Microbiological understandings and mysteries of noma (cancrum oris)

Abstract

The microbiologic history of noma was reviewed. Studies have associated the disease process with large numbers of fusiform bacilli and spirochetal organismS. In order to study the microbiology of the staging and infection periods of noma 62 Nigerian children, aged 3–14 years, 22 children had acute necrotizing ulcerative gingivitis (ANUG) and were also malnourished, 20 exhibited no acute necrotizing ulcerative gingivitis but were malnourished and 20 were free of acute necrotizing ulcerative gingivitis and in good nutritional state) were evaluated for the presence of viruses and oral microorganisms. The ANUG cases in the malnourished children had a higher incidence of Herpesviridae, the main virus being detected was cytomegalovirus. There were more anaerobic microorganisms recovered, with Prevotella intermedia as the predominant isolate, in the malnourished children as compared to the healthy children. A study of the predominant microflora in active sites of noma lesions was carried out in eight noma patients, 3–15 years of age, in Sokoto State, northwestern Nigeria.Fusobacterium necrophorum was recovered from 87.5% of the noma lesionS. Oral microorganisms isolated 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, Veil‐lonella parvula, Staphylococcus aureus and Pseudomonas spp.were each recovered from one lesion. 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 pathogenic mechanisms of F.necrophorum as a trigger organism were discussed. The isolation from human noma lesions of F.necrophorum, a pathogen primarily associated with animal diseases, may have important etiologic and animal transmission implications.

NOMA: A Preventable “Scourge” of African Children

“…The primary reason for this obscurity is obvious: the epicenter of noma development, the oral cavity, is inhabited by several hundred species of normal commensal bacteria [48][49][50][51]. A long held notion is that noma is caused by spirochetes and fusobacteria [5,6,52]. This notion partly stems from an extrapolation of the microbiological culprits of the presumed noma antecedent, NUG, which also includes spirochetes and fusobacteria, and partly because the levels of these organisms appear to be elevated in noma.…”

“…Nevertheless, recent reports suggest that noma is caused by a mixed infection of oral and extraoral opportunistic pathogens [3,5,6,54] while incorporating the proposal that some noma cases may be the result of zoonotic infection with Fusobacterium necroforum. Using culture-independent molecular methods, Paster et al [54] reported the detection of 67 bacterial species or phylotypes in advanced noma lesion of four Nigerian patients.…”

Noma management in a child with systemic lupus erythematosus

“…It has been speculated that B�rrelia vincentii and F�s��acteri�� are prominent bacteria in such lesions. 2,8 Recent reports suggest that besides fusiform bacilli and spirochetes, other anaerobic bacteria are present in a relatively high proportion of noma lesions. 8 F. necr����r�� is considered a key component.…”

“…2,8 Recent reports suggest that besides fusiform bacilli and spirochetes, other anaerobic bacteria are present in a relatively high proportion of noma lesions. 8 F. necr����r�� is considered a key component. This organism produces dermatotoxins, which could explain the rapid progression of the disease.…”

“…1 It is postulated that the disease is triggered by a consortium of micro organisms of which F�s��acteri�� necr����r�� is a key component. 2,8 Symbiotic relationship between fusiform bacilli and non-hemolytic streptococci and staphylococci has been considered a significant factor in the development of noma. Anaerobic bacteria may be present in rapidly progressing disease.…”