Coryneform Bacteria Infection And Immunity

WC Noble, Department of Microbial Diseases, The Institute of Dermatology, United Medical and Dental Schools of Guy's and St Thomas' Hospital, St Thomas' Hospital, London, UK

Coryneform bacteria from mammalian sources can be assigned to five genera: Brevibacterium, Coryne-bacterium, Dermabacter, Propionibacterium and Rhodococcus. All are gram-positive, nonspore-forming bacilli, distinguished chiefly on their cell wall composition; speciation within the genera is incomplete.

Brevibacterium spp. are aerobic, nonlipid-requir-ing organisms which are sometimes referred to as 'large colony coryneforms'. Their pathogenic role is uncertain except in forms of tinea pedis associated with malodor caused by proteolytic destruction of the skin. Bloodstream infections are reported on rare occasions.

Corynebacterium spp. include many of the best speciated organisms; they frequently need lipid for adequate growth in vitro and are often microaero-phils; they may be called the 'small colony coryneforms'. The localized skin disease erythrasma is caused by an overgrowth of the normal skin inhabitant C. minutissimum, whilst a variety of normal axillary inhabitants are associated with pronounced axillary odor which results from microbial modifications of apocrine steroid secretions.

Cory neb acterium diphtheriae, the best studied and most serious pathogen, gives rise to toxinogenic pharyngeal diphtheria and also to less severe skin infections. Toxin production occurs following lyso-genization of C. diphtheriae by tox+ phages, several of which have been described though most have similar DNA structures. Tox+ phages are also able to lysogenize C. pseudotuberculosis (C. ovis) and C. ulcerans, causing these organisms to produce diphtheria toxin. The toxin is a 535 amino acid polypeptide of 58.3 kDa. When nicked by trypsin at specific sites, it forms two dissimilar fragments which remain joined to form an enzymically active molecule catalyzing ADP ribosylation of elongation factor 2 (EF2) with nicotinamide adenine dinucleotide as substrate. F,F2 is an enzyme present in the cytoplasm of eukary-otic cells and is essential for peptide synthesis. Ribosylation of this enzyme inhibits protein synthesis and results in the necrotic lesions of diphtheria. A single molecule of the A fraction of toxin, which contains the ribosylating activity, is lethal to a cell within hours if introduced into the cytoplasm but neither A nor B fragment is toxic extracellularly. Since the toxins produced by all strains of C. diphtheriae are immunologically identical, immunity is achieved by immunizing with a single toxoid; there is no type-specific immunity. The immunized individual is not protected against infection but against the systemic and local necrotic effects of the toxin; the degree of immunity conferred is high but not complete.

Caseous lymphadenitis in sheep and goats and ulcerative lymphangitis in horses results from infection with C. pseudotuberculosis. The disease is pyogenic despite the fact that C. pseudotuberculosis may produce its own toxin ('C. ovis toxin') as well as diphtheria toxin. The toxins appear to play little part in animal disease. C. ulcerans is also able to produce both these toxins and has given rise to classical diphtheria in humans. The C. renale, C. pilosum, C. cysti-tidis group cause bovine cystitis and pyelonephritis associated with extensive necrosis.

Corynebacterium jeikeium is most frequently characterized by resistance to most common antibiotics. Although found on normal human skin it causes low-grade bacteremias, generally in the immunosuppressed and particularly in males with leukemia. The mechanism of pathogenesis is unknown. C. urealyticum is similarly a skin resident and resistant to many antibiotics, it is a rare cause of kidney stones.

Dermabacter hominis is a recently described large colony coryneform from human skin which is re cognized as a rare cause of bacteremia and deep infection.

Propionibacterium spp. require lipid and anaerobic conditions for successful cultivation in vitro. P. acnes and P. granulosum are isolated from highly sebaceous areas of human skin in all those past puberty; P. avidum is similarly found in the axilla. The first two species are associated with acne and are occasionally recovered from deep infections in humans. There is no consensus on the role of Propionibacteria in acne. Not all acne lesions contain microorganisms but a potential role for Propionibacteria may be as follows: they reside in the ducts of sebaceous glands which become blocked as a result of changes in keratinization; sebum continues to be produced so that the blocked duct forms a closed comedo. In vitro, P. acnes has sharp pH and p02 optima for the production of hyaluronidase and protease; production of these enzymes in vivo, if it occurs, would render the comedo wall leaky to host-defense mechanisms; triggering of the alternative complement pathway by the cell wall of P. acnes or by protease would account for erythema and the recruitment of white cells to form a pustule. The serological picture is complicated by the almost universal existence of antibody to P. acnes. There is switch from predominantly immunoglobulin M (IgM) in children to IgG in adults. Antibodies to hyaluronidase are found in only about 10% of adults and this may indicate that exocellular enzymes have-little role in acne. Cellular immunity in acne is a late event which probably does not contribute to lesion formation. The immunostimulator 1 Corynebacterium parvum' is a mixture of Propionibacteria similar to that found on the skin.

Propionibacterium propionicus ( Arachnid propio-nica) is a normal inhabitant of the human oral cavity which causes lachrymal duct infections.

Rhodococcus spp. may be difficult to distinguish from Corynebacterium spp. unless red pigmented colonies are seen or details of mycolic acid structure obtained, since the two grow under similar conditions in vitro. R. equi, a facultative intracellular organism, produces a potentially fatal suppurative bronchopneumonia in foals with intense inflammation of the lymph nodes. Rhodococcus spp. are rare pathogens of humans, occurring most frequently in the severely immunosuppressed.

See also: Bacterial cell walls; Immunopotentiation; Toxins.

Further reading

Colman G, Weaver E and Efstratiou A (1992) Screening tests for pathogenic corynebacteria. Journal of Clinical

Pathology 45: 46-48.

Coyle iVtB and Lipsky BA (1990) Coryneform bacteria in infectious disease: clinical and laboratory aspects. Clinical Microbiology Reviews 3: 227-246. DeZoysa A, Efstratiou A, George RC et al (1995) Molecular epidemiology of Corynebacterium diphtheriae from northwestern Russia and surrounding countries studied by using ribotyping and pulsed field electrophoresis. Journal of Clinical Microbiology 33: 1080-1083.

Dixon JMS, Noble WC and Smith GR (1990) Diphtheria: other corynebacterial and coryneform infections. In: Smith GR and Easmon CSF (eds) Topley and Wilson's Principles of Microbiology and Immunity, vol 3, pp 55-79. London: Edward Arnold.

Funke G, von Graevenitz A, Clarridge JE et al (1997) Clinical microbiology of coryneform bacteria. Clinical Microbiology Reviews 10: 125-159.

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