dip h tetanus

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    EPIDEMIOLOGY

    ANDCONTROL OF

    DIPHTHERIAAND

    TETANUS

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    Epidemiology:

    Identification

    Infectious agent

    Occurrence

    Reservoir

    Mode of transmission

    I.P.

    Period of communicability

    Susceptibility and resistance

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    Methods of Control:

    A.Preventive measures: Vaccination

    Public education

    Others

    B.Control of patients, contacts andenvironment:

    C.Epidemic Measures: Prompt reporting

    IG for outbreaks

    Priorities if short of vaccine

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    DIPHTHERIA

    Epidemiology:

    Identification: an acute bacterial disease oftonsils, pharynx, largnx, nose, occasionally of

    other mucous membranes or skin and

    sometimes the conjunctiva or genitalia.

    The characteristics lesion, caused by liberation ofa specific cytotoxin secondary to proliferation of

    bacteria at a focus of infection. Patches of an

    adherent grayish membrane with surrounding

    inflammation.

    The focus is usually the throat, spreading to the

    fauces, pharynx and larynx.

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    Infectious Agent:

    Coryndbacterium diphtheria of biotype:Gravis,

    Mitis,Intermedius

    Reservoir: Man

    Carriers: Do exist but are less infective than cases.

    Mode of transmission:

    Pts. * or carriers (direct droplet).Soiled articles (indirect).

    Raw milk (served as a vehicle).

    Occurrence:

    * Geography: World wide.A disease of colder months

    ( temperate zones).

    Prevalence depends on:

    - the extent of immunization

    - population density.

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    Age:

    - Unimmunized children < 15 yrs.,

    - often found among adults ( where immunization wasneglected).

    - Unusual among infants.

    Sex:

    No sex difference.

    I.P.:

    Usually 2-5 days.

    Period of Communicability:

    - Variable

    (until virulent bacilli disappear from discharges and lesions(usually 2 wks or less and seldom > 4 wks).

    ** Rarely chronic carriers may shed organisms for 6/12 or >.

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    Susceptibility and Resistance:

    - Infants born to immune mothers are

    relatively * immune for up to 6/12.

    - Recovery from clinical attacks are (in the

    majority) followed by lasting immunity.

    - Immunity acquired through inapp.infectn.

    - In tropics, cutaneous dipth. can pass

    unnoticed and induces significant

    immunity.

    - In U.S.A. > 40% of adults lack protective

    levels of circulating antitoxin.

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    Clinical Manifestations

    - The S & S depend upon:Site of infection,

    Immunization status,

    escape of toxin to ciculation.- Diphtheria is classified clinically on the

    basis of the anatomic location of the initial

    infection, and the dipth. Membrane:1-Nasal Diphtheria: initially resemble mild

    common cold with rhinorrhea and paucity

    of systemic symptoms.

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    2- Tonsillar and pharyngeal diphtherias:(insidious and more severe)

    Accompanying symptoms& signs:anorexia, malaise, low grade fever andpharyngitis. Within 1-2 days a memb. appearsof various extent (depending on the immune

    status of the host).Cervical lymphadenitis is variable.

    Bull Neck: edema of soft tissue of neck.

    3- Laryngeal diphtheria:- downwards extensionof memb. from pharynx,

    Occasionally, only laryn. Involvement ispresent (pts. toxicity less prominent).

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    4- Cutaneous, vulvovaginal, conjunctival and auraldipheria also occur.

    Complications:-1. Respiratory Obstruction leading to death (young

    children with laryng. or tracheal diph. due toocclusion of airway by dipht. memb. + edema ofneck).

    2. Myocarditis may follow both severe and mild casesof dipht. esp. among pts. with extensive local lesionswho experienced delay in administn. of antitoxin (2ndweek).

    3. Neurologic Complications:- Usually appear after a variable latent period,

    - predominantly bilateral motor > sensory ,

    - usually resolves completely.

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    Control and Prevention

    Preventive Measures:1- Active immunizatn. with diph. toxoid, including

    an adequate program to maintain immunity.

    Triple Antigen DPT.

    Schedules:

    a- < 6-7 yrs: 4 doses of DPT Ist 3 doses to be

    given at 4-8 wks. Intervals beginning when

    infant is 6-8 wks. Old (2 and 4 and 6 monthsin S.A.) The 4th dose given 1 yrafter the 3rd

    dose. A 5th dose, usually given at school

    entry.1

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    b. For persons > 7 yrs., : for previously unimm.

    Individual, a primary series of 3 doses of

    tetanus and dipth. Toxoids (adult type, Td) isgiven. The Ist 2 doses at 4-8 wks. Intervals, the

    3rd dose 6/m 1 yr. After 2nd dose.

    c. Active protectn. Should be maintained byadministering a dose of Td every 10 yrs.

    thereafter, (esp. for persons who are at higher

    risk to pt. exposure e.g. health workers).

    2 . Educational measures:

    to inform the public and esp. parents of young

    children of the hazards of diptheria and the imp.

    of immunization.

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    Control of pt., contacts and immediateenviron.:-

    - Report to local health authority.

    - Isolation :

    Strict for pharyn. diph.

    Contact isolatn. for cutan. diph.

    {Until 2, cultures from both throat and nose (orskin lesions) taken at least 24 hrs. apart, andnot less than 24 hrs. after cessatn. Ofantimicrob. therapy, fail to show dipht. bacilli.}

    Or when culture is impractical, isolatn. may beended after 14 days of appropriate antibioticRx.

    Concurrent disinfectn.: of all articles in

    contact with pts.

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    Management of case:-

    1 . DAT and antibiotics to be started

    immediately without waiting for lab. results.2. Rest and observation, to cover the period of

    potential cardiac damage and paralysis ,

    3. Avoid limbs deformity + ensure joint mobility.4. Tracheostomy and artificial respiration .

    Management of Contacts:

    1. For those who are previously immunised ,

    adminst . a booster dose (Td).

    2. For those not imm. they should be cultured

    and given DAT followed by immun. later on.

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    Tetanus

    Infectious Agent:Clostridium tetani

    Identification:An acute disease induced by an exotoxin

    of the tetanus bacillus, which grows

    anaerobically at the site of an injury. Thedisease is characterised by painful ms.

    contractions, primarily of the masseter

    and neck ms., secondarily of trunk ms.

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    Clinical Picture: ( common early S & S ) -

    lock jaw and muscular pain,

    - Abdominal rigidity,

    - Generalised spasms ,

    ( frequently induced by sensory stimuli)

    typical features of the tetanic spasm are the

    facial expression known as

    risus sardonicus.

    Note : Dysphagia is an uncommon

    but

    important early symptom.

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    Period of onset:

    The time bet. the Ist symptom and the appearance ofreflex ms. spasm.

    ( A typical tetanus pt. is apprehensive and alert. Allvoluntary ms. are hypertonic esp. on face, neck, spineand abd. wall).

    Complications: Tetanus is not simply a disorder of motor function. Theautonomic N.S. is also rendered unstable by the actionof the toxin.

    - Death occurs mainly due to eitherasphyxia orautonomic instability (e.g. sudden changes in pulserate, bl.P., and cardiac output).

    - Serious cardiac arrythmias, excessive sweating and fevermay occur.

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    I.P.: Usually 5-10 days (36 hrs and severalmonths have been reported).

    Reservoir:- Intestine of animals, in which theorganism is a harmless normal inhabitant. Soilcontaminated with animal and rarely humanfeces.

    Mode of Transmission:- Tetanus spores introduced into the body,usually through a puncture wound contaminatedwith soil etc.

    - The *umbilical wound when (unhyg.) dressed isthe main portal of entry in T. neonatorum.

    - The presence of necrotic tissues, foreignbodies, poor local bl. supply, favours growth of

    the anaerobic pathogen.

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    Period of Comm.:-

    - Not directly transmitted from person toperson.

    Susceptibility and Resistance:-

    - Suscept. is general.- Active immunity is induced by tetanus

    toxoid and persists for at least 10 yrs. after

    full immunizatn.Recovery from tetanus may not result in

    immunity. Second attack can occur.

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    2. Education on:

    - the necessity of complete immunization

    with T. Toxoid,

    - the kind of injury particularly liable to be

    complicated by tetanus, the potentialneed after injury for passive and *active

    phrophylaxis.

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    Control of pt., contacts and

    immediate environment:

    1. Report to local health authority.

    2.No isolatn.

    3. Immunizatn. Of contacts: None

    4. Investigatn. of contacts and source of infectn.:

    5. Specific Rx: human tetanus immunoglobulin*

    (TIG) i.m. follow a wound. If TIG not available,

    give tetanus antitoxin* in a single large i.v.

    dose + parentral penicillin in large doses for

    10-14 days.

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    Specific Treatmentb. Wound should be debrided widely.

    c. Maintain an adequate airway.

    d.Employ sedatn. (as indicated) or ms. relaxant.

    e.Active imm. should be initiated concurrently with

    therapy.

    6.Destruction of environmental spores:

    - esp. in operating theaters.

    - Special air-flow equipment and filtered ventilation.- Reduce airborne particles. Surgical instruments

    and dressing sterilizatn (use of autoclaves).

    Disinfectn. e.g. formaldehyde.