Corynebacterium diphtheriae (diphtheria): Morphology, Pathogenesis, Clinical Findings, Treatment

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Summary

This video provides a detailed overview of Corynebacterium diphtheriae, the bacterium responsible for diphtheria. It covers its classification, morphology, habitat, transmission, pathogenesis, clinical findings, laboratory diagnosis, treatment, and prevention strategies.

Highlights

Introduction & Classification of Corynebacterium diphtheriae
00:00:00

The video introduces Corynebacterium diphtheriae, explaining its classification as a Gram-positive, non-spore-forming, non-filamentous rod. It is pleomorphic, meaning it exists in various shapes (V, L, club-shaped rods), and is catalase-positive. It ferments carbohydrates to produce lactic acid and produces diphtheria toxin responsible for the disease.

Morphology of Corynebacterium diphtheriae
00:03:48

Corynebacterium diphtheriae are Gram-positive rods, appearing club-shaped. They arrange in palisades or V and L-shaped formations. The rods have a beaded appearance due to metachromatic granules, which are highly polymerized phosphate storage mechanisms that stain red while the rest of the cell is blue. The bacterium is 2 micrometers in length, non-capsulated, non-motile, and produces diphtheria toxin.

Habitat and Transmission of Diphtheria
00:05:25

Humans are the only host for Corynebacterium diphtheriae. Both toxigenic and non-toxigenic strains reside primarily in the upper respiratory tract but can also be found in gastrointestinal and genitourinary tracts. Diphtheria is transmitted via respiratory or airborne droplets and can infect skin at pre-existing lesions. Risk factors include tropical regions, poor skin hygiene, and children.

Pathogenesis of Diphtheria
00:06:15

Corynebacterium diphtheriae becomes pathogenic when infected by a bacteriophage carrying the gene for diphtheria toxin, an AB toxin. This toxin inhibits protein synthesis by ADP-ribosylation of elongation factor 2 (eEF2), leading to cell death. The toxin's binding domain attaches to host cells, and the active domain performs the ribosylation. The phage integrates its DNA into the bacterial chromosome during the lysogenic phase, enabling toxin production. Non-lysogenized cells are non-pathogenic.

Clinical Findings of Diphtheria
00:08:42

Diphtheria presents in two main types: respiratory and cutaneous. Respiratory diphtheria involves local inflammation in the throat, forming a tough, adherent gray pseudomembrane composed of necrotic tissue, bacterial cells, lymphocytes, plasma cells, and fibrin. It causes non-specific upper respiratory tract symptoms like fever, sore throat, and cervical adenopathy. Cutaneous diphtheria causes ulcerating skin lesions covered by a gray membrane, which are often indolent. Complications include airway obstruction, myocarditis, and nerve paralysis.

Laboratory Diagnosis of Diphtheria
00:11:58

Diagnosis can be made by throat swab, Gram staining (showing purple/blue Gram-positive pleomorphic rods), and methylene blue staining (showing red metachromatic granules). Culture on selective media like Loeffler's medium and tellurite plate (forming black colonies with a small zone of hemolysis) is crucial. Other tests include gel diffusion toxin assays, PCR for the toxin gene, ELISA for toxin protein, and the Schick test to assess patient immunity.

Treatment and Prevention of Diphtheria
00:14:52

Immediate treatment involves diphtheria antitoxin derived from horses, which neutralizes unbound toxin in the blood. Maintaining an airway is critical due to potential obstruction. Antibiotics like penicillin G and erythromycin are used. Prevention relies on the DTaP vaccine (Diphtheria toxoid, Tetanus toxoid, and acellular Pertussis), which provides immunity by administering toxoids.

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