Characterization of protease activities in Capnocytophaga spp., Porphyromonas gingivalis, Prevotella spp., Treponema denticola and Actinobacillus actinomycetemcomitans

Gazi, M. I.; Cox, Susanne; Clark, Douglas; Eley, B M

doi:10.1111/j.1399-302x.1997.tb00386.x

Cited by 31 publications

(46 citation statements)

References 40 publications

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“…Prevotella intermedia could add to tissue destruction with its ability to degrade lipid materials 50 and the production of proteolytic enzymes such as dipeptidyl peptidases and cysteine proteases, with the latter also involved in the breakdown of IgG. [89][90][91] The degradation of immunoglobulin molecules would limit opsonic activity and complement-mediated lysis of these gram-negative microorganisms.…”

Section: Discussionmentioning

confidence: 99%

Isolation of Fusobacterium necrophorum from cancrum oris (noma).

Falkler¹,

Enwonwu²,

Idigbe³

1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. A study of the predominant microflora in active sites of noma (cancrum oris) lesions was carried out in eight noma patients 3-15 years of age in Sokoto State in northwestern Nigeria. Paper point sampling and conventional anaerobic microbiologic techniques were used. Fusobacterium necrophorum was recovered from 87.5% of the noma lesions. Oral microorganisms included Prevotella intermedia, alpha-hemolytic streptococci, and Actinomyces spp. which were isolated from 75.0%, 50.0%, and 37.5% of the patients, respectively. Peptostreptococcus micros, Veillonella parvula, Staphylococcus aureus, and Pseudomonas spp. were each recovered from one lesion. The F. necrophorum and P. intermedia isolates were tested for antibiotic sensitivity to clindamycin, tetracycline, metronidazole, and penicillin using the E-test, and all strains were observed to be sensitive to all of the antibiotics tested with the exception of one strain of P. intermedia, which showed resistance to penicillin. The first reported isolation from human noma lesions of F. necrophorum, a pathogen primarily associated with animal diseases, may have important etiologic and animal transmission implications.Noma (cancrum oris) is a destructive gangrenous stomatitis occurring mainly in children. It may lead to devastating facial deformity, circumferential scarring, stenosis of the mouth, and in many cases death. This disease occurs almost exclusively among poor malnourished children in developing countries.

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Section: Discussionmentioning

confidence: 99%

Isolation of Fusobacterium necrophorum from cancrum oris (noma).

Falkler¹,

Enwonwu²,

Idigbe³

1999

The American Journal of Tropical Medicine and Hygiene

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“…P. intermedia has also been isolated from nonoral infections such as abscesses of the head and neck and pleuropulmonary infections (Johnson and Holdeman, 1983;Finegold et al, 1993). P. intermedia could add to tissue destruction with its ability to degrade lipid materials ) and the production of proteolytic enzymes such as dipeptidyl peptidases and cysteine proteases, the latter also involved in the breakdown of IgG (Slots, 1981;Jansen et al, 1995;Gazi et al, 1997). It is not clear whether P. intermedia could be the black-pigmented member of the organisms considered as Bacteroides melaninogenicus in earlier work associated with noma lesions (MacDonald, 1962;Adekeye and Ord, 1983).…”

Section: Microbiological Reviewmentioning

confidence: 99%

Oro-Facial Gangrene (Noma/Cancrum Oris): Pathogenetic Mechanisms

Enwonwu

Falkler

Idigbe

2000

Critical Reviews in Oral Biology & Medicine

126

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Cancrum oris (Noma) is a devastating infectious disease which destroys the soft and hard tissues of the oral and para-oral structures. The dehumanizing oro-facial gangrenous lesion affects predominantly children ages 2 to 16 years, particularly in sub-Saharan Africa, where the estimated frequency in some communities varies from I to 7 cases per 1000 population. The risk factors are poverty, malnutrition, poor oral hygiene, residential proximity to livestock in unsanitary environments, and infectious diseases, particularly measles and those due to the herpesviridae. Infections and malnutrition impair the immune system, and this is the common denominator for the occurrence of noma. Acute necrotizing gingivitis (ANG) and oral herpetic ulcers are considered the antecedent lesions, and ongoing studies suggest that the rapid progression of these precursor lesions to noma requires infection by a consortium of micro-organisms, with Fusobacterium necrophorum (Fn) and Prevotella intermedia (Pi) as the suspected key players. Additional to production of a growth-stimulating factor for Pi, Fn displays a classic endotoxin, a dermonecrotic toxin, a cytoplasmic toxin, and a hemolysin. Without appropriate treatment, the mortality rate from noma is 70-90%. Survivors suffer the two-fold afflictions of oro-facial mutilation and functional impairment, which require a time-consuming, financially prohibitive surgical reconstruction.

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“…Being anaerobic, they reside mainly in the subgingival area. However, they may take hold in opportunistic infections such as periodontal diseases, which are destructive, inflammatory processes of the tooth attachment tissues, caused by Gram-negative proteolytic anaerobic bacteria (Gazi et al, 1997). Various spirochetal morphotypes can be observed in periodontal pockets, but many of these morphotypes are as yet uncultivable (Moter et al, 1998).…”

mentioning

confidence: 99%

Role of Treponema Denticola in Periodontal Diseases

Sela

2001

Critical Reviews in Oral Biology & Medicine

163

153

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Among periodontal anaerobic pathogens, the oral spirochetes, and especially Treponema denticola, have been associated with periodontal diseases such as early-onset periodontitis, necrotizing ulcerative gingivitis, and acute pericoronitis. Basic research as well as clinical evidence suggest that the prevalence of T. denticola, together with other proteolytic Gram-negative bacteria in high numbers in periodontal pockets, may play an important role in the progression of periodontal disease. The accumulation of these bacteria and their products in the pocket may render the surface lining periodontal cells highly susceptible to lysis and damage. T. denticola has been shown to adhere to fibroblasts and epithelial cells, as well as to extracellular matrix components present in periodontal tissues, and to produce several deleterious factors that may contribute to the virulence of the bacteria. These bacterial components include outer-sheath-associated peptidases, chymotrypsin-like and trypsin-like proteinases, hemolytic and hemagglutinating activities, adhesins that bind to matrix proteins and cells, and an outer-sheath protein with poreforming properties. The effects of T. denticola whole cells and their products on a variety of host mucosal and immunological cells has been studied extensively (Fig. 1). The clinical data regarding the presence of T. denticola in periodontal health and disease, together with the basic research results involving the role of T. denticola factors and products in relation to periodontal diseases, are reviewed and discussed in this article.

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Characterization of protease activities in Capnocytophaga spp., Porphyromonas gingivalis, Prevotella spp., Treponema denticola and Actinobacillus actinomycetemcomitans

Cited by 31 publications

References 40 publications

Isolation of Fusobacterium necrophorum from cancrum oris (noma).

Isolation of Fusobacterium necrophorum from cancrum oris (noma).

Oro-Facial Gangrene (Noma/Cancrum Oris): Pathogenetic Mechanisms

Role of Treponema Denticola in Periodontal Diseases

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