1. CORYNEFORM BACTERIA

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

3. 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.

4. 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.

5. 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 (β phage) infection of the bacterium.

6. 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).

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

8. Grey tonsillar membrane in acute diphtheria

9. 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)

10. Clinical Manifestation (Continued)
Less Commonly:
Cutanous
Vaginal
Conjunctival or otic

11. 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

12. 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.

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

14. 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 β phage infected C.diphtheriae.

15. 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.

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

17. Elek plate demonstrating toxin from Corynebacterium diphtheriae

18. 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.

19. Management Fatality with delay (0 -20%) Patient: 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

20. 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.

21. 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.

22. 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%

23. 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.

24. 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