DIPTHERIA tetanus pertussis infection,............................................

Diptheria pertussis tetanus infection

1. DIPTHERIA PRESENTER - DR.VINAY(JR 2) MODERATOR – DR .UDDHAV KINHAL

2. Diphtheria is an acute toxic infection caused by Corynebacterium species typically corynebacterium diphtheriae 95% and corynebacterium ulcerans 5%.

3. Corynebacterium are aerobic, non-encapsulated, non-spore-forming, mostly nonmotile , pleomorphic gram positive bacilli

4. Corynebacterium diphtheria is most common isolated agent of diptheria . Corynebacterium ulcerans is more often isolated from animal source and can cause human infection. The ability to produce diptheria toxin results from acquisition of a lysogenic corynebacteriophage by either C.diptheriae or C.ulcerans which encodes the diptheria toxin gene and confers diptheria producing potential on these strains.

5. Epidemiology C.diptheriae is an exclusive inhabitant of human mucosa membrane and skin. Spread is by airborne respiratory droplets or exudate from infected skin lesion. Asymptomatic respiratory tract carriage is important in transmission .

6. Skin infection and skin carriage are silent reservoirs of C.diptheriae . Transmission through contaminated milk and through an infected food handler has been proved

7. CLINICAL MANIFESTATIONS RESPIRATORY TRACT INFECTION - Incubation period – 2-4 days Infants – infection of anterior nares is most common serosanguineous ,purulent ,erosive rhinitis with membrane formation Shallow ulceration of external nares and upper lip is characteristic

8. In 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 is followed by unilateral or bilateral tonsillar membrane formation, which can extend to involve the uvula (which may cause toxin-mediated paralysis), soft palate, posterior oropharynx , hypopharynx , or glottic areas . Underlying sott tissue edema and enlarged lymph nodes can cause a bull-neck appearance.

9. The characteristic adherent membrane, extension beyond the faucial area, dysphagia , and relative lack of fever help differentiate diphtheria from exudative pharyngitis caused by other organisms

10. CUTANEOUS DIPTHERIA Classic cutaneous diphtheria is an indolent, nonprogressive infection characterized by a superficial, ecthyma -like, nonhealing ulcer with a gray-brown membrane. Diphtheria skin infections cannot always be differentiated from streptococcal or staphylococcal impetigo and these conditions frequently coexist.

11. In most cases a primary process such as dermatosis , laceration, burn, bite, or impetigo, becomes secondarily infected with C. diphtheria. Extremities are more often affected than the trunk or head.

12. INFECTION AT OTHER SITES C . diphtheria occasionally causes mucocutaneous infections at other sites, such as the ear ( otitis externa ), the eye (purulent and ulcerative conjunctivitis), and the genital tract (purulent and ulcerative vulvo-vaginitis ).

13. Sporadic cases of endocarditis occur, and clusters among intravenous drug users have been reported in several countries; skin was the probable portal of entry, and almost all strains were nontoxigenic . Sporadic cases of pyogenic arthritis, mainly from nontoxigenic strains, have been reported in adults and children

14. DIAGNOSIS Specimens for culture should be obtained 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 . Evaluation of a direct smear using Gram stain or specific fluorescent antibody is unreliable.

15. Culture isolates of coryneform organisms should be identified to the species level, and toxigenicity and antimicrobial susceptibility tests should be performed for C. diphtheria isolates. It is recommended that all isolates be sent to a reference laboratory.

16. TREATMENT S pecific antitoxin is the mainstay of therapy based on the clinical diagnosis. Antitoxin is administered as a single empirical dose of 20,000-100,000 units based on the degree of toxicity, site and size of the membrane, and duration of illness. Skin testing must be performed before administration of antitoxin. Patients with positive sensitivity testing or with a history of hypersensitivity reaction to horse equine protein should be desensitized.

17. Antitoxin is probably of no value for local manifestations of cutaneous diphtheria, but its use is prudent because toxic sequelae can occur. Antitoxin is not recommended for asymptomatic carriers.

18. The role of antimicrobial therapy is to halt toxin production. Appropriate therapy is erythromycin (40-50 mg/kg/day ) divided every 6 hour by mouth (PO) or intravenously maximum (2 g/day) aqueous crystalline penicillin G (1,00,000-1,50,000 units/kg/day divided every 6 hours IV or intramuscularly [IMI) procaine penicillin (300,000 unit every 12 hr IM for those <10 kg in weight, 600,000 units every 12 hr for those >10 kg in weight) for 14 days. Once oral medications are tolerated, oral penicilin V (250 mg four times daily) may be .

19. Some patients with cutaneous diphtheria have been treated for 7-10 days. 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. Treatment with erythromycin is repeated if either culture yields C. diphtheria

20. ASYMPTOMATIC CASE CONTACT All household contacts and people who have had intimate respiratory or habitual physical contact with a patient are closely monitored for illness for 7 days. Cultures of the nose, throat, and any cutaneous lesions are performed.

21. Antimicrobial prophylaxis is presumed effective and is administered regardless of immunization status, using a single injection of benzathine penicillin G (600,000 units IM for patients <6 yr old, or 1,200,000 units IM for patients >6 yr old) or erythromycin (40-50 mg/ kg/day divided qid PO for 10 days; max 2 g/day). Diphtheria toxoid vaccine, in age-appropriate form, is given to immunized individuals who have not received a booster dose within 5 yr.

22. 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 should be immunized with an age-appropriate preparation on a primary schedule

23. ASYMPTOMATIC CARRIERS When an asymptomatic carrier is identified, antimicrobial prophylaxis is given for 10-14 days and an age-appropriate preparation of diphtheria toxoid is administered immediately if a booster has not been given within 1 yr. Droplet precautions (respiratory tract colonization) or contact precautions ( cutaneous colonization only) are observed until at least 2 subsequent cultures obtained 24 hr apart after cessation of therapy have negative results

24. VACCINE Universal immunization with diphtheria toxoid throughout life, to provide constant protective antitoxin levels and to reduce severity of C. diphtheriae disease, is the only effective control measure. Although immunization does not preclude subsequent respiratory or cutaneous carriage of toxigenic C. diphtheriae , it decreases local tissue spread, prevents toxic complications, diminishes transmission of the organism, and provides herd immunity when at least 70-80% of a population is immunized

25. DTwP Disease against Diphtheria Pertusis Tetanus T ype of vaccine Toxoid (20-30 Lf) flocculation content Killed whole cell bacilli (>4 IU) Toxoid (5-25 Lf) Nature/ diluent Aluminium salts adjuvants Thiomersal - preservative Storage At 2-8 °C; Never to be frozen (discard if frozen) Dose/route/site 0.5 ml/ intramuscularly/ anterolateral thigh (left) Efficacy 95% Antibody titre > 0.1 IU/ml 70-90% 95% Antibody titre > 0.01 IU/ mL Schedule 6, 10 and 14 weeks, Booster at 18 months and 5 yrs Catch-up schedule <7yrs-0, 1 and 6 months; Booster need not be given if last vaccine was given after 4 yrs After 7 yrs- Tdap , Td, and Td at 0, 1 and 6 months Adverse effects Fever, local pain and induration , persistant crying( 4-8.8/1000 dose) , encephalopathy> 24 h, hypotonic hyporesponsive episodes( 0.06-0.8/1000 dose) , hyperpyrexia (temp > 40.5 °C) Contraindications Severe hypersentivity to previous dose Progressive neurological disease- active epilepsy Pertusis - Beyond 7 yrs of age Both DTwP and DTap

26. DTaP Acellular pertusis toxin Use of purified antigens and the removal of LPS and other parts of the bacterial cell wall during the purification of soluble antigenic material. These vaccines contain ≥ 1 of the separately purified antigens pertussis toxin (PT), filamentous hemagglutinin (FHA), pertactin (PRN), and fimbrial hemagglutinins 1, 2 & 3 (FIM type 2 and type 3) Both DTwP & DTaP must not be given in children >7 years of age because of reactogenecity .

27. T d a p Reduced antigen acellular pertusis and diphtheria toxoid Single dose at 10- 12 yrs; booster Td every 10 yrs Catch up – up to 18yrs Catch up above 7 years: Tdap , Td, Td at 0, 1 and 6 months ( Tdap only 1 dose) Diphtheria Pertusis Tetanus 2 Lf Toxoid - 8 mcg FH- 8 mcg Pertactin - 2.5 mcg 5 Lf

28. THANK YOU

29. PERTUSSIS

30. Pertusis is acute highly contagious disease which cause classic spasm ( paroxyms ) of uncontrollable coughing, that is violent and persistence followed by a sharp,high pitched intake of air which create characteristic"WHOOP " sound. Children who have typically illness of pertusis try to take deep breath between cough result in whooping Whooping cough is also known as 100 days cough. Habbit pattern of coughing may longer or subscquent weeks & month,so chiniese call it;"100 DAYS COUGH".

31. ETIOLOGY Bordetella pertussis is the cause of epidemic pertussis and the usual cause of sporadic pertussis . Bordetella parapertussis is an occasional cause of sporadic pertussis . B. pertussis and B. parapertussis are exclusive pathogens of humans and some primates . Bordetella holmesii , first identified as a cause of bacteremia in immunocompromised hosts without cough illness, also is reported to cause pertussis -like cough illness in small outbreaks in healthy persons. Protracted coughing (which in some cases is paroxysmal) is attributable sporadically to Mycoplasma , parainfluenza viruses, influenza viruses, enteroviruses , respiratory syncytial virus (RSV), or adenoviruses.

32. Before vaccination was available, pertussis was the leading cause of death from communicable disease among children <14 yr old. Widespread use of whole cell pertussis vaccine (DTP) led to a >99% decline in cases. Neither natural disease nor vaccination provides complete or lifelong immunity against pertussis reinfection or disease. Subclinica reinfection undoubtedly contributed significantly to immunity against disease ascribed previously to both vaccine and prior infection.

33. INCUBATION PERIOD The incubation period is typically 3 to 12 days in infants or young children, after which there are usually mild respiratory symptoms, mild coughing, sneezing,or runny nose.

34. MODE OF TRANSMISSION Tiny droplets that comes from mouth & nose of infected patient . Respiratory Aerosoles (Droplets) Close Contact It spreads through close contact with oral secretions or respiratory droplets. So it's easily spread through the cough, especially when people are in close contact, like living in the same house with a person who has whooping cough. It can also be spread through sneezes .

35. AGE GROUP & SEX It is primarily disease of pre schoolar (3-5 years) & may occur in infants, new born, pregnant lady . Pre schoolar are responsible for about 50% of total case It is more common in females then males.

36. pathogenisis

37. CLINICAL MENIFESTATION Clinical menifestation include '3‘ stages 1.Catarrhal Stage (Pre paroxymal stage, o-2 weeks ) 2.Paroxymal Stage (Spasmodic stage, 2-6 weeks) 3.Convulscent Stage (Last 2 weeks)

38. STAGE-I CATARRHAL STAGE Catarrhal symptoms appear that are : Fever Rhinitis Sneezing Anorexia- Nausea & Vomiting Lacrimation Irritating cough at night (nocturnal but later becomediurnal )

39. STAGE- I I PAROXYMAL STAGE Cough means in paroxymus ( repeatating ) & is accompanied by vomiting. • A typical attack consist of repeated series of many cough in expiration followed by sudden deep, violent inspiration with characterise crowing sound"WHOOP “ Ulcer of franulum of tounge . Congestion of neck & scalp vein. Patient appears suffocated with congested (red) face with or without cyanosis Mouth opened, periorbital oedema Sub conjuctional haemorrhage Convulsion may be present.

40. STAGE-I|I CONVULSCENT STAGE Disturbing cough & vomiting stops and appetite too improves (start of hungerness ) Habit pattern of coughing may be longer to several weeks & month . Infants less than 3 months do not show classical stages

41. Adolescents and previously immunized children have foreshortening of all stages of pertussis . Adults have no distinct stages. Classically, adolescents and adults describe a sudden feeling of strangulation followed by uninterrupted coughs

42. Findings on physical examination generally are uninformative. Signs of lower respiratory tract disease are not expected unless complicating secondary bacterial pneumonia is present. Conjunctival hemorrhages and petechiae on the upper body are common.

43. COMPLICATIONS Otitis media is quite frequent . Respiratory complications are Pneumonia (specially in infants ) Atelectasis Bronchiectasis Emphysema Neurological complication Intra cranial h aemorrhage Seizures (due to cerebral hypoxia ) Encephalopathy (Encephalitis) (Due to cerebral anoxia)

44. diagnosis Pertussis should be suspected in any individual who has a pure or predominant complaint of cough, especially if the following features are absent: fever, malaise or myalgia , exanthem or enanthem , sore throat, hoarseness, tachypnea , wheezes, and rales . For sporadic cases, a clinical case definition of cough of > 14 days' duration with at least 1 associated symptom of paroxysms, whoop, or posttussive vomiting has sensitivity of 81% and specificity of 58% for confirmation of pertussis .

45. Pertussis should be suspected in infants <3 mo old with gagging, gasping, apnea, cyanosis, or an apparent life-threatening event. Sudden infant death occasionally is caused by B.pertusis

46. DIAGNOSTIC EVALUATION Pertusis is difficult to diagnose because coughing maybe due to common cold, bronchitis or chest infection. For accurate diagnosis :- CBC ( Lymphocytosis is characteristic in the catarr hal stage ) Chest X-Ray ( Perihilar infiltration, atelectasis,emphysema ) ELISA (To detect IgM , IgG , IgA ) Nasophrayngeal swab (Mainly in stage-I)

47. Thank you