Showing papers on "Noma published in 2000"

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

Abstract: 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 1 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.

Noma (cancrum oris): case report in a 4-year-old HIV-positive South African child.

Abstract: Cancrum oris (noma) is a gangrenous infection that develops in the mouth and spreads rapidly to other parts of the face. The disease occurs mostly in conditions of poverty, poor hygiene and malnutrition. In sub-Saharan Africa the frequency in several countries is estimated to be 1-7 cases per 1,000 population, and as many as 12 cases per 1,000 in the most affected communities. About 90% of these children die without receiving any care, yet the disease can, and should, be prevented. With increasing numbers of children who are malnourished and who have compromised immune systems (compounded by the HIV pandemic) the prevalence of conditions such as noma is likely to increase. Among the earliest features of noma are excessive salivation, marked fetor oris, facial oedema and a greyish-black discolouration of the skin in the affected area. This devastating gangrenous lesion may involve the cheek, the chin, the infra-orbital margin, palate, nose, antrum and virtually any part of the face. This report describes a 4-year-old HIV-positive African girl, who was abandoned, discharged from the Plastics Unit and now lives in a child care sanctuary. Little is known about her history prior to her arrival at the home a few weeks previously. The clinical examination revealed a delay in growth and physical development equivalent to that of a 2-year-old child. The left cheek had a perforating ulcer in a healing phase. The perforation, about 1 cm in diameter, was surrounded by oedematous tissues showing a mild to moderate erythema. The peripheral oedema extended to the lower palpebral, the upper labial, left labial commissural, mandibular and pre-parotid regions. Submental, submandibular and cervical lymph nodes were mildly painful upon palpation. The child was not pyretic. The intra-oral examination revealed the features of acute necrotising gingivitis (ANG). ANG was generalised and showed classic interdental crater-like ulcers covered with whitish debris. Halitosis was pronounced. Examination of the second quadrant revealed a large ulcer extending from the distal aspect of the deciduous canine to the distal aspect of the second deciduous molar. The adjacent palatal mucosa was severely oedematous. The alveolar bone supporting the first and the second molars was completely exposed to the fundus of the vestibulum. It was not possible to obtain intraoral photographs or radiographs. Chlorhexidine gluconate (0.2% solution) and metronidazole tablets, 200 mg twice daily for 15 days were prescribed. The child was seen every alternate day for 10 days and her condition improved rapidly. Halitosis had subsided. She was then referred to the Johannesburg Hospital for further treatment under general anaesthesia. The proposed treatment plan was as follows: removal of dental accretions and polishing of all teeth, extraction of the left maxillary teeth supported by non-vital bone, resection of the necrotic bone in the left maxilla and reconstructive surgery in the left cheek.