CORYNEFORM BACTERIA. Diphteroids Pleomorphic gram-positive rods. Club Shaped (Chinese Letter like,...

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CORYNEFORM BACTERIA

Transcript of CORYNEFORM BACTERIA. Diphteroids Pleomorphic gram-positive rods. Club Shaped (Chinese Letter like,...

Page 1: CORYNEFORM BACTERIA. Diphteroids  Pleomorphic gram-positive rods.  Club Shaped (Chinese Letter like, V forms)  Catalase +ve  Non sporing  Non acid.

CORYNEFORM BACTERIA

Page 2: CORYNEFORM BACTERIA. Diphteroids  Pleomorphic gram-positive rods.  Club Shaped (Chinese Letter like, V forms)  Catalase +ve  Non sporing  Non acid.

DiphteroidsDiphteroids

Pleomorphic gram-positive rods.Pleomorphic gram-positive rods. Club Shaped (Club Shaped (Chinese Letter like, V formsChinese Letter like, V forms)) Catalase +veCatalase +ve Non sporing Non sporing Non acid fast Non acid fast

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DiphteroidsDiphteroids (Continued) (Continued)

Commensals of the throat and skin of low Commensals of the throat and skin of low pathogenicity.pathogenicity.

Morphologically similar to the pathogenic Morphologically similar to the pathogenic C.diphtheriae.C.diphtheriae.

Can be found as contaminants of blood cultures Can be found as contaminants of blood cultures and CSF.and CSF.

Can cause opportunestic infections in Can cause opportunestic infections in Immunosupressed patients.Immunosupressed patients.

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Corynebacterium diphtheriae Corynebacterium diphtheriae (diphtheria)(diphtheria)

Local infection of the throat with grayish Local infection of the throat with grayish adherent exudate (adherent exudate (PseudomembranePseudomembrane) and ) and generalized toxaemia due to production and generalized toxaemia due to production and dissemination of a highly potent toxindissemination of a highly potent toxin..

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Etiology Etiology Corynebacterium diphtheriaeCorynebacterium diphtheriae

3 Types of Colony:3 Types of Colony: Mitis (Mild disease)Mitis (Mild disease) Intermedius (Intermedius (Intermediate dis.Intermediate dis.)) Gravis (Gravis (severesevere))

Strains may be toxegenic or non-toxegenic.Strains may be toxegenic or non-toxegenic. Production of toxin is mediated by bacteriophage Production of toxin is mediated by bacteriophage

((ββ phage phage) infection of the bacterium.) infection of the bacterium.

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Etiology Etiology Corynebacterium diphtheriae Corynebacterium diphtheriae (Continued)(Continued)

The demonstration of toxin production is The demonstration of toxin production is essential to differentiate toxegenic from essential to differentiate toxegenic from commensal corynebacteria.commensal corynebacteria.

Toxogenicity is demonstrated by the agar gel Toxogenicity is demonstrated by the agar gel precipitation (precipitation (ElekElek) test or by the polymerase ) test or by the polymerase chain reaction (chain reaction (PCRPCR).).

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Clinical ManifestationClinical Manifestation

Usually gradual onset of local infection.Usually gradual onset of local infection. Membranous nasopharyngitisMembranous nasopharyngitis Obstructive laryngotrachitisObstructive laryngotrachitis With low grade feverWith low grade fever MalaiseMalaise FatigueFatigue Sore throatSore throat

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Grey tonsillar membrane in acute diphtheria

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Clinical Manifestation Clinical Manifestation (Continued)(Continued)

Clinically:Clinically: Nasal diphNasal diph.. thick nasal discharge thick nasal discharge

(intoxication rare)(intoxication rare) Pharyngial Pharyngial thick, adherent pseudomembranethick, adherent pseudomembrane

(intoxication common)(intoxication common) (tonsillar)(tonsillar) Odema, Heat + Tenderness of Odema, Heat + Tenderness of

tissue of neck (tissue of neck (Bull neckBull neck)) Laryngial Laryngial extension of membrane extension of membrane

((asphyxiaasphyxia))

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Clinical Manifestation Clinical Manifestation (Continued)(Continued)

Less Commonly:Less Commonly: CutanousCutanous VaginalVaginal Conjunctival or oticConjunctival or otic

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Clinical Manifestation Clinical Manifestation (Continued)(Continued)

Life threating complication include:Life threating complication include: Upper airway obstruction Upper airway obstruction (extension of (extension of

membrane)membrane) Myocarditis Myocarditis (heart failure)(heart failure) Neurologic Neurologic Peripheral neuritisPeripheral neuritis

Vocal cord paralysisVocal cord paralysis Ascending paralysisAscending paralysis Difficulty in swallowingDifficulty in swallowing Visual disturbanceVisual disturbance

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EpidemiologyEpidemiology

Humans are the only reservoir.Humans are the only reservoir. Sources of Infections:Sources of Infections:

Discharges from nose, throat, eye and skin lesions of Discharges from nose, throat, eye and skin lesions of infected patients or carriers (direct contact)infected patients or carriers (direct contact)

Most common in low socioeconomic groups in Most common in low socioeconomic groups in crowded conditions.crowded conditions.

Since 1990 – epidemics in Soviet Union, Russia Since 1990 – epidemics in Soviet Union, Russia with 50,000 cases – 1750 deaths.with 50,000 cases – 1750 deaths.

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EpidemiologyEpidemiology (Continued) (Continued)

Case fatality 3% - 23%Case fatality 3% - 23% Children are susceptable after 3-6 months (highest Children are susceptable after 3-6 months (highest

incidence).incidence). Latent skin infection Latent skin infection immunity.immunity. Communicability Communicability 2 weeks (untreated 2 weeks (untreated

person)person)

<4 days (treated patients)<4 days (treated patients) Incubation Period is 2- 5 days.Incubation Period is 2- 5 days.

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PathogenesisPathogenesis

Powerful exotoxin ( blood stream):Powerful exotoxin ( blood stream):

Toxin Toxin local and systemic toxicity local and systemic toxicity

(toxin mediated disease)(toxin mediated disease) Cause of mortality in clinical diphtheria.Cause of mortality in clinical diphtheria. Affinity for heart muscles, nerve endings and Affinity for heart muscles, nerve endings and

adreral glands.adreral glands. Produced by Produced by ββ phage infected phage infected C.diphtheriae.C.diphtheriae.

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Pathogenesis Pathogenesis (Continued)(Continued)

Rapidly diffused from local lesion Rapidly diffused from local lesion irreversibly irreversibly bound to tissues.bound to tissues.

ADP ribosylating toxin ADP ribosylating toxin protein synthesis protein synthesis inhibition cell death necrosis and inhibition cell death necrosis and neutroxic effects.neutroxic effects.

Bacilli (local effect), no deep penetration to Bacilli (local effect), no deep penetration to blood or underlying tissue.blood or underlying tissue.

Inflammatory exudate and necrosis of Inflammatory exudate and necrosis of pharyngeal muscles pharyngeal muscles respiratory respiratory obstruction.obstruction.

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DiagnosisDiagnosis

Clinical diagnosis:Clinical diagnosis: Lab should not delay management.Lab should not delay management. Specimen for culture Specimen for culture

Nose Nose From bothFrom both ThroatThroat Patient and carrierPatient and carrier Lesions Lesions

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Elek plate demonstrating toxin from Corynebacterium diphtheriae

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DiagnosisDiagnosis (Continued) (Continued)

Direct stained smear unreliable (Commensals)Direct stained smear unreliable (Commensals)

Special media (Special media (Potassium -telluritePotassium -tellurite) and enriched ) and enriched Loefflers slope (selective) grey black colonies.Loefflers slope (selective) grey black colonies.

Albert stain Albert stain metachromatic granules. metachromatic granules. Toxogenicity test (Toxogenicity test (Elek test, PCRElek test, PCR) is most ) is most

important, guinea pig inoculation.important, guinea pig inoculation. Elek test: agar gel precipitation.Elek test: agar gel precipitation.

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ManagementManagementPatient:Patient:

Fatality with delay (Fatality with delay (0 -20%)0 -20%)1- 1- AntitoxinAntitoxin

Equine antitoxin – neutralize the toxin Start soon if clinically suspected.

2- Isolation of the patient (droplet precautions)3- Antibiotics (no effect on toxin)

to eradicate organism and prevent spread (a) Penicillin – oral (b) Erythromycin

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Management Management (Continued)(Continued)

3- 3- Contacts (Close) Contacts (Close) Investigated for signs of disease

Carriage (nose, throat)

Chemoprophylaxis (erythromycin) Immunization of susceptiable contacts

(diph. toxoid) Carriers isolated and treated.

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Prevention and ControlPrevention and Control

Universal immunization with diph. toxoid the only Universal immunization with diph. toxoid the only effective control measure.effective control measure.

High immunization rate among children (High immunization rate among children (3 doses of 3 doses of DPT + 2 boosters at 2 month ageDPT + 2 boosters at 2 month age))

Regular booster (Regular booster (Td every 10 yearsTd every 10 years).). Vaccine = formalin treated toxin – highly antigenic, Vaccine = formalin treated toxin – highly antigenic,

not toxic.not toxic.