Presentation is loading. Please wait.

Presentation is loading. Please wait.

DIPHTHERIA, PERTUSSIS & TETANUS Dr Sarika Gupta, Asst. Professor.

Similar presentations


Presentation on theme: "DIPHTHERIA, PERTUSSIS & TETANUS Dr Sarika Gupta, Asst. Professor."— Presentation transcript:

1 DIPHTHERIA, PERTUSSIS & TETANUS Dr Sarika Gupta, Asst. Professor

2 Diphtheria (Corynebacterium diphtheriae) Diphtherais Greek word for leather Bull-neck appearance of diphtheritic cervical lymphadenopathy

3 INTRODUCTION  An acute toxic infection caused by Corynebacterium diphtheriae and rarely toxigenic strains of Corynebacterium ulcerans  aerobic, nonencapsulated, non–spore-forming, mostly nonmotile, pleomorphic, gram-positive bacilli  Differentiation of C. diphtheriae from C. ulcerans is based on urease activity, C. ulcerans is urease-positive  Four C. diphtheriae biotypes - mitis, intermedius, belfanti, gravis; differentiated by colonial morphology, hemolysis, and fermentation reactions

4 INTRODUCTION  Diphtheritic toxin production occurs only after acquisition of a lysogenic Corynebacteriophage by either C. diphtheriae or C. ulcerans, which encodes the diphtheritic toxin gene and confers diphtheria-producing potential on these strains  Demonstration of diphtheritic toxin production or potential for toxin production by an isolate is necessary to confirm disease  The former is done in vitro using the agar immunoprecipitin technique (Elek test) or in vivo with the toxin neutralization test in guinea pigs, the latter by polymerase chain reaction testing for carriage of the toxin gene  Toxin is lethal in human beings in an amount 130μg/kg BW

5 EPIDEMIOLOGY  Transmission: airborne respiratory droplets, direct contact with respiratory secretions of symptomatic individuals, or exudates from infected skin lesions  Asymptomatic respiratory tract carriage is important in transmission. Where diphtheria is endemic, 3-5% of healthy individuals can carry toxigenic organisms  Diphtheria is endemic in INDIA.  Skin infection and skin carriage are silent reservoirs and organisms can remain viable in dust or on fomites for up to 6 months  Transmission through contaminated milk and an infected food handler has been documented

6 EPIDEMIOLOGY  Children aged 1-5yrs are commonly infected  A herd immunity of 70% is required to prevent epidemics  Contaminated objects like thermometers, cups, spoons, toys and pencils can spread the disease  Overcrowding, poor sanitation and hygiene, illiteracy, urban migration and close contacts can lead to outbreak

7 PATHOGENESIS Within the first few days of respiratory tract infection, a dense necrotic coagulum of organisms, epithelial cells, fibrin, leukocytes and erythrocytes forms, advances, and becomes a gray-brown, leather-like adherent pseudomembrane. Removal is difficult and reveals a bleeding edematous submucosa The major virulence of the organism lies in its ability to produce the potent 62-kd polypeptide exotoxin, which inhibits protein synthesis and causes local tissue necrosis Entry into nose or mouth The organism remains in the superficial layers of skin lesions or respiratory tract mucosa, inducing local inflammatory reaction

8  Local effect of diphtheritic toxin:  Paralysis of the palate and hypopharynx  Pneumonia  Systemic effects (Toxin absorption ):  kidney tubule necrosis  hypoglycemia  myocarditis and/or demyelination of nerves  Myocarditis:10-14 days  Demyelination of nerves: 3-7 weeks

9 CLINICAL MANIFESTATIONS  Influenced by the anatomic site of infection, the immune status of the host and the production and systemic distribution of toxin  Incubation period: 1-6 days  Classification (location):  nasal  pharyngeal  tonsillar  laryngeal or laryngotracheal  skin, eye or genitalia

10 CLINICAL MANIFESTATIONS  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  Accurate diagnosis of nasal diphtheria delayed-paucity of systemic signs and symptoms

11  Tonsillar and pharyngeal diphtheria: sore throat is the universal early symptom  Only half of patients have fever and fewer have dysphagia, hoarseness, malaise, or headache  Mild pharyngeal injection unilateral or bilateral tonsillar membrane formation extend to involve the uvula, soft palate, posterior oropharynx, hypopharynx, or glottic areas  Underlying soft tissue edema and enlarged lymph nodes: bull- neck appearance

12

13  Laryngeal diphtheria: At significant risk for suffocation because of local soft tissue edema and airway obstruction by the diphtheritic membrane  Classic cutaneous diphtheria is an indolent, nonprogressive infection characterized by a superficial, ecthymic, nonhealing ulcer with a gray-brown membrane

14 Infection at Other Sites: ear (otitis externa), the eye (purulent and ulcerative conjunctivitis), the genital tract (purulent and ulcerative vulvovaginitis) and sporadic cases of pyogenic arthritis Diagnosis  Clinical features  Culture: from the nose and throat and any other mucocutaneous lesion. A portion of membrane should be removed and submitted for culture along with underlying exudate  Elek test: rapid diagnosis (16-24 hrs)

15  Enzyme immunossay  PCR for A or B portion of the toxic gene “tox”  Hypoglycemia, glycosuria, BUN, or abnormal ECG for liver, kidney and heart involvement Differential diagnosis: 1. Common cold 2. Congenital syphilis snuffle 3. Sinusitis 4. Adenoiditis and foreign body in nose 5. Streptococcal pharyngitis 6. Infectious mononucleosis

16 COMPLICATIONS 1. Respiratory tract obstruction by pseudomembranes: bronchoscopy or intubation and mechanical ventilation 2. Toxic Cardiomyopathy: -in 10-25% of patients -responsible for 50-60% of deaths -the risk for significant complications correlates directly with the extent and severity of exudative local oropharyngeal disease as well as delay in administration of antitoxin -Tachycardia out of proportion to fever -prolonged PR interval and changes in the ST-T wave -Elevation of the serum aspartate aminotransferase concentration closely parallels the severity of myonecrosis

17 3. Toxic Neuropathy:  Acutely or 2-3 wk after: 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.

18 TREATMENT 1. Antitoxin:  Mainstay of therapy  Neutralizes only free toxin, efficacy diminishes with elapsed time  Antitoxin is administered as a single empirical dose of 20, ,000 U based on the degree of toxicity, site and size of the membrane, and duration of illness 2. Antimicrobial therapy  Halt toxin production, treat localized infection and prevent transmission of the organism to contacts  erythromycin (40-50 mg/kg/day 6 hrly [PO] or [IV]), aqueous crystalline penicillin G (100, ,000 U/kg/day 6 hrly IV or [IM]), or procaine penicillin (25,000-50,000 U/kg/day 12 hrly IM) for 14 days

19  Elimination of the organism should be documented by negative results of at least 2 successive cultures of specimens from the nose and throat (or skin) obtained 24 hr apart after completion of therapy  Prognosis: depends on the virulence of the organism (subspecies gravis), patient age, immunization status, site of infection and speed of administration of the antitoxin  The case fatality rate of almost 10% for respiratory tract diphtheria  At recovery, administration of diphtheria toxoid is indicated to complete the primary series or booster doses of immunization, because not all patients develop antibodies to diphtheritic toxin after infection

20 PREVENTION Asymptomatic Case Contacts:  Antimicrobial prophylaxis -erythromycin (40-50 mg/kg/day divided qid PO for 10 days) or a single injection of benzathine penicillin G (600,000U IM for patients <30 kg, 1,200,000U IM for patients ≥30 kg)  Diphtheria toxoid vaccine-to immunized individuals who have not received a booster dose within 5 yr. Children who have not received their 4th dose should be vaccinated. Those who have received fewer than 3 doses of diphtheria toxoid or who have uncertain immunization status are immunized with an age-appropriate preparation on a primary schedule Asymptomatic Carriers:  Same+Repeat cultures are performed about 2 wk after completion of therapy. if results are positive, an additional 10-day course of oral erythromycin should be given and follow-up cultures performed VACCINE

21 W hooping cough: whooping sound made when gasping for air after a fit of coughing Cough of 100 days PERTUSSIS (WHOOPING COUGH)

22 INTRODUCTION  A highly contagious acute bacterial infection caused by the bacilli Bordetella pertussis  Currently worldwide prevalence is diminished due to active immunization  However it remains a public health problem among older children and adults  It continues to be an important respiratory disease afflicting unvaccinated infants and previously vaccinated children and adults (waning immunity)

23 EPIDEMIOLOGY  Transmission: through the respiratory route in the form of droplet infection  Adolescents and adults are the reservoir. No animal or insect reservoir  A highly communicable disease. SAR 80% among households contacts  In the catarrhal stage and 2 weeks after the onset of cough

24 ETIOLOGY  Bordetella pertussis – aerobic gram-negative coccobacilli  Produces toxins namely pertussis toxin, filamentous hemagglutinin, hemolysin, adenylate cyclase toxin, dermonecrotic toxin and tracheal cytotoxin- responsible for clinical features (toxin mediated disease) and the immunity

25 PATHOGENESIS -This exudate predisposes to atelectasis, cough, cyanosis and pneumonia -Organism causes local tissue damage and systemic effects mediated through its toxin The organism get attached to the respiratory cilia and toxin causes paralysis of cilia muocopurulent-sanguineous exudate forms in the respiratory tract

26 CLINICAL MANIFESTATIONS  Incubation period: 7-10 days  Infection lasts for 6 weeks – 10 weeks  Stage I (catarrhal stage; 1-2 weeks): insidious onset of coryza, sneezing, low grade fever and occasional cough  Stage II (paroxysmal cough stage; 1-6 weeks): due to difficulty in expelling the thick mucous form the tracheobronchial tree  At the end of paroxysm long inspiratory effort is followed by a whoop  In between episodes child look well. During episode of cough the child may become cyanosed, followed by vomiting, exhaustion and seizures

27 CLINICAL MANIFESTATIONS  Cough increase for next 2-3 weeks and decreases over next 10 weeks  Absence of whoop and/or post-tussive vomiting does not rule out clinical diagnosis of pertussis paroxysmal cough>2 weeks with or without whoop and/or post-tussive vomiting is the hallmark feature of pertussis  Stage III (convalecence stage): period of gradual recovery even up to 6 months

28 COMPLICATIONS 1. Secondary pneumonia (1 in 5) and apneic spells (50%; neonates and infant<6 months of age) 2. Neurological complications: seizures (1 in 100) and encephalopathy (1 in 300) due to the toxin or hypoxia or cerebral hemorrhage 3. Otitis media, anorexia and dehydration, rib frcture, pneumothorax, subdural hematoma, hernia and rectal prolapse Differential diagnosis: 1. B. parapertussis, adenovirus, mycoplasma pneumonia, and chlamydia trachomatis 2. Foreign body aspiration, endobronchial tuberculosis and a mass pressing on the airway

29 DIAGNOSIS 1. Suspected on the basis of history and clinical examination and is confirmed by culture, genomics or serology 2. Elevated WBC count with lymphocytosis. The absolute lymphocyte count of ≥20,000 is highly suggestive 3. Culture: gold standard specially in the catarrhal stage. A saline nasal swab or swab from the posterior pharynx is preferred and the swab should be taken using dacron or calcium alginate and has to be plated on to the selective medium

30 DIAGNOSIS However culture are not recommended in clinical practice as the yield is poor because of previous vaccination, antibiotic use, diluted specimen and faulty collection and transportation of specimen. 4. PCR: most sensitive to diagnose; can be done even after antibiotic exposure. It should always be used in addition with cultures 5. Direct fluorescent antibody testing: low sensitivity and variable specifity

31 TREATMENT 1. Avoidance of irritants, smoke, noise and other cough promoting factors 2. Antibiotics: effective only if started early in the course of illness. Erythromycin (40-50 mg/kg/day 6 hrly orally for 2 weeks or Azithromycin 10 mg/kg for 5 days in children 6 months 10 mg/kg on day 1, followed by 5mg/kg from day2-5 or Clarithromycin 15 mg/kg 12 hrly for 7 days 3. Supplemental oxygen, hydration, cough mixtures and bronchodilators (in individual cases)

32 PREVENTION  All household contacts should be given erythromycin for 2 weeks  Children <7 years of age not completed the four primary dose should complete the same at the earliest  Children <7 years of age completed primary vaccination but not received the booster in the last 3 years have to be given a single booster dose  VACCINE

33 Tetanus LOCKJAW

34 INTRODUCTION  Tetanus is an acute, fatal, severe exotoxin mediated nervous system disorder characterized by muscle spasm  Caused by the toxin producing anaerobe, Clostridium tetani  Tetanus is the only vaccine preventable disease that is infectious but not contagious from person to person

35 EPIDEMIOLOGY  C. tetani is a part of the normal flora in human and animal intestines and is disseminated through excreta  In spore form they are hard and long lasting in soil and dust  The contamination of wound, unhygienic and improper handling of the umbilical cord in newborns, lack of hygienic habits and aseptic care during and after delivery are the main risk factors for infection

36 PATHOGENESIS Net effect is disinhibition of anterior horn cells and autonomic nervous system resulting in increased muscle tone, painful spasms and widespread autonomic instability After reaching the spinal cord and brainstem via retrograde axonal transport and binding tightly and irreversibly to receptor, tetanus toxin blocks neurotransmission Tetanus occurs when spores of C.tetani found in soil gain access to damaged human tissue After inoculation, C. tetani transforms into a vegetative rod shaped bacterium and produces the metalloprotease, tetanospasmin

37 PREDISPOSING FACTORS  A penetrating injury – inoculation of C. tetani spores  Coinfection with other bacteria  Devitalized tissue  A foreign body  Localized ischemia  Therefore tetanus develop in these clinical settings: neonates, obstetric patients, postsurgical patients, patients with dental infection, diabetic patients with infected extremity ulcers, patients who inject illicit and/or contaminated drugs

38 CLINICAL MANIFESTATIONS  Incubation period: 1-8 days  Generalized tetanus:  Presenting feature is trismus  Symptoms of autonomic overactivity such as irritability, restlessness, sweating, tachycardia, cardiac arrhythmias, labile hypotension or hypertension and fever  Tonic contractions of skeletal muscles (stiff neck, opisthotonus, risus sardonicus, board like rigid abdomen) and intermittent intense muscular spasms with no impairment of consciousness  Painful spasms, triggered by loud noises or other sensory stimuli such as physical contact or light

39 CLINICAL MANIFESTATIONS  Period of apnea and/or upper airway obstruction due to contraction of thoracic muscles and/or glottal or pharyngeal muscle  Neonatal tetanus:  Manifested by rigidity, spasms, trismus, inability to suck and seizures Diagnosis: mainly clinical

40 TREATMENT  Best in the ICU as child may need early and aggressive airway management  The goals of treatment include 1. Halting toxin production  Wound debridement  Antimicrobial therapy: metronidazole or penicillin G for days 2. Neutralization of unbound toxin:  HTIG-3,000-6,000 units i.m.  Equine antitoxin 1,500-3,000 units i.m. or i.v.

41 TREATMENT 3. Control of muscle spasms  Avoidance of sensory stimuli  Sedatives: diazepam 4. Management of autonomic dysfunction:  Magnesium sulfate, beta blockers, morphine sulfate 5. Airway management and other supportive measures  Main treatment as bound tetanus toxin can not be displaced from the nervous system  Endotracheal intubation/tracheostomy, nutritional support, physical therapy as soon as spasms have ceased

42 PREVENTION  Immunization and proper treatment of wounds and traumatic injuries  PROGNOSIS:  The average mortality of tetanus is 45-55%  Neonatal tetanus: 60-70%  Most important factor influencing outcome is supportive care

43 PREVENTION VACCINE:  DPT vaccine: 3 primary doses starting at 6 weeks of age  1 st booster at months of age, 2 nd booster at 5 years of age  At 10 years of age Tdap/Td followed by Td every 10 years  Catch-up vaccination:  Below 7 years: DPT at 0,1 and 6 months


Download ppt "DIPHTHERIA, PERTUSSIS & TETANUS Dr Sarika Gupta, Asst. Professor."

Similar presentations


Ads by Google