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03. CORYNEFORM by xiaohuicaicai



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

   Commensals of the throat and skin of low
   Morphologically similar to the pathogenic
   Can be found as contaminants of blood cultures
    and CSF.
   Can cause opportunestic infections in
    Immunosupressed patients.
      Corynebacterium diphtheriae

   Local infection of the throat with grayish
    adherent exudate (Pseudomembrane) and
    generalized toxaemia due to production and
    dissemination of a highly potent toxin.
     Corynebacterium diphtheriae
3 Types of Colony:
    Mitis (Mild disease)
    Intermedius (Intermediate dis.)
    Gravis (severe)
 Strains may be toxegenic or non-toxegenic.

 Production of toxin is mediated by bacteriophage
  (β phage) infection of the bacterium.
    Corynebacterium diphtheriae (Continued)

   The demonstration of toxin production is
    essential to differentiate toxegenic from
    commensal corynebacteria.
   Toxogenicity is demonstrated by the agar gel
    precipitation (Elek) test or by the polymerase
    chain reaction (PCR).
       Clinical Manifestation

Usually gradual onset of local infection.
   Membranous nasopharyngitis
   Obstructive laryngotrachitis
   With low grade fever
   Malaise
   Fatigue
   Sore throat
Grey tonsillar membrane in acute diphtheria
      Clinical Manifestation (Continued)

   Nasal diph.      thick nasal discharge
                     (intoxication rare)
   Pharyngial       thick, adherent pseudomembrane
                     (intoxication common)
   (tonsillar)       Odema, Heat + Tenderness of
    tissue of neck (Bull neck)
   Laryngial          extension of membrane
      Clinical Manifestation (Continued)

Less Commonly:
 Cutanous

 Vaginal

 Conjunctival or otic
      Clinical Manifestation (Continued)

Life threating complication include:
 Upper      airway obstruction (extension   of
 Myocarditis (heart failure)
 Neurologic       Peripheral neuritis
     Vocal cord paralysis
     Ascending paralysis
     Difficulty in swallowing
     Visual disturbance

   Humans are the only reservoir.
   Sources of Infections:
     Discharges from nose, throat, eye and skin lesions of
      infected patients or carriers (direct contact)
   Most common in low socioeconomic groups in
    crowded conditions.
   Since 1990 – epidemics in Soviet Union, Russia
    with 50,000 cases – 1750 deaths.
       Epidemiology (Continued)

   Case fatality 3% - 23%
   Children are susceptable after 3-6 months (highest
   Latent skin infection           immunity.
   Communicability           2 weeks (untreated person)
                              <4 days (treated patients)
   Incubation Period is 2- 5 days.

Powerful exotoxin (   blood stream):

   Toxin      local and systemic toxicity
               (toxin mediated disease)
   Cause of mortality in clinical diphtheria.
   Affinity for heart muscles, nerve endings and
    adreral glands.
   Produced by β phage infected C.diphtheriae.
        Pathogenesis (Continued)

   Rapidly diffused from local lesion       irreversibly
    bound to tissues.
   ADP ribosylating toxin         protein synthesis
    inhibition        cell death     necrosis and neutroxic
   Bacilli (local effect), no deep penetration to blood or
    underlying tissue.
   Inflammatory exudate and necrosis of pharyngeal
    muscles         respiratory obstruction.

Clinical diagnosis:
 Lab should not delay management.

 Specimen for culture
   Nose         From both
   Throat       Patient and carrier
   Lesions
Elek plate demonstrating toxin from Corynebacterium diphtheriae
            Diagnosis (Continued)

Direct stained smear unreliable (Commensals)

   Special media (Potassium -tellurite) and enriched
    Loefflers slope (selective)       grey black colonies.
   Albert stain      metachromatic granules.
   Toxogenicity test (Elek test, PCR) is most
    important, guinea pig inoculation.
   Elek test: agar gel precipitation.
    Fatality with delay (0 -20%)
1- Antitoxin
    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
   Management (Continued)

3- Contacts (Close)
     Investigated for signs of disease
                       Carriage (nose, throat)
     Chemoprophylaxis (erythromycin)
     Immunization of susceptiable contacts
      (diph. toxoid)
     Carriers         isolated and treated.
          Prevention and Control

   Universal immunization with diph. toxoid the only
    effective control measure.
   High immunization rate among children (3 doses of
    DPT + 2 boosters at 2 month age)
   Regular booster (Td every 10 years).
   Vaccine = formalin treated toxin – highly antigenic,
    not toxic.
Listeria monocytogenes

    Listeria monocytogenes is widespread in
     nature and has been
    isolated from the stools of 5% healthy
     adults. A variety of foods are contaminated
     with LM. It has been recovered from raw
     vegetables, raw milk, fish, poultry, soft
     cheese and meats at
    rates ranging from 15% to 70%
   Resistance to LM infection is predominantly cell-
     Evidence of this is provided by the overwhelming
   association between Listeria infections and
    conditions associated with impaired cellular
    immunity, including lymphomas, pregnancy, AIDS
    and corticosteroid-induced immunosupression
     in transplant recipients.
   Listeria monocytogenes (LM) meningitis is rare in
    patients with a normal immune status. Most
    reported cases have been associated with
    immunosupression produced by drugs (steroids and
     cytotoxic drugs), chronic renal disease, diabetes,
   and HIV . Additional groups include neonates ,
     women and elderly

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