CORYNEFORM BACTERIA

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CORYNEFORM BACTERIA
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Diphteroids

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

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Diphteroids (Continued)

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

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Corynebacterium diphtheriae (diphtheria)

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

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Etiology 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
  (ß phage) infection of the bacterium.

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Etiology 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).

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Clinical Manifestation

• Usually gradual onset of local infection.
• Membranous nasopharyngitis
• Obstructive laryngotrachitis
• With low grade fever
• Malaise
• Fatigue
• Sore throat

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Grey tonsillar membrane in acute diphtheria
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Clinical Manifestation (Continued)

• Clinically
• 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
• (asphyxia)

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Clinical Manifestation (Continued)

• Less Commonly
• Cutanous
• Vaginal
• Conjunctival or otic

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Clinical Manifestation (Continued)

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

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Epidemiology

• 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.

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Epidemiology (Continued)

• Case fatality 3 - 23
• Children are susceptable after 3-6 months
  (highest incidence).
• Latent skin infection immunity.
• Communicability 2 weeks (untreated
  person)
• lt4 days (treated patients)
• Incubation Period is 2- 5 days.

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Pathogenesis

• 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 ß phage infected C.diphtheriae.

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Pathogenesis (Continued)

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

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Diagnosis

• Clinical diagnosis
• Lab should not delay management.
• Specimen for culture
• Nose From both
• Throat Patient and carrier
• Lesions

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Elek plate demonstrating toxin from
Corynebacterium diphtheriae
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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.

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Management

• Patient
• 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

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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.

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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.

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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

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• Resistance to LM infection is predominantly
  cell-mediated
• Evidence of this is provided by the
  overwhelming clinical
• association between Listeria infections and
  conditions associated with impaired cellular
  immunity, including lymphomas, pregnancy, AIDS
  and corticosteroid-induced immunosupression
• in transplant recipients.

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• 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, malignancy
• and HIV . Additional groups include neonates ,
  pregnant
• women and elderly