Corynebacterium diphtheriae Diphtheria

Morphology and culturing. Diphtheria bacteria are Gram-positive, pleomorphic, often club-shaped rods. The individual cells tend to group in V, Y, or palisade arrangements (Fig. 4.9). Neisser staining reveals the polar bodies (polyphosphates stored at one end of the rod).

Loffler nutrient medium, which consists of coagulated serum and nutrient broth, is still used for the primary cultures. Selective indicator mediums containing tellurite are used in selective culturing. K tellurite is used to inhibit the accompanying flora. The K tellurite is also reduced to tellurium, coloring the colonies a brownish black.

Extracellular toxin. Diphtheria toxin consists of two functionally distinct fragments, A and B, whereby B stands for binding to receptors of target cells and A stands for toxic activity. Fragment A irreversibly blocks protein synthesis translation in the target cells, which then die. The toxin gene is always a prophage genome component (see lysogenic conversion, p. 186).

— Corynebacterium diphtheriae-

Fig. 4.9 Gram staining of a wound secretion preparation in wound diphtheria: typical configuration of

— Corynebacterium diphtheriae-

Fig. 4.9 Gram staining of a wound secretion preparation in wound diphtheria: typical configuration of

Wound Diphtheria

Diphtheria toxin

Fragment A is an ADP ribosyl transferase. The enzyme transfers adenosine diphosphate ribose from NAD to the elongation factor eEF2, thereby inactivating it:

eEF2 "translocates" the peptidyl tRNAfrom the amino acid position A to the peptide position P on the eukaryotic ribosome. Although the toxin gene is integrated in a phage genome, its activity is regulated by the gene product DtxR of the dtxR gene of the bacterial cell's genome. DtxR combines with Fe2+ to become an active repressor that switches off the transcription of the toxin gene.

4 Pathogenesis and Clinical Picture

■ Local infection. Infection of the mucosa of tonsils, pharynx, nose, and conjunctiva (Fig. 4.10). Wounds and skin lesions can also be infected. The pathogens invade the host through these portals, reproduce, and produce toxin, resulting in local cell damage. The inflammatory reaction leads to collection of a grayish-white exudate, the matrix of the "diphtherial pseudomembrane" consisting of fibrin, dead granulocytes, and necrotic epithelial cells. This coating adheres quite strongly to the mucosa. It may extend into the larynx, thus eventually hindering respiration. Regional lymph nodes are highly swollen.

■ Systemic intoxication. Parenchymal degeneration in the cardiac muscle, liver, kidneys, and adrenal glands. Motor cranial nerve paralysis. Late sequel damage due to the intoxication is frequently seen after the acute infection has subsided.

Toxin-negative strains of C. diphtheriae are occasionally observed as pathogens in endocarditis or dermal infections. The pathogenicity of such strains corresponds to that of commensal corynebacteria (see Table 4.3, p. 261).

Diagnosis. The method of choice is detection and identification of the pathogen in cultures from local infection foci. The culture smear, which arrives at the laboratory in transport medium, is plated out on Loffler medium and a selective indicator medium. Identification is based on both morphological and physiological characteristics. The toxin is detected by the Elek-Ouchter-lony immunodiffusion test. A molecular method is now also being used to identify the toxin gene. Toxin detection is necessary for a laboratory diagnosis of diphtheria because of the occurrence of toxin-negative strains.

Therapy. Antitoxic serum therapy is the primary treatment and it must commence as soon as possible if diphtheria is suspected. This treatment is supplemented by administration of penicillin or erythromycin.

— Nose and Throat (Nasopharyngeal) Diphtheria

— Nose and Throat (Nasopharyngeal) Diphtheria

Bullneck And Corynebacterium Diphtheriae
Fig. 4.10 a Hemorrhaging of the nasal mucosa (endothelial damage). Pronounced cervical adeno-pathy and swelling, creating a bull neck appearance. b Thick coating (membrane) on highly swollen tonsils (so-called diphtherial pseudomembrane), causing respiratory stridor.

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