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Diptheria
Corynebacterium diphtheriae is the bacterium responsible for diphtheria, a serious infectious disease characterized by a potent exotoxin that can cause severe respiratory complications and systemic effects. The pathogenesis of diphtheria involves its ability to colonize and produce diphtheria toxin, which can lead to life-threatening conditions. Control measures include immunization with diphtheria toxoid and antibiotics, with prompt administration of antitoxin being crucial to reduce mortality rates.
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Diptheria
- 1. Corynebacterium diphtheriae A paradigm ofthe toxigenic infectious diseases Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
- 2. Edwin Klebs In 1883,Klebs demonstrated that Corynebacterium diphtheriae was the agent of diphtheria
- 3. Introduction By 1888, Rouxand Yersin showed that animals injected with sterile filtrates of C diphtheriae developed symptoms similar to that of human diphtheria; this demonstrated that a potent exotoxin was the major virulence factor. Alexandre Yersin Pierre Paul Émile Roux
- 4. General Characters • Itis also known as the Klebs-Löffler bacillus • Gram-positive, highly pleomorphic organisms with no particular arrangement • Special stains like Albert’s stain and Ponder's stain are used to demonstrate the metachromatic granules formed in the polar regions
- 5. General Characters • Itis also known as the Klebs-Löffler bacillus • Gram-positive, highly pleomorphic organisms with no particular arrangement • Special stains like Albert’s stain and Ponder's stain are used to demonstrate the metachromatic granules formed in the polar regions
- 6. General Characters • Corynebacteriumdiphtheriae is a nonmotile, noncapsulated, club-shaped, gram-positive bacillus • Toxigenic strains are lysogenic for one of a family of corynebacteriophages that carry the structural gene for diphtheria toxin, tox • Corynebacterium diphtheriae is classified into biotypes (mitis, intermedius, and gravis) according to colony morphology on tellurite containing media, as well as into lysotypes based upon corynebacteriophage sensitivity
- 7. Classification • Long Rods •curved shaped • pleomorphic • Prominent granules • greyish black, opaque colonies • Glycogen and starch fermentation • Paralytic and epidemic • Short Rods • Uniform Staining • Few or no granules • May be pleomorphic • gray colony, dark center shining • Non-hemolytic • Hemorrhagic and epidemic • Long-barred forms, clubbed end • Poor Granulation • Very pleomorphic • gray, opaque glossy, smooth surface, poached egg colonies, • Obstructive and Endemic
- 8. DIphtheria • Diphtheria ismost commonly an infection of the upper respiratory tract and causes • Fever • sore throat • malaise • A thick, gray-green fibrin membrane, the pseudomembrane, often forms over the site(s) of infection as a result of the combined effects of • bacterial growth • toxin production • necrosis of underlying tissue • host immune response
- 9. Diseases • Symptoms ofpharyngeal diphtheria vary from mild pharyngitis to hypoxia due to airway obstruction by the pseudomembrane • The involvement of cervical lymph nodes may cause swelling of the neck (bull neck diphtheria), and the patient may have a fever (≥ 103 °F) • The skin lesions in cutaneous diphtheria are usually covered by a gray-brown pseudomembrane • Life-threatening systemic complications, principally loss of motor function (e.g., difficulty in swallowing) and congestive heart failure, may develop as a result of the action of diphtheria toxin on peripheral motor neurons and the myocardium. There are two types of clinical diphtheria: nasopharyngeal and cutaneous.
- 10. Pathogenesis The pathogenesis ofdiphtheria is based upon two primary determinants: 1. the ability of a given strain of C diphtheriae to colonize in the nasopharyngeal cavity and/or on the skin 2. its ability to produce diphtheria toxin
- 11. Pathogenesis • The structuralgene for diphtheria toxin, tox, is carried by a family of closely related corynebacteriophages • The regulation of diphtheria tox expression is mediated by an iron-activated repressor, DtxR, which is encoded on the C diphtheriae genome • When iron become the growth limiting diphtheria toxin is synthesized and secreted at maximal rates
- 12. Pathogenesis • Diphtheria toxinis extraordinarily potent: as little as 100 to 150 ng/kg of body weight is lethal • Diphtheria toxin is composed of a single polypeptide chain of 535 amino acids • Intoxication of a single eukaryotic cell by diphtheria toxin can lead to complete irreversible inhibition of protein synthesis (by binding to elongation factor – 2, EF-2)
- 13. Diagnosis • laboratory confirmationof toxigenic C diphtheriae in throat or lesion cultures • Sterile cotton-tipped applicators are used to swab the pharyngeal tonsils or their beds. • Swabs may be inserted through both nares to collect nasopharyngeal samples for culture. Since diphtheritic lesions are often covered with a pseudomembrane, the surface of the lesion may have to be carefully exposed before swabbing • The most common in vitro assay for toxigenicity is the Elek immunodiffusion test • This test is based on the double diffusion of diphtheria toxin and antitoxin in an agar medium. • A sterile, antitoxin-saturated filter paper strip is embedded in the culture medium, and C diphtheriae isolates are streak-inoculated at a 90° angle to the filter paper • The production of diphtheria toxin can be detected within 18 to 48 hours by the formation of a toxin-antitoxin precipitin band in the agar
- 14. Elek immunodiffusion test •Sterile filter paper impregnated with diphtheria antitoxin is imbedded in agar culture medium. Isolates of C diphtheriae are then streaked across the plate at an angle of 90° to the antitoxin strip. Toxigenic C diphtheriae is detected because secreted toxin diffuses from the area of growth and reacts with antitoxin to form lines of precipitin.
- 15. Signs and symptoms •The symptoms of diphtheria usually begin two to seven days after infection • fever of 38 °C (100.4 °F) or above, chills, fatigue, bluish skin coloration (cyanosis), sore throat, hoarseness, cough, headache, difficulty swallowing, painful swallowing, difficulty breathing, rapid breathing, foul-smelling and bloodstained nasal discharge, and lymphadenopathy • Within two to three days, diphtheria may destroy healthy tissues in the respiratory system • Dead tissue forms a thick, gray coating that can build up in the throat or nose. This thick gray coating is called a “pseudomembrane.” • It can cover tissues in the nose, tonsils, voice box, and throat, making it very hard to breathe and swallow. • Symptoms can also include cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies
- 16. Signs and symptoms Anadherent, dense, grey pseudomembrane covering the tonsils is classically seen in diphtheria. A diphtheria skin lesion on the leg Diphtheria can cause a swollen neck, sometimes referred to as a bull neck
- 17. Control • The controlof diphtheria depends upon adequate immunization with diphtheria toxoid: ormaldehyde-inactivated diphtheria toxin that remains antigenically intact • Immunization against diphtheria should begin in the second month of life with a series of three primary doses spaced 4 to 8 weeks apart, followed by a fourth dose approximately 1 year after the last primary inoculation • Diphtheria toxoid is widely used as a component in the DPT (diphtheria, pertussis, tetanus) vaccine. • Diphtheria vaccine is usually combined at least with tetanus vaccine (Td) and often with pertussis (DTP, DTaP, TdaP) vaccines, as well. • The adult population should be reimmunized with diphtheria toxoid every 10 years
- 18. Control • Although antibiotics(e.g., penicillin and erythromycin) are used as part of the treatment of patients who present with diphtheria, prompt passive immunization with diphtherial antitoxin is most effective in reducing the fatality rate • The long half-life of specific antitoxin in the circulation is an important factor in ensuring effective neutralization of diphtheria toxin; however, to be effective, the antitoxin must react with the toxin before it becomes internalized into the cell. • Metronidazole, Erythromycin, Procaine penicillin G, rifampin or clindamycin • diphtheria toxin spreads through the blood and can lead to potentially life-threatening complications that affect other organs, such as the heart and kidneys. Damage to the heart caused by the toxin affects the heart's ability to pump blood or the kidneys' ability to clear wastes. It can also cause nerve damage, eventually leading to paralysis.
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- 20. How did theymake diphtheria antitoxin?