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Premium member Presentation Transcript Diphtheria : Diphtheria Dr.N.Bayapa Reddy ASST.PROFESSOR DEPT.OF COMMUNITY MEDICINE CHENNI MEDICAL COLLEGE HOSPITAL & RESEARCH CENTERSlide 2: EPIDEMIOLOGY OF DIPHTHERIAINTRODUCTION: INTRODUCTION Diphtheria is an highly infectious and communicable disease characterized by involvement of the respiratory system , the local production of membrane and general symptoms caused by absorption of toxin .History : History The disease was first recognized as a clinical entity by Bretonneau (1826) who called it as diphtherite . The Diphtheria bacillus was : First observed and described by - KLebs  . First Cultivated by - Loeffler  . Hence it is also known as Klebs – Loeffler bacillus. Roux and Yersan - discovered the Diphtheria exotoxin and established its pathogenic effect Von Behring - described the antitoxin . Shick  - Introduced the test for susceptibility which bears his name. Problem Statement: Problem Statement WORLD Developed countries – rare Developing countries - endemic The true number of cases and deaths are unknown because of incomplete reporting from most countries. Problem Statement: Problem Statement Recent Outbreak in Afghanistan Time : Aug 2003 Place : Kandahar No of cases : 50 Deaths : 3 (Case fatality rate 6%) Age group : 74% of cases were 5 to14 yrs Problem Statement : Problem Statement India ☺ Endemic Disease ☺ Declining trend due to increasing cover of immunization . 1987 – 12952 2005 - 10231 Declined by 21%Agent Factors: Agent Factors Agent Corynebacterium diphtheria coryne – club diphtheros - leather Gram positive , Non- sporing , non capsulated non motile , and slender rod shaped bacteria .Gram +ve Bacilli and Colonies: Gram +ve Bacilli and Colonies Agent Factors: Agent Factors Arrangement – They are usually seen in pairs , palisades or small groups , the bacilli being at various angles to each other to each other resembling the letters V or L . Chinese letter or cuneiform Agent Factors: Agent Factors Classification - Mc Leod Gravis Intermedius MitisAgent Factors: Agent Factors Source of infection Carrier Case Temporary Permanent Nasal ThroatSlide 13: Case : Range from sub clinical to frank clinical cases . Temporary Carrier : State may last for about a month . Permanent Carrier : State may persist for a year or so unless the patient is treated. Carriers are more numerous and are the common source of infection than cases (95 : 5) . Source of infectionSlide 14: Source of infection Nasal Carriers are more dangerous than throat carriers as source of infection because of frequent shedding of organisms into environment. Immunization does not prevent the carrier state. Agent Factors: Agent Factors Infective Material Nasopharyngeal Secretions . Discharge from Skin Lesions . Contaminated fomites and possibly infected Dust. Period of Infectivity Cases – 14 to 28 days Carriers - Longer periodsHost factors : Host factors Age Particularly affects 1 – 5 years of age . In countries where wide spread immunization is practiced a shift in age incidence has been observed from pre school to school age. Sex Both sexesSlide 17: Immunity One attack of the disease generally leads to lasting immunity . There are however instances of multiple attacks . Infants are protected from birth to the age of 3 months 60 % 4 months 50 % 6 months 17% But by one year of age nearly all are susceptible to the disease . Host factorsSlide 18: Environmental Factors All seasons , although cold months favour its spread . Mode of transmission Mainly by droplet infection . Infected cutaneous lesions . By fomites (ex : Cups, Thermometers) contaminated by the nasopharyngeal secretions of the patient.Slide 19: Portal of EntrySlide 20: Portal Of Entry ` Respiratory Route – Most common . ` Non respiratory routes ~ Skin – cuts , wounds & Ulcers . ~ Umbilicus of new born . ~ Eye , genitalia and middle ear Incubation Period ~ 2 – 6 Days .Pre-disposing Causes: Pre-disposing Causes Operation in the area of nose and throat . Economic status . Lack of proper nutrition . Over Crowding .Slide 22: CLINICAL FEATURES OF DIPHTHERIASlide 23: ONSET OF THE DISEASE It is rarely sudden and the symptoms are infrequently severe. Moderate temperature 102 F , Malaise, sore throat, tired feeling. Sore throat is not marked initially. This delays the discovery of the illness which results in considerable amount of membrane formation. Membrane formation is due to necrosis of epithelial cells, sero-fibrinous material liberated which form greenish white memb. Edges are curled or separated from the underlying mucus membrane. Bleeds on peeling and there is increased toxin absorptionSlide 24: Usually one tonsil is involved and soon spreads to opposite side Patient discovered late shows extension from tonsil to fauces to pharynx. In mixed infections by secondary bacterial invasion ( streptococci) is called septic diphtheria. a) High grade fever b) Atypical appearing membrane c) Greater inflammation in surrounding structures Bleeds on peeling and results in is increased toxin absorption CHARACTERISED BY :Slide 25: CLINICAL FEATURES Manifestations : (b) Membrane formation. (c) Toxaemia. Forms of Diphtheria: (a) Tonsillar. (b) Pharyngeal. (c) Laryngeal. (d) Anterior nasal (e) Other forms. (a) Local inflammation.Slide 26: Tonsillar diphtheria Most common form Initially it is a thin membranous spot few mm on one tonsil More often identified on two tonsils as greyish yellow membrane Narrow area of redness surrounds the membrane Tender and enlarged sub mandibular lymphnodes Fauces is normalSlide 27: MEMBRANE OVER FAUCESSlide 28: MEMBRANE OVER TONSILSlide 29: Pharyngeal diphtheria Membrane spreads to sides of uvula. Spread of membrane : (a) Anteriorly upto teeth. (b) From post pillar to naso pharynx & then to nostrils. Early formed membrane gets necrotic as newer parts advance. This necrotic material produces foul smell Foetor oris Throat tissue is congested. When bleeding occurs the mem becomes foul black mass of tissue BULL NECK - Swelling of tissues in front of neck. Lymph nodes are not palpable. Patient is drowsy ,pale & tired.Slide 30: BULL NECKThick Membrane: Thick MembraneSlide 32: Laryngeal Diphtheria Primary - Most commonly due to mitis. Secondary - Spread from fauces. May spread to trachea ,bronchi& bronchioles. Symptoms - Due to obstruction. (a) Huskiness of voice. (b) Croupy cough. (c) inspiratory distress. (d) Stridor ,more common in children. Danger of laryngeal diphtheria is - ASPHYXIA TRACHEOSTOMY can bring relief.Slide 33: Anterior Nasal Discharge Which is initially thin & blood stained which later turn into thick & mucopurulent. The discharge contains in large numbers Thin yellowish membrane is present.Slide 34: Others These include non respiratory forms They are (a) skin. (b) Eye. (c) Intestines. (d) Genito urinary system. (e) Diphtheritic endocarditis.Slide 35: SKIN Common in tropics. Seen mostly on fingers & back of the hands which spread from fauces. Punched out ulcers are seen. EYES Secondary to ant nasal. Spreads through naso lachrymal duct. It manifests as conjunctival diphtheria. Sloughing of conjunctiva & corneal damage occurs. Rarely pan ophthalmitis.Slide 36: SKIN SORESlide 37: INTESTINES Secondary to Faucial Diphtheria. Dysphagia & bloody diarrhoea with intestinal casts are seen. Usually diagnosed at autopsy. UROGENITAL SYSTEM Transmitted through fingers by contact. In males coronal sulcus & glans are involved In females vulva & vagina are involved DIPHTHERITIC ENDOCARDITIS High fatality rate but rarest. Caused by c . Xerosis , valves are involved.Slide 38: COMPLICATIONS OF DIPHTHERIA Causes of complications is toxin. Severe complications are seen in (a) nasopharyngeal . (b) laryngeal. Complications are rare in nasal ,tonsillar diphtheria Earliest severe complication in N.P. diphtheria is myocarditis. These rarely cause otitis media ,albuminuria & perutonsillar abscess.Slide 39: CARDIOVASCULAR COMPLICATIONS. It includes (a) early Myocarditis (b) Late PARALYTIC COMPLICATIONS Palatine Eyes Pharynx , larynx , respiratory muscles. limbs . Heart , EncephalitisSlide 40: EARLY MYOCARDITIS Peripheral changes which include pallor , rapid & thready pulse , collapse of B.P. Vomiting & upper abd pain are ominous signs. Shock -due to toxins affecting adrenals & vas deferens. If the pt survives there are signs of cardiac involvement. Pt dies within 10 days without cardiac involvement. Time of occurrence is in between 3-7 day. Heart sounds &heart rhythm are normal.Slide 41: LATE MYOCARDITIS Time of onset is in between 5-14 days. Severe pallor ,weak , slow & thready pulse . S1 is absent ,S2 is soft. Heart rate is irregular & gallop rhythm is present. Severe abd pain is present. Peripheral & splanchnic vasculature dilation. Apex is shifted outwards & down wards.Slide 42: ECG changes . T – wave is inverted or flattened . Lengthening of PR or QT interval. Usually pt recovers without any evidence of cardiac damage.Slide 43: PARALYTIC COMPLICATIONS PALATAL PARALYSIS Sets in 3 rd week & lasts for 2 wks. Pronunciation is difficult because pt is unable to direct lips . EYES Blurred vision, paralysis of accommodation. Persists for week. Convergent squint - lat rectus paralysis. Most common.Slide 44: PHARYNGEAL PARALYSIS Difficulty in swallowing. . Saliva collected in back of throat. If larynx is also involved aspiration into bronchial tree. LARYNGEAL PARALYSIS Loss of voice. Ineffective cough is present. LIMBS Most commonly involved parts are dorsi flexors.Slide 45: DIAGNOSIS OF DIPHTHERIA It is necessary for control and epidemiological purpose but not for treatment Treatment should be started immediately after suspicion of disease. A ) Clinical diagnosis B ) Laboratory diagnosis C ) Diagnosis of susceptibilitySlide 46: Clinical Diagnosis Onset of the disease The patient looks ill Bull neck is present Lymph nodes are not palpable Thick tough yellowish grey membrane grey black in center Faucial diphtheria Pharyngeal diphtheriaSlide 47: Laryngeal Diphtheria Membrane observed with a laryngoscope Dry croupy cough is present Nasal Diphtheria Membrane is seen along the septum and turbinates Diphtheric Paralysis No clinical features of Diphtheric paralysis are able to distinguish from other paralytic diseases (especially Polio myelitis)Slide 48: LABORATORY DIAGNOSIS Swabs from throat ,nose ,larynx ,skin& tracheal exudates are cultured. Culture medium is loefflers serum slope In doubtful cases animal inoculation may be done, by S.C. route. Smear staining is by albert stain. Serological tests are also done.Slide 49: CORYNEBACTERIUM DIPHTHIRIA ALBERT STAINSlide 50: VIRULENCE TESTS To test toxigenicity for the bacteriological examination to be complete. Two types - (a) in vivo test (b) In vitro test In vivo test done on guinea pigs by s.c tests & intradermal tests. In vitro tests are (a) Eleks gel ppt test (b) Tissue culture test.Slide 51: DIAGNOSIS OF SUSCEPTIBILITY SCHICK TEST Used to test (a) Presence of anti toxins in the body. (b) Hypersensitivity to diphtheria toxin. Test proper 0.2ml of fluid containing measured dose of D.T. is injected intradermally into pts left forearm. Similar amount of heat inactivated toxin is injected into arm. It is a quantitative test, with regarding to circulating antitoxin. It is a reliable test of susceptibility useful in investigation of outbreaks and as a criterion of a patients need for immunizationSlide 52: CLINICAL INTERPRETATION POSITIVE If red circumscribed flush is seen in test arm measuring 10-50 mm Peak during 4 th to 7 th day. The subject is susceptible. NEGATIVE The subject is immune to D.T. No reaction. OF SCHICK TEST Interpretation is negative. COMBINED Test arm --- true positive. Susceptible to diphtheria. A person who is susceptible ,but allergic should be cautiously immunized. PSEUDO POSITIVE Red flush equally on both arms, but less circumscribed. Allergic reaction.Diphtheria Complications: Diphtheria Complications Mostly attributable to toxin Severity generally related to extent of local disease Most common complications are myocarditis and toxic neuritis with palsy Death occurs in 5%-10% for respiratory diseaseSlide 54: PREVENTION AND CONTROL OF DIPHTHERIASlide 55: MANAGEMENT OF DIPHTHERIA DIAGNOSIS: Clinical examination Direct microscopy using ALBERTS STAIN Culture (LOEFFLER’S SERUM SLOPE) Flourescent Ab technique Toxigenicity testing by ELEK’S GEL PPT Diagnosis of susceptibility by SHICK TESTSlide 56: DIFFERENTIAL DIAGNOSIS NASAL DIPHTHERIA: FB in Nose Rhinorrhoea Snuffles (due to congenital Syphilis) FAUCIAL DIPHTHERIA: Acute Strep. membranous Tonsillitis Viral membranous Tonsillitis Herpetic tonsillitis Thrush Infectious MononucleosisSlide 57: LARYNGEAL DIPHTHERIA: Croup Acute Epiglottitis LaryngoTracheobronchitis Retropharyngeal abscess Peritonsillar abscess BronchopneumoniaSlide 58: TREATMENT OF A CASE OF DIPHTHERIA PRINCIPLES: Neutralisation of free circulating toxin by administration of ANTITOXIN ANTIBIOTICS to eliminate bacteria Supportive and symptomatic therapy Management of complications IsolationSlide 59: 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 hrs. apart should be negative before terminating isolationSlide 60: ANTITOXIN Administered as soon as infection with Diphtheria is suspected. Given by i.m or i.v injection after testing sensitivity to antitoxin serum. Antitoxin interferes with the action of toxin and modifies the attack. After administration of antitoxin Pt. is observed closely for anticipated reduction in constitutional symptoms & toxemia.Slide 61: DOSAGE Cases: Anti toxin 10,000 to 80,000 units Penicillin 2.5 lakh units every 6 hours 5-6 days or oral erythromycin 250 mg every 6 hours for 5-6 days Carriers: oral erythromycin 250 mg every 6 hours for 10 daysSlide 62: ANTIBIOTICS : To terminate toxin production. To limit proliferation of bacteria. To prevent spread of organism to contacts. To prevent development of carrier state. PROCAINE PENICILLIN 3-6 lac units i.m at 12hrly intervals is recommended till the pt. is able to swallow. ORAL PENICILLIN 125-250mg q.i.d or ERYTHROMYCIN 25-30mg/kg/day is substituted when the pt. is able to swallow for a total period of 14 days. Clinical infection does not result in immunity. The attack should be followed by active immunisation.Slide 63: SUPPORTIVE THERAPY : Bed rest for 2-3 wks. 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.Slide 64: TREATMENT OF COMPLICATIONS TOXEMIA AND MYOCARDITIS : Absolute bed rest and only essential nursing care Hypertonic sols of glucose in 10-20% dil Steroids Digoxin (only if signs of C.H.F occur) TREATMENT OF PARALYSIS: Palate Pharynx Per nasal gastric tube Suction of mucus Respiratory obstruction Humidified oxygen TracheostomySlide 65: TREATMENT OF CONTACTS Based on IMMUNITY STATUS of person PRIMARY IMMUNISATION or BOOSTER Within 2-years >2-years NON IMMUNISED CLOSE CONTACT NO action required BOOSTER Prophylactic antibiotics ANTITOXIN 1000-2000u ACTIVE IMMUNISATION CONTACTS SHOULD BE PLACED UNDER MEDICAL SURVEILLANCE & EXAMINED DAILY FOR EVIDENCE OF DIPHTHERIA FOR ATLEAST A WEEK AFTER EXPOSURESlide 66: TREATMENT OF CARRIERS The carriers should be treated with 10 day course of oral erythromycin. Patient convalescent from diphtheria or persons harboring organisms 2 wks. or longer are termed as carriers of Diphtheria.Slide 67: PROGNOSIS: Depends on Extent of membrane. Ability of organism to produce toxin. Immunity status of pt. If memb. Is limited to nostrils, toxicity is negligible. If memb. Present on both tonsils, pt. may develop palatal paralysis. If memb.extends beyond tonsils involving palate and nasopharynx, pt. may suffer from any or all of severe complications. If there is hemorrhage the prognosis is grave. Diphtheric paralysis is a temporary condition & recovery when occurs is complete.Slide 68: Four key strategies are required to ensure continued prevention and control of diphtheria E nsuring high population immunity; S trengthened surveillance; E arly diagnosis and high quality case management; R apid investigation and the management of close contacts. PREVENTIONSlide 69: PREVENTION IMMUNISATION HEALTH EDUCATION ACTIVE PASSIVE COMBINED VACCINES SINGLE VACCINES DPT DTaP DT dT FT APT PTAP PTAHTAF ANTISERA COMBINEDSlide 70: DPT VACCINE : 2 Types PLAIN & ADSORBED Adsorbtion is usually done on a mineral carrier. Adsorbtion increases the immunological effectiveness of the vaccine. COMPOSITION: CONTENTS (per 0.5ml) GLAXO KASAULI Diph. Toxoid 25 Lf 30 Lf Tet. Toxoid 5 Lf 10 Lf B.pertussis(millions) 20,000 32,000 Al.Phosphate 2.5 mg 3.0 mg Thiomersal,B.P 0.01% 0.01% It is a combined vaccine.Slide 71: STORAGE : DPT/DT VACCINES SHOULD NOT BE FROZEN. Stored in a refrigerator between 2-8 C (35-46 F). When issued to a subcentre it should be used C in a WEEK. If they r suspected to be frozen they can be determined by SHAKE TEST . Procedure: 1.Prepare a frozen control sample. 2.Choose a test sample. 3.Shake the control and test samples for 10-15 sec. 4.Allow to rest. 5.Compare the vials.Slide 72: If the vaccine is allowed to freeze, the link between Antigen &Al. adsorbent gets broken. Al. tends to come together in lumps and becomes heavier. This is why sedimentation occurs faster in a vaccine vial which has been frozen. View both vials against light to compare the rate of sedimentation. If sed. rate of test is same as that of control vaccine vial has been damaged. If the test sample show a much slower sedimentation rate than control, the test sample is potent & can be used.Slide 73: OPTIMUM AGE: Can be safely &effectively given as early as 6 wks. ADMINISTRATION: ROUTE: Deep I.M. injection SITE: Lateral aspect of thigh. DOSE: 0.5ml INTERVAL OF DOSES : 4 weeks between first 3 doses. DPT I : 6 weeks DPT II :10 weeks DPT III: 14 weeks BOOSTER: 18-24 months BOOSTER: 5-6 yrs. (DT only) Additional boosters (dT) every 10 yearsSlide 74: REACTIONS FOLLOWING IMMUNISATION: LOCAL : Pain, swelling, redness .(30-40%) It persists for 24-72 hrs. & responds well to paracetamol. Occasionally a nodule forms soften & form abscess. SYSTEMIC : Fever, lassitude, anorexia, vomiting, irritability, excessive crying & screaming spells for >4hrs , convulsions Of these fever bet 100-102F, Pain, redness, swelling, vomiting, anorexia are common. FEVER (>105F),SEIZURES, CONVULSIONS, COLLAPSE,DIFFICULTY IN BREATHING are serious side effects.Slide 75: CONTRAINDICATIONS: Allergy/Anaphylactic reaction to a previous dose of DPT. RELATIVE: ABSOLUTE: Hypotonic Hypo-responsive Episodes (HHE) DEFERRAL: Deferral of ‘ P ’ component of DPT should be considered in children with a progressive neurological conditions including Seizures. Reinstituted when cond has resolved. Elective immunization of individuals>6 months. Should be deferred during an outbreak of Poliomyelitis.Slide 76: DTaP: Unlike ‘ P ’ comp. IN DPT which contains toxic whole cell of pertussis bacteria,DTaP contains only a few detoxified comp. which can still spark immunity. If immunisation with ‘ P ’ containing vaccine is contraindicated/ deferred DTaP can be given. DT: Can be given to children>7yrs. Old. It is given by injection into arm or thigh dT: It is the adult vaccine that protects against Diphtheria and Tetanus. It has 1/10 th dose of Diphtheria toxoid than present in DPT/DT. If full dose of Diphtheria toxoid is given as present in DT/DPT to children above 10yrs.it can lead to serious side effects like heart toxicity etc.Slide 77: FORMOL TOXOID: Also known as fluid toxoid . By incubating toxin with formalin at p 7.4-7.6 for 3-4 weeks at 37 C until the product is devoid of toxicity while still retaining immunogenicity. H 0 ADSORBED TOXOID: Purified toxoid is adsorbed onto insoluble Al. compounds usually Al. phosphate or Al. hydroxide. It is much more immunogenic than fluid toxoid.Slide 78: PASSIVE IMMUNISATION: By administration of serum containing antitoxin prepared in Horse serum. DOSE: Prophylactic : 500-2000 Units by S.C/I.M. Therapeutic:10,000-30,000 units by i.m inj. or 40,000-1,00,000 units by i,.v inj. In 2 divided doses with an interval of ½ - 2 hrs.Summary: SummaryAgent Factors: Agent Factors Agent Corynebacterium diphtheria coryne – club diphtheros - leather Gram positive , Non- sporing , non capsulated non motile , and slender rod shaped bacteria .Host factors : Host factors Age Particularly affects 1 – 5 years of age . In countries where wide spread immunization is practiced a shift in age incidence has been observed from pre school to school age. Sex Both sexesDiphtheria Epidemiology: Diphtheria Epidemiology Reservoir Human carriers Usually asymptomatic Transmission Respiratory Skin and fomites rarely Temporal pattern Winter and spring Communicability Up to several weeks without antibioticsDiphtheria Clinical Features: Diphtheria Clinical Features Incubation period 2-8 days May involve any mucous membrane Classified based on site of infection anterior nasal pharyngeal and tonsillar laryngeal cutaneous ocular genitalSlide 84: THANK YOU You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.