, adherent pseudomembrane composed of a mixture of fibrin, dead cells, and bacteria. Toxin absorption can lead to systemic manifestations: kidney tubule necrosis, thrombocytopenia, cardiomyopathy, and demyelination of nerves.  DIPTHERIA Clinical Manifestations : Respiratory Tract Diphtheria : average incubation period is 2-4 days(range 1-10 days). anterior Nasal diphtheria. Pharyngeal and Tonsillar diphtheria: Sore throat Malaise mild-to-moderate fever grayish membrane Cervical adenopathy and soft tissue edema result in the typical bull neck appearance and stridor. Laryngeal diphtheria :manifested as hoarseness, stridor and dyspnea.  Cutaneous diphtheria : Classic cutaneous diphtheria is an indolent, nonprogressive infection characterized by a superficial , non healing ulcer with a gray-brown membrane.  Diagnosis : Specimens for culture should be obtained from the nose and throat and any other mucocutaneous lesion. Gram stain is used to accurately identify the organism. special stain like Albert’s stain, Ponders stain to detect metachromatic granular structure. selective media like tellurite agar or specially enriched Loeffler, Tinsdale medium.  Differential diagnosis : streptococcal and viral tonsillopharyngitis, infectious mononucleosis, Vincent’s angina, candidiasis acute epiglottitis.  Management : The goals of treatment : - neutralize the toxin rapidly. - eliminate the infecting organism. - provide supportive care. - prevent further transmission The mainstay of therapy is equine diphtheria antitoxin. A single dose ranging in quantity from 20,000 units for localized tonsillar diphtheria up to 100,000 units is given for extensive disease with severe toxicity. Route of administration :intramuscularly or intravenously  Management : Antimicrobial therapy : Erythromycin (40-50 mg/kg/day divided every 6 hr by mouth [PO] or intravenously [IV]; maximum 2 g/day). Aqueous crystalline penicillin G (100,000-150,000 units/kg/day divided every 6 hr IV or intramuscularly [IM]). Procaine penicillin (300,000units every 12 hr IM for those ≤10 kg in weight; 600,000 units every 12 hr IM for those >10 kg in weight) for14 days. Once oral medications are tolerated, oral penicillin V (250  Complications : Myocarditis. Conduction disturbances like ST-T wave abnormalities, arrhythmias, and heart block. Neurologic complications : cranial nerve palsies and polyneuritis , Palatal or pharyngeal paralysis.  Prognosis : depends on : The virulence of the organism. Patient age. Immunization status. Site of infection. Speed of administration of the antitoxin.  Prevention : immunization. minimum protective level for diphtheria antitoxin is 0.01-0.10 IU/mL. Asymptomatic Case Contacts : All house hold contacts and people who have had intimate respiratory or habitual physical contact with a patient are closely monitored for illness for 7 days. a single injectionof benzathine penicillinG(600,000 units IM forpatients 6 yr old) or erythromycin (40-50 mg/kg/day divided qid PO for 10 days. Pertussis  Pertussis is an infection of the respiratory tract characterized by a paroxysmal cough. Bordetella pertussis and Bordetella parapertussis cause whooping cough. Bacteria spread via aerosolized droplets from coughing of infected individuals. The global incidence is 48.5 million cases and 295,000 deaths annually. The case-fatality rate among infants in low-income countries is 4%. Neither natural infection, nor vaccination provides lifelong immunity.  Pathogenesis : Bordetella organisms are small, fastidious, gram- negative coccobacilli that colonize only ciliated epithelium. B. pertussis expresses pertussis toxin (PT), the major virulence protein. Tracheal cytotoxin, dermonecrotic factor, and adenylate cyclase are responsible for the local epithelial damage that produces respiratory symptoms and facilitates absorption of PT.  Clinical Manifestations : Incubation period 3-12 days (up to 21 days) Insidious onset, similar to minor upper respiratory infection with nonspecific cough Fever usually minimal throughout course Apnea & Cyanosis in infant  Clinical Manifestations : STAGES : 1st Stage- Catarrhal Stage 1 to 2 weeks ,URI, very contagious 2nd Stage- Paroxysmal Stage 1to 6 weeks , worsening cough ,post –tussive emesis, inspiratory whooping ,cyanosis, exhaustion. 3rd Stage - Covalescent Stage 2 to 3weeks, cough decreases, symptoms may return or woren.  Diagnosis : A pure or predominant complaint of cough. Cough of ≥14 days’ duration with at least 1 associated symptomof paroxysms, whoop, or post tussive vomiting has sensitivity of 81% and specificity of 58%. Pertussis should be suspected in older children whose cough illness is escalating at 7-10 days and whose coughing comes in bursts. Pertussis should be suspected in infants