Pathophysiology Processes & Consequences of Noma
Chamberlain College of Nursing
NR283: Pathophysiology
May 2016, Professor (Name Here)

Pathophysiology Processes & Consequences of Noma Noma disease, commonly referred to as cancrum oris, fusospirochetal gangrene, necrotizing ulcerative stomatitis, and stomatitis gangrenosa is a devastating disease that is famously quoted as “the face of poverty”. This rare disease with high prevalence in Sub-Saharan countries is lethal and has been linked to acute and rapid disease progression in persons that are immunocompromised. Evidence based research suggests a high prevalence of the disease is observed in populations experiencing extreme poverty, malnourishment, and exposure to infectious diseases, while living in a continued state of poor hygiene. This gangrenous infection has a microbial origin, often found in the mouth. It is exacerbated by poor hygiene that give rise to the bacterial micro-organisms responsible for aggressive manifestations observed on individuals infected.
Etiology of Noma The exact etiology of Noma disease is unknown. However, it is believed to be multifactorial in nature (Ashok, Tarakji, Darwish, Rodrigues , & Altamimi, 2016). The spread of the disease is due to deteriorating sanitation and inadequate nutrition, most common in underdeveloped countries. Noma is an opportunistic infection, which typically show dominance after a weakened immune system is present, preceding multiple risk factors that work together increasing risk potential for the disease. The most prevalent risk factors associated to development of this disease include malnutrition, poor oral hygiene, potentially including oral lesions from gingivitis, a compromised immune system (i.e., viral infections), an unidentified triggering micro-organism, previously hypothesized as a member of Fusobacterium or Prevotella (Whiteson, et al., 2014). Noma was first discovered in concentration camps during World War II, and is most commonly found in children. Noma, for most people is a disease of shame; the prevalence and processes from derivations are completely unknown due to only 15% of acute cases seeking medical care while others go into isolation.
Pathophysiological Process The rapid destruction and deterioration of the hard and soft tissues that display physiologic characteristics in response to the pathological processes of Noma, can be attributed to an immuno-pathological response to microbial factors rather than the microbiological factors alone (Ashok, Tarakji, Darwish, Rodrigues , & Altamimi, 2016). Noma’s multifactorial nature and origin is considered infectious and mostly recognized as opportunistic rather than communicable. The onset of Noma with mucosal ulcerations may show limited activity for an extended period of time prior to progressing to associated tender stomatitis and edema. A painless necrotic center develops, with an outward expansion following a sharp perimeter; the infection will rapidly spread across local tissue types and planes, affecting skin turgor dramatically. The sloughing of tissue on the face exposes mandibular and maxillary bone leading to facial deformities, oral incontinence, and severe pain. This consumptive gangrene progression for survivors require surgical reconstruction to achieve and regain functionality (Tonna, Lewin, & Mensh, 2010).
Clinical Manifestations & Complications Noma’s early and progressed clinical manifestations include signs of edema in the cheek, malodorous breath, excessive salivation, anemia, severe dehydration, and symptoms of both acute and chronic kwashiorkor (Tonna, Lewin, & Mensh, 2010). A greyish-black area appears on the outside of the opposite cheek within a couple days, which then becomes a black necrotic spot. Physiologic manifestations include fever, tachycardia, increased respiratory rate, general edema, leukocytosis and lymphadenopathy, indicating acute infection. High, rapid mortality rates used to be a common result of Noma, however with recent use of antibiotics and better nutrition, the mortality rate has reduced from 90% to 8 -10% (Ashok, Tarakji, Darwish, Rodrigues , & Altamimi, 2016). Other complications presented by Noma include trismus, alveolar bone destruction, and sepsis. Many survivors of Noma experience trouble chewing due to the loss of tissue and pain, leading to malnutrition and death.
Diagnostics
Noma disease presents with underlying illnesses, systemic inflammatory response, malnutrition (usually secondary to oral incontinence), aspiration pneumonia, and septicemia may all contribute to diagnosis, however even when treated death may occur due to the acute nature of the disease (Tonna, Lewin, & Mensh, 2010). Lesion sites are tested using Koch’s Postulates by way of lab swabs, and DNA based culture testing to identify its origin and driving force. Potential indicators of Noma were researched using 16S rRNA gene community profiles, according to (Whiteson, et al., 2014), Peptostreptococcus and Prevotella, both were identified as precursors that exacerbated the disease. This finding further supports the notion that one dominant pathogen is not the underlying characteristic of Noma, rather this disease has a diverse community of species attributing to its prevalence. Treatment efforts include fluid hydration, balancing of abnormal electrolytes, vitamin supplements and improved nutrition, along with a compilation of antibiotics and pain medications used as the first line of treatment administered.
Affected Health Patterns with Specific Impact. The most common affected by Noma are children between the ages of 2 and 5, they typically reside in extremely malnourished areas and underdeveloped countries. Geographical areas in Africa, known as the “Noma belt” has been identified by researchers to present the most cases edema associated with acute infection, leading to Noma disease onset. According to (Tonna, Lewin, & Mensh, 2010), “Noma is most common in populations with extreme poverty, severe malnutrition, unsafe drinking water, poor sanitation, poor oral health, high infant mortality rate, limited access to high quality healthcare, and intrauterine growth retardation”. In research studied by (Huyghe, et al., 2013), it is noted that “recently an increased incidence of Noma has been reported in patients with HIV”. Prevention measures for Noma include, “administration of nutritious food, exclusive breast feeding during the first three to six months of life, inculcation of proper oral hygiene practices, immunization against endemic diseases like measles, segregation of animals from human living areas, improved sanitation practices and creating a proper awareness about Noma (Ashok, Tarakji, Darwish, Rodrigues , & Altamimi, 2016)
Conclusion
Noma disease and its debilitating components affecting exposed individuals prove most prevalent among underprivileged populations, whereas individuals within these affected communities have little or no access to good medical care. Proactive efforts taken by the government and health organizations may help reduce or prevent the occurrence of Noma. Improvement of social living conditions in areas susceptible to the disease, along with providing improved medical care that give community members better access to care, good nutrition with improved water consumption facilities, education and promotion of good hygiene practices, and routine vaccinations will collectively provide maintenance and eliminate future onset with diagnosis of this fatal disease.

References
Ashok, N., Tarakji, B., Darwish, S., Rodrigues , J. C., & Altamimi, M. A. (2016, April). A Review on Noma: A Recent Update. Global Journal of Health Science, 8(4), 53-59. doi:10.5539/gjhs.v8n4p53
Tonna, J. E., Lewin, M. R., & Mensh, B. (2010, December 21). A Case and Review of Noma. (C. Franco-Paredes, Emory University , & United States of America, Editors) doi:10.1371/journal.pntd.0000869
Whiteson, K. L., Lazarevic, V., Tangomo-Bento, M., Girard, M., Maugham, H., Pittet, D., . . . the GESNOMA study group. (2014, December 4). Noma Affected Children from Niger Have Distinct Oral Microbial Communities Based on High-Throughput Sequencing of 16S rRNA Gene Fragments. Retrieved from plos.org: http://dx.doi.org/10.1371/journal.pntd.0003240