Version May 2024
INTRODUCTION — Noma is a severe disfiguring gangrene of the mouth and face that begins as a gingival ulcer and spreads rapidly through the tissues of the mouth and face [1-5]. Unlike other infectious processes of the face, which may progress along anatomic spaces of the head and neck, noma disrupts anatomic barriers and spreads through muscle and bone [4]. The resulting gangrene may involve the maxilla, the mandible, and extend to the nose and infraorbital margins (picture 1). The word noma derives from the Greek "voun," meaning to devour, emphasizing the rapid progression of the disease [6,7].
Noma is categorized by the World Health Organization (WHO) as a necrotizing ulcerative stomatitis. Synonyms include cancrum oris and fusospirochetal gangrene. The name "cancrum oris" was introduced in Britain in the mid-17th century and is still in common usage in the British Commonwealth countries [7,8]. Most of these countries are former African colonies of Britain. According to an 1848 description, orofacial noma is a "gangrenous affection of the mouth, especially attacking children in whom the constitution is altered by bad hygiene and serious illness, especially from the eruptive fevers, beginning as an ulcer of the mucous membrane, with edema of the face, extending from within out, rapidly destroying the soft parts and the bone, and almost always quickly fatal" [9].
Mortality due to noma can be reduced with prompt, appropriate treatment. Noma is one of the most devastating human diseases worldwide and has been designated a health priority by the WHO [3,10-13].
MICROBIOLOGY — Noma is a polymicrobial infection associated predominantly with anaerobic organisms [3,14].
Fusobacterium necrophorum has been observed most frequently in culture in Nigerian cases and appears to be an important organism for the development of noma [15-18]. Virulence factors of F. necrophorum include proteolytic enzymes and toxins capable of tissue destruction [18]. F. necrophorum also produces a growth stimulating factor for Prevotella intermedia, which facilitates lipid degradation.
Other microorganisms cultivated from noma lesions among Nigerian children are similar to those seen in adult periodontitis and are also capable of releasing enzymes that can degrade host tissues [19]. These include P. intermedia, alpha-hemolytic streptococci, Pseudomonas spp, Actinomyces spp, and Peptostreptococcus micros [3,15-18,20-22]. Spirochetes have also been observed at the advancing edge of active lesions with dark-field microscopy [15]. Molecular studies have demonstrated the complex diversity of microorganisms associated with noma, including 67 bacterial species, of which 25 have not yet been grown in vitro [23]. Herpes viruses have also been implicated, particularly herpes simplex virus and cytomegalovirus [1,21,24-26].
Development of noma has been attributed to an imbalance of oral bacterial flora in some studies, noting reduced bacterial diversity and a prominently increased proportion of organisms in the Prevotella genus [27,28]. One study in the Niger Republic observed larger counts of P. intermedia and members of the Peptostreptococcus genus in noma lesions than in non-noma cases [27]. P. intermedia is a gram-negative obligate anaerobic pathogen involved in periodontal infections, including acute necrotizing gingivitis.
Coinfection is common, particularly in resource-limited settings. As an example, HIV infection may play a role in the pathogenesis of oral soft tissue lesions [29]. In addition, herpesviruses may play a role in the pathogenesis of acute necrotizing gingivitis, a precursor of noma [24,30].
EPIDEMIOLOGY — The global distribution of noma is poorly understood. Many affected individuals die in the acute stage of the disease before presenting for clinical attention; most reside in rural areas, and some hide deliberately because of the stigma associated with the disease [3,10,31].
The incidence of noma is highest in sub-Saharan Africa; the disease also occurs in Asia and Latin America [7,10,13,31-34]. The World Health Organization estimates the global incidence of noma to be around 100,000 to 140,000 new cases per year [35]. In countries such as Gambia, Niger, Nigeria, and Senegal, the annual incidence of noma based on hospital records ranges from 0.28 to 1.9 per 1000 children [31,36,37]. In West Africa, the peak age range for acute illness is one to six years, although late stages do occur in adolescents and adults [3,6,7,10,38]. The fatality rate in the absence of prompt treatment is about 80 percent [35]. With appropriate treatment, mortality rates are less than 10 percent [6,10].
The HIV/AIDS epidemic has been associated with an increase in the number of noma cases [1,8,39,40]. Among 48 patients with noma seen at the University of Zimbabwe between 2002 and 2006, all were seropositive for HIV [41]. In Sub-Saharan Africa the prevalence of HIV-associated acute necrotizing gingivitis (ANG, a major precursor of noma) is high [29,42,43].
Noma occurred worldwide until the early 20th century, when it essentially disappeared from the developed countries; some cases occurred in concentration camps during World War II [44,45]. The near eradication of noma from developed countries coincided with improvements in living standards, prior to the discovery of penicillin [2,7,10].
Risk factors — Poverty is a critical risk factor for noma [1,7,38,46]. Additional associated risk factors include food insecurity, poor sanitation, poor oral hygiene, limited access to health care services, close residential proximity to livestock, nomadic lifestyle, and residence in an area with high prevalence of infectious diseases including malaria, measles, HIV/AIDS, diarrhea, tuberculosis, and other neglected tropical diseases [3,10,25,46-49]. Infants and children are particularly susceptible. Noma does not appear to be a transmissible disease in humans; cases have not been reported in caregivers of children with the disease.
Malnutrition — Chronic malnutrition is common in communities at risk for noma, as it increases susceptibility to infection [3,17,31,38,50]. Nigerian studies have noted reductions in plasma levels of micronutrients (particularly retinol, ascorbate, and zinc) among children with noma compared with children without noma [2,32,38]. These observations may reflect an acute phase response associated with infections that accompany nutritional deficiency states [51].
Chronic malnutrition has been associated with increased numbers of mouth anaerobes (particularly P. intermedia) among malnourished children in Nigeria compared with well-nourished children, regardless of presence or absence of overt oral pathology [52]. This is consistent with increased circulating level of steroids, which is a feature of the stress of infection and malnutrition [3,53,54]. P. intermedia uses steroids as growth factors. Other important growth factors for this bacterium include hemin-iron containing compounds present in the gingival/periodontal ulcer sites [55].
Malnutrition is often intergenerational, commencing prenatally in the setting of poor maternal health during pregnancy [1,3,38]. The developing immune system is influenced by malnutrition during the prenatal period [3,56-59]. In communities at risk for noma, the prevalence of intrauterine growth retardation leading to infants who are small for gestational age (SGA) is high; in such settings, the infant mortality rate may be as high as 114 per 1000 live births [38,60,61].
Acute necrotizing gingivitis — ANG is an important risk condition for noma and is a precursor of the disease [1,2,28,42]. ANG is characterized by ulceration involving one or more interdental papillae, pain, fetid breath, bad taste, fever, and lymphadenopathy (picture 2) [26,62,63]. The most common sites of ANG are the premolar and molar area, followed by the mandibular incisor area. Ulceration of the overlapping inner cheek may also occur concurrently.
In sub-Saharan Africa, ANG typically occurs among malnourished children two to six years of age. The prevalence ranges from 2 to 18 percent in some rural communities [3,10,31,53]. In developed settings, ANG is rare, particularly in children; it is occasionally observed in severely immunocompromised individuals such as patients with HIV infection and those receiving organ transplants [26,62,64].
As with noma, ANG is likely attributable to periodontal bacteria and herpesviruses [24,65]. Molecular studies support the hypothesis that ANG may be a precursor of noma [66]. Studies in the Zinder region of Southeast Niger Republic [42] have confirmed earlier reports in many underprivileged African communities that ANG might be an immediate clinical precursor of noma [2,3,38,67]. In the malnourished, immunologically compromised child, ANG may evolve from a purely gingival lesion and spread to the underlying mucosa and alveolar bone, thus setting the stage for development of noma [26,42,68]. It is suggested that prevention of noma should pay particular attention to undernourished communities with a high prevalence of ANG [3,42].
Other factors — Additional risk factors for noma include antecedent infections (particularly measles and malaria) and immunosuppressing conditions.
Measles infection alters cytokine activity, leading to immunosuppression that can persist up to six months after acute infection [54,69-71]. Some have suggested that measles infection promotes development of acute noma in poor African children [1,6,10,25,72,73]. Studies in the Congo Republic (formerly Zaire) have noted noma-like oral ulcerations following measles in severely malnourished children one to six years of age [25]. The prolonged immunosuppressive effects elicited by measles infection compromise overall immunity [74]; for example, stomatitis resulting from measles infection may promote reactivation of latent herpes viruses, resulting in peribuccal, perinasal, and infraorbital ulcerative lesions [25,67,72,75].
Acute noma has been described in association with malaria infection in children [2,40,46,76,77]. Malaria infection is associated with profound immune impairment [78-81]. Effects of placental malaria include impaired utero-placental blood flow as well as reduced transplacental transfer of maternal antibodies to infectious diseases such as measles [82-85]. (See "Malaria: Clinical manifestations and diagnosis in nonpregnant adults and children", section on 'Concomitant infection'.)
Noma has been reported in association with the following conditions (see "Periodontal disease in children: Associated systemic conditions"):
●HIV infection/AIDS [41,86-88]
●Type 2 diabetes mellitus [89]
●Immune-deficient states such as familial neutropenia, histiocytosis syndromes, and severe combined immunodeficiency (SCID) [20,90-94]
●Immunosuppressive therapy [95]
●Autoimmune diseases in the absence of immunosuppressive therapy [90]
●Hypophosphatasia (an inborn error of metabolism caused by deficiency of tissue-nonspecific alkaline phosphatase) [92]
CLINICAL MANIFESTATIONS AND DIAGNOSIS — The diagnosis of noma is based on clinical manifestations. Suggestive clues include recent or concurrent infections preceding onset of facial swelling and excessive salivation in the setting of malnutrition. In general, there are at least three well-defined stages of noma (which may overlap): an acute phase, a gangrenous phase, and a scarring phase [4,7,10,18].
Acute phase — Symptoms associated with the acute phase of noma include mouth soreness, facial swelling, fetid breath, excessive salivation, and difficulty eating [6,10,11]. The medical history is frequently notable for recent or concurrent infections such as diarrheal illness, malaria, measles, tuberculosis, or HIV [3,7,10,24,96].
In general, children with acute noma are malnourished, as evidenced by growth retardation, hair discoloration, and/or limb edema [2,25]. In one study of Nigerian children <4 years of age with acute noma, about 90 percent had stunted growth and were underweight; more than two-thirds were severely affected [38]. Among age- and sex-matched neighborhood children without noma, about 40 percent were stunted and underweight; less than one-third were severely affected [38].
Laboratory findings may include severe anemia (hemoglobin levels as low as 5 to 6 g/dL), white blood cell counts of 20,000 to 30,000 per microL, and hypoalbuminemia [2,25,97]. Anemia is often most severe among the most stunted children with noma.
Gangrenous phase — Noma likely begins as a gingival inflammatory lesion that spreads to the labiogingival fold and then to the mucosal surface of the cheek and lip [2,6]. Subsequently, an area of bluish-black discoloration may appear on the cheek (picture 1) [6,98]. After this finding, progression of the disease resulting in perforation of the cheek is very rapid (usually a matter of days) [1,2,6,98]. During this time, there is extensive intraoral destruction (picture 3). Soft tissue sloughing leaves a well-demarcated deep wound with exposed bones and teeth. Ulcerative gingivitis or periodontitis is considered to have progressed to noma once there is exposure of the alveolar bone [2,67].
The disease is usually unilateral but can occur bilaterally. Some cases may occur with ectopic lesions involving the scalp, neck, shoulders, perineum, and vulva [6,99].
Scarring phase — Scarring sets in following the acute and gangrenous stages, leading to trismus and severe facial disfigurement [71,86,98]. Sequelae of noma depend on the sites affected and the extent of tissue destruction; they may include displacement or exfoliation of teeth, facial mutilation, bony fusion between the maxilla and mandible, trismus, poor speech, and difficulty feeding [6,71,98]. Persistent leakage of saliva is a major problem in patients with extensive destruction of the maxilla, lower lip, cheek, and/or floor of the mouth [3,6].
Trismus refers to limited mobility of the mandible. In the setting of noma, trismus may occur following necrosis of the mandible, which may be associated with dense scarring of the posterior part of the lining of the cheek, just anterior to the temporomandibular joint (TMJ). In some cases, bony fusion may occur between the mandible and maxilla. Patients with moderate to severe trismus (mouth aperture less than half of normal) may be associated with intubation difficulty as well as impairments of speech and feeding following surgery.
If possible, patients with trismus should be evaluated with radiographs of the mouth, skull (including the TMJ) and chest, in addition to blood counts. The extent of tissue defects may be evaluated using the classification system in the Table (table 1) to plan for surgery [71,100]. (See 'Surgical repair' below.)
A WHO international consultation has reclassified the stages of noma as follows: ANG stage with or without fetid breath, ulceration of the gum, pain, and increased salivation; edema stage with fever, rapid extension of the gingival and mucosal ulcer; gangrenous stage; scarring stage; and sequelae stage [101].
PATHOGENESIS — The pathogenesis of noma is not fully understood. The following sections summarize observed findings [3].
Histopathology — Histopathology generally demonstrates necrosis of the epidermis with acanthosis around the rim of the epithelium [4,95,98]. The necrotic area is well circumscribed; at the margins, there is hyperplasia with ballooning of the epithelial cells. The dermis typically has a heavy infiltrate of polymorphonuclear neutrophils; phagocytosed bacteria may be observed. Separation of collagen bundles due to edema may be observed. Blood vessels are frequently dilated and filled with inflammatory cells. Small and large cocci of various morphologies and gram-negative coccobacilli may be seen.
Role of malnutrition — Noma is associated with very low levels of most essential amino acids and significant reductions in plasma levels of vitamin A, vitamin C, zinc, albumin, and hemoglobin [17,25,32,56,97,102-104]. Given the frequency of multiple concurrent deficiencies, no single nutrient deficiency has been causally related.
Leptin, a polypeptide produced by adipose tissue involved in the inflammatory response and immune function, is significantly diminished in children with noma [105-108]. The prolonged inflammatory response in the setting of noma may downregulate or exhaust leptin production; similar observations have been described in the setting of tuberculosis with associated wasting and chronic inflammation [109].
Inflammatory mediators — Children with noma have higher inflammatory cytokine levels than neighborhood village children without noma; both groups have higher levels than age-matched healthy urban children [17]. In the setting of noma, there appears to be disruption of complex interactions involving tumor necrosis factor (TNF) and the TNF family receptor herpes virus entry mediator (HVEM), leading to T cell stimulation and promotion of mucosal inflammation [110-112].
The circulating cytokine patterns observed in children with noma and acute necrotizing gingivitis resemble findings in other diseases characterized by necrotic lesions [17]. Increased systemic concentrations of cytokines (particularly TNF and interleukin-18) are also features of inflammatory bowel disease as well as measles, malaria, and sepsis [14,113-121].
DIFFERENTIAL DIAGNOSIS — The diagnosis of noma is straightforward in the gangrenous stage [122]. The disease is readily recognized by the rapid course of inflammation in the setting of antecedent infection (measles, malaria, tuberculosis, etc). Diseases with similar characteristics include (see related topics):
●Noma neonatorum resembles noma in children but occurs during the first few weeks of life in premature and low birthweight infants [123-126]. The gangrene generally involves the oronasal region, eyelids, and perineum. Cultures may demonstrate Pseudomonas aeruginosa, Escherichia coli, Klebsiella spp, or staphylococci.
●Ecthyma gangrenosum – Ecthyma gangrenosum refers to a necrotic skin lesion associated with P. aeruginosa infection that may involve the oral cavity, nose, or perineum. Ecthyma gangrenosum resembles noma histopathologically [127]. The diagnosis of ecthyma gangrenosum is established based on clinical manifestations and culture results. (See "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Ecthyma Gangrenosum'.)
●Mycobacterial infection – Mycobacteria associated with ulcerating lesions include Mycobacterium tuberculosis and Mycobacterium leprae infection, which may present with oral ulceronecrotic lesions. The diagnosis of mycobacterial infection is established by biopsy with evidence of acid-fast bacilli. (See "Leprosy: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Cutaneous manifestations of tuberculosis".)
●Mucocutaneous leishmaniasis – Mucocutaneous leishmaniasis causes disfiguring destruction of the mucous membranes of the nose and mouth; the majority of cases occur in South America. The diagnosis of leishmaniasis is established via histology or molecular techniques. (See "Cutaneous leishmaniasis: Clinical manifestations and diagnosis", section on 'Mucosal leishmaniasis'.)
●Oral and maxillofacial myiasis – Myiasis may cause a skin lesion resembling noma in adults and older children. It is caused by deposition of tumbu fly larvae in subdermal tissue [128]. The diagnosis is established based on clinical manifestations and history of exposure in an area where the fly is endemic. (See "Skin lesions in the returning traveler", section on 'Myiasis'.)
●Necrotizing fasciitis – Necrotizing fasciitis involving the head and neck typically originates from an odontogenic abscess or trauma and may be associated with gangrene of the cheek. Cervical necrotizing fasciitis typically occurs in older adults with diabetes; the diagnosis is established via surgical exploration. (See "Necrotizing soft tissue infections".)
●Osteonecrosis of the jaw – Osteonecrosis of the jaw is typically associated with medications such as bisphosphonates and generally occurs in adults in association with underlying malignancy. The diagnosis is established via radiographic imaging such as computed tomography (CT). (See "Medication-related osteonecrosis of the jaw in patients with cancer" and "Risks of bisphosphonate therapy in patients with osteoporosis".)
●Ludwig's angina – Ludwig's angina is an infection of the submandibular space that most commonly arises from an infected tooth in adults or children. The diagnosis is established based on clinical manifestations and radiographic imaging (CT scan). (See "Ludwig angina".)
●Oral tumor – Tumors of the oral cavity typically present as a nonhealing ulcer or mass. The diagnosis of oral tumor is established via biopsy. (See "Oral lesions", section on 'Oral squamous cell carcinoma'.)
●Syphilis – In late syphilis, gummatous lesions may occur on the skin and present as ulcers or heaped-up lesions. The diagnosis of syphilis is based on serologic testing. (See "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV", section on 'Gummatous syphilis'.)
TREATMENT — Treatment of noma in the acute phase consists of antibiotics, wound care, and replacement of needed fluids, electrolytes, and good nutrition. Oral physiotherapy to relieve trismus resulting from fibrous strictures should start immediately following containment of the acute phase [5]. Subsequently, surgery is performed for correction of trismus and flap creation. Oral physiotherapy is continued after surgery.
Attention to psychosocial needs is also an important component of treatment, given the cosmetic and functional debilitation associated with noma.
Antibiotics — The optimal approach to antimicrobial therapy for treatment of noma is uncertain. The dose and type of antibiotic depend on individual circumstances and available clinical tools. Reasonable regimens include penicillin in combination with metronidazole or streptomycin [10,27,95,129]. Some favor a combination of amoxicillin and metronidazole; a study in the Niger Republic involving 82 patients with noma treated with this regimen noted a mortality rate of 8 percent [27]. Others prefer monotherapy with metronidazole, since noma is associated predominantly with anaerobic organisms [11,129].
For children who can swallow oral medication, antibiotics may be given in tablet or syrup form. Dosing for penicillin VK is 25 to 50 mg/kg/day in three divided doses; dosing for metronidazole is 30 mg/kg/day in three or four divided doses. For children who cannot tolerate oral medication, parenteral therapy with penicillin may be administered.
Wound care — The wound should be dressed daily with gauze soaked in antiseptic [10,11,98]. If possible, the mouth should be rinsed with a solution of chlorhexidine digluconate (0.12 to 0.20%) daily [10,11]. This may be continued for up to one week.
Fluid, electrolytes, and nutrition — Management of acute noma requires rehydration with correction of electrolyte abnormalities followed by nutritional rehabilitation with a high protein diet enriched with essential micronutrients. At the Noma Children Hospital in Sokoto, Nigeria, a highly enriched nutrition formula (Enfortal, donated through the Dutch Noma Foundation) has yielded good results [71]. Feeding by mouth is preferred. If this is not possible due to pain, tissue destruction, or severe trismus, parenteral nutrition may be administered [6,71,98]. (See "Maintenance intravenous fluid therapy in children" and "Oral rehydration therapy" and "Overview of enteral nutrition in infants and children".)
Surgical repair — The goal of surgery is to improve cosmetic appearance as well as oral function including eating, drinking, swallowing, and speech [6,10,11,98,100]. In the acute phase, intervention for control of secondary hemorrhage, removal of loose teeth, and wound debridement may be needed to prevent secondary infection and promote healing [86]. To allow time for resolution of necrosis, more definitive surgery is performed several months to one year after the acute phase.
The techniques for correction of deformities depend on location and severity of the lesions, available resources, and abilities of the surgical team [71,100,130,131]. Preoperative classification of the tissue defects is essential for planning surgical intervention (table 1) [6,10,100,131]. In patients with mild to moderate trismus, it may be reasonable to defer surgery because given the high rate of relapse and associated morbidity, especially in children [131]. (See 'Clinical manifestations and diagnosis' above.).
For patients with trismus who undergo surgery, oral physiotherapy should be initiated prior to surgery. Surgical correction of trismus requires excision of fibrous bands restricting jaw opening [6,10,98,100,129,130,132,133]. Following surgery, physiotherapy is important to prevent recurrence of trismus [11,100,129,130]. During the first few days after surgery, a bundle of wooden tongue spatulas may also be useful to help keep the mouth open.
Additional surgical intervention may include tissue flaps and/or bone grafting [5]. Options for flap techniques range from simple flaps to complex procedures involving microsurgery [6,100,133,134].
Surgical intervention requires general anesthesia with intubation, which may be difficult in settings with limited facilities [100,129,135]. Regional centers for noma surgical rehabilitation have been established in a number of resource-limited settings, including the Noma Children Hospital (Sokoto, Nigeria), Stiftung Kinderhilfe (a German nongovernmental organization), and the Dutch Noma Foundation [71]. Another organization, the German Hilfsaktion Noma, treats some cases in the Niger Republic and transfers very difficult cases to Germany.
Following surgical repair, some functional and cosmetic defects may persist. Therefore, attention to psychosocial needs is also an important component of treatment [129,133].
Other measures — The patient should undergo evaluation for predisposing systemic diseases including malaria, measles, tuberculosis, HIV infection, and other parasitic diseases endemic in the region. In addition, routine immunizations should be administered if necessary.
PREVENTION — Prevention of noma requires a multidisciplinary approach with attention to routine health care needs, sanitation, nutrition, vaccination, and public awareness.
Health care personnel should know the risk factors for and early signs of noma and screen children at risk accordingly. The risk factors include:
●Severe growth failure in the first 6 to 12 months of life
●Severe malnutrition and poor eating habits
●Persistent diarrhea
●Presence of oral mucosal ulcers
●Malodorous breath
Proper oral hygiene practices must be taught and promoted. For areas in which toothbrushes and toothpaste are not available, children should be taught to use soft chewing sticks or sponges, under adult supervision. Many chewing sticks are fashioned from plants containing active medicinal properties; several are from the tea plant family and may concentrate fluoride from the soil [136-139]. For very young children, cotton buds may substitute for chewing sticks. Saline solution is helpful for mouth rinsing.
As oral ulcers are frequently preceded by antecedent infection, administration of routine immunizations is also a priority. Other vaccines include DPT (diphtheria, pertussis, tetanus), Haemophilus influenzae serotype b (Hib), and polio vaccine.
Sanitation inside and outside of the residential quarters requires careful attention to the following issues:
●Clean drinking water must be readily available.
●Human waste must be removed in a timely fashion.
●Livestock should be segregated from human living quarters.
Adequate nutrition in the first three to six months of life is an important priority; breastfeeding should be encouraged. Weaning foods for infants should be prepared under hygienic conditions.
Noma occurs almost exclusively in resource-limited settings in which the general understanding of the causes of disease may be limited and illness may be interpreted within the framework of superstitious beliefs. Information campaigns are needed at regional and global levels.
SUMMARY AND RECOMMENDATIONS
●Noma is a severe disfiguring gangrene of the mouth and face that starts as a gingival ulcer and spreads rapidly through the tissues of the mouth and face. It is associated with poverty, malnutrition, and poor sanitation. (See 'Introduction' above.)
●Noma is a polymicrobial infection associated predominantly with anaerobic organisms, although identifying a specific causative infectious agent can be difficult. Fusobacterium necrophorum and P. intermedia are observed most frequently in culture and are suspected to be important for the development of noma. (See 'Microbiology' above.)
●The incidence of noma is highest in sub-Saharan Africa; the disease also occurs in Asia and Latin America. Risk factors include poor oral hygiene, limited access to health care services, close residential proximity to livestock, nomadic lifestyle, and high prevalence of infectious diseases including malaria, measles, AIDS, diarrhea, and tuberculosis. Infants and children are particularly susceptible. (See 'Epidemiology' above.)
●The diagnosis of noma is based on clinical manifestations. Suggestive clues include recent or concurrent systemic infection, particularly measles and/or malaria, preceding onset of facial swelling, and excessive salivation in the setting of malnutrition. (See 'Clinical manifestations and diagnosis' above.)
●Acute treatment consists of antibiotics, wound care, and replacement of needed fluids, electrolytes, and nutrition. We suggest treatment with penicillin or amoxicillin, with or without metronidazole (Grade 2C). Dosing is as outlined above; the duration is 10 to 14 days. (See 'Treatment' above.)
●Several months to one year after the acute phase, surgery is performed for correction of trismus and flap creation. Physiotherapy to reduce fibrous scarring should be initiated during the healing phase and continued after surgery. Attention to psychosocial needs is also an important component of treatment, given the cosmetic and functional debilitation associated with noma. (See 'Treatment' above.)
●Prevention of noma requires a multidisciplinary approach with attention to routine health care needs, sanitation, nutrition, and awareness. Measles immunization reduces the risk of noma. Prevention of malaria in pregnant women receiving antenatal care is also important, since placental malaria impairs transplacental transfer of maternal antibodies to the infant. (See 'Prevention' above.)
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