Herpesviruses have been implicated in the pathogenesis of human periodontitis. The present study investigated whether herpesviruses are present in the lesions of acute necrotizing ulcerative gingivitis. Sixty-two Nigerian children, aged 3-14 years, were studied. Twenty-two children had acute necrotizing ulcerative gingivitis 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 a good nutritional state. Polymerase chain reaction methods were used to determine the presence of human cytomegalovirus (HCMV), Epstein-Barr virus type 1 and type 2 (EBV-1, EBV-2), herpes simplex virus (HSV), human herpes virus 6 (HHV-6), human papilloma virus and human immunodeficiency virus type 1 in crevicular fluid specimens collected by paper points. Of the 22 acute necrotizing ulcerative gingivitis patients, 15 (68%) revealed viral infection and 8 (36%) viral coinfection. Thirteen (59%) acute necrotizing ulcerative gingivitis patients demonstrated HCMV, 6 (27%) EBV-1, 5 (23%) HSV and 1 (5%) HHV-6. Only 2 (10%) subjects from each group not affected by acute necrotizing ulcerative gingivitis showed viral presence, and no control subject revealed viral coinfection. These findings suggest that HCMV and possibly other herpesviruses contribute to the onset and/or progression of acute necrotizing ulcerative gingivitis in malnourished Nigerian children.

The purpose of this study was to determine the bacterial diversity in advanced noma lesions using cultureindependent molecular methods. 16S ribosomal DNA bacterial genes from DNA isolated from advanced noma lesions of four Nigerian children were PCR amplified with universally conserved primers and spirochetal selective primers and cloned into Escherichia coli. Partial 16S rRNA sequences of approximately 500 bases from 212 cloned inserts were used initially to determine species identity or closest relatives by comparison with sequences of known species or phylotypes. Nearly complete sequences of approximately 1,500 bases were obtained for most of the potentially novel species. A total of 67 bacterial species or phylotypes were detected, 25 of which have not yet been grown in vitro. Nineteen of the species or phylotypes, including Propionibacterium acnes, Staphylococcus spp., and the opportunistic pathogens Stenotrophomonas maltophilia and Ochrobactrum anthropi were detected in more than one subject. Other known species that were detected included Achromobacter spp., Afipia spp., Brevundimonas diminuta, Capnocytophaga spp., Cardiobacterium sp., Eikenella corrodens, Fusobacterium spp., Gemella haemoylsans, and Neisseria spp. Phylotypes that were unique to noma infections included those in the genera Eubacterium, Flavobacterium, Kocuria, Microbacterium, and Porphyromonas and the related Streptococcus salivarius and genera Sphingomonas and Treponema. Since advanced noma lesions are infections open to the environment, it was not surprising to detect species not commonly associated with the oral cavity, e.g., from soil. Several species previously implicated as putative pathogens of noma, such as spirochetes and Fusobacterium spp., were detected in at least one subject. However, due to the limited number of available noma subjects, it was not possible at this time to associate specific species with the disease.

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 (cancrum oris) is an infectious disease which destroys the oro‐facial tissues and other neighboring structures in its fulminating course. It affects predominantly children aged 2–16 years in sub‐Saharan Africa where the estimated frequency in some communities may vary from one to seven cases per 1000 children. The key risk factors are poverty, malnutrition, poor oral hygiene, deplorable environmental sanitation, close residential proximity to livestock, and infectious diseases, particularly measleS. Malnutrition acts synergistically with endemic infections in promoting an immuno‐deficient state, and noma results from the interaction of general and local factors with a weakened immune system as the common denominator. Acute necrotizing gingivitis (ANG) is considered the antecedent lesion. Current studies suggest that evolution of ANG to noma requires infection by a consortium of microorganisms with Fusobacterium necrophorum and Prevotella intermedia as the suspected key playerS. Without appropriate treatment, mortality rate is 70–90%.Survivors suffer the twofold affliction of oro‐facial disfigurement and functional impairment. Reconstructive surgery of the resulting deformity is time‐consuming and financially prohibitive for the victims who are poor.

SUMMARY. Modulation of Bordetella pertussis was induced by growth in Hornibrook medium with a high content of magnesium sulphate (C-medium); four pathophysiological activities in the cells or in the whole culture were measured at intervals. Modulation, shown by the extensive loss of protective antigen, histamine-sensitising factor, leukocytosis-promoting factor, heat-labile toxin and X-mode specific envelope proteins, occurred during the first 10 h of incubation of X-mode cells in C-medium at 35°C and before the onset of the logarithmic phase of growth. The rapidity of these losses was greater than could be explained by a simple growth-dilution effect and did not appear to be due to release of activity into the culture fluid. It seemed, therefore, that there was selective destruction of pathophysiological activities as well as cessation of synthesis. The activities appeared to be lost at different rates. Mouse-protective activity was lost more rapidly than histaminesensitising and leukocytosis-promoting activities; heat-labile toxicity was lost more slowly or less completely. Modulation was shown to be easily reversed.