Reoviruses vaccines are advocated (in dams or in broilers) do not entirely solve the problem.

General hygiene and correct breeding conditions (especially correct brooding temperatures) may be efficient, but the disease often disappears as it had appeared, which makes it difficult to appreciate the effectiveness of control measures.

Causing agents may include

- viruses : reovirus (often considered as unique cause), adenoviruses, enteroviruses, rotaviruses, parvoviruses.

- bacteria like Escherichia coli, Proteus mirabilis, Enterococcus faecium, Staphylococcus cohnii, Clostridium perfringens, Bacteroides fragilis and Bacillus licheniformis, often isolated in affected birds.

Nodding syndrome is debilitating both physically and mentally. In 2004, Peter Spencer stated: "It is, by all reports, a progressive disorder and a fatal disorder, perhaps with a duration of about three years or more." While a few children are said to have recovered from it, many have died from the illness. Seizures can also cause children to collapse, potentially causing injury or death.

It is currently not known what causes the disease, but it is believed to be connected to infestations of the parasitic worm "Onchocerca volvulus", which is prevalent in all outbreak areas, and a possible explanation involves the formation of antibodies against parasite antigen that are cross-reactive to leiomodin-1 in the hippocampus. "O. volvulus", a nematode, is carried by the black fly and causes river blindness. In 2004, most children suffering from nodding disease lived close to the Yei River, a hotbed for river blindness, and 93.7% of nodding disease sufferers were found to harbour the parasite — a far higher percentage than in children without the disease. A link between river blindness and normal cases of epilepsy, as well as retarded growth, had been proposed previously, although the evidence for this link is inconclusive. Of the connection between the worm and the disease, Scott Dowell, the lead investigator into the syndrome for the US Centers for Disease Control and Prevention (CDC), stated: "We know that ["Onchocerca volvulus"] is involved in some way, but it is a little puzzling because [the worm] is fairly common in areas that do not have nodding disease". Andrea Winkler, the first author of a 2008 Tanzanian study, has said of the connection: "We could not establish any hint that "Onchocerca volvulus" is actually going into the brain, but what we cannot exclude is that there is an autoimmune mechanism going on." In the most severely affected region of Uganda, infection with microfilariae in epileptic or nodding children ranged from 70% to 100%.

The CDC is investigating a possible connection with wartime chemical exposure. The team is also investigating whether a deficiency in vitamin B (pyridoxine) could be a cause, noting the seizures of pyridoxine-dependent epilepsy and this common deficiency in disease sufferers. Older theories include a 2002 toxicology report that postulated a connection with tainted monkey meat, as well as the eating of agricultural seeds provided by relief agencies that were covered in toxic chemicals.

There is most likely a link between children's linear growth and household sanitation practices. The ingestion of high quantities of fecal bacteria by young children through putting soiled fingers or household items in the mouth leads to intestinal infections. This affect children's nutritional status by diminishing appetite, reducing nutrient absorption, and increasing nutrient losses.

The diseases recurrent diarrhoea and intestinal worm infections (helminthiasis) which are both linked to poor sanitation have been shown to contribute to child stunting. The evidence that a condition called environmental enteropathy also stunts children is not conclusively available yet, although the link is plausible and several studies are underway on this topic. Environmental enteropathy is a syndrome causing changes in the small intestine of persons and can be brought on due to lacking basic sanitary facilities and being exposed to faecal contamination on a long-term basis.

Research on a global level has found that the proportion of stunting that could be attributed to five or more episodes of diarrhoea before two years of age was 25%. Since diarrhoea is closely linked with water, sanitation and hygiene (WASH), this is a good indicator for the connection between WASH and stunted growth. To what extent improvements in drinking water safety, toilet use and good handwashing practices contribute to reduce stunting depends on the how bad these practices were prior to interventions.

Poor maternal nutrition during pregnancy and breastfeeding can lead to stunted growth of their children. Women who are underweight or anemic during pregnancy, are more likely to have stunted children which perpetuates the inter-generational transmission of stunting.

In dairy breeds, the disease may occur in calves between birth and 4 months of age. In rustic breeds or beef cattle, heifers and young steers up to 12 months of age can be affected. In calves, muscles in upper portion of the front legs and the hind legs are degraded, causing the animal to have a stiff gait and it may have difficulty standing. The disease may also present in the form of respiratory distress.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

Diarrhea and other infections can cause malnutrition through decreased nutrient absorption, decreased intake of food, increased metabolic requirements, and direct nutrient loss. Parasite infections, in particular intestinal worm infections (helminthiasis), can also lead to malnutrition. A leading cause of diarrhea and intestinal worm infections in children in developing countries is lack of sanitation and hygiene. Other diseases that cause chronic intestinal inflammation may lead to malnutrition, such as some cases of untreated celiac disease and inflammatory bowel disease.

Children with chronic diseases like HIV have a higher risk of malnutrition, since their bodies cannot absorb nutrients as well. Diseases such as measles are a major cause of malnutrition in children; thus immunizations present a way to relieve the burden.

In lambs, the disease typically occurs between 3 to 8 weeks of age, but may occur in older lambs as well. Progressive paralysis occurs, which is evident through the following symptoms: arched back, difficulty moving and an open shouldered stance. Cardiac failure may occur in two forms: sudden heart failure or gradual cardiac failure characterized by lung anemia that causes death due to suffocation.

Ewes may be given an injection of vitamin E/selenium prior to lambing to prevent deficiencies in lambs. In areas, such as Ontario, where lambs are highly susceptible to the condition, management practices should include vitamin E/selenium injections.

In almost all countries, the poorest quintile of children has the highest rate of malnutrition. However, inequalities in malnutrition between children of poor and rich families vary from country to country, with studies finding large gaps in Peru and very small gaps in Egypt. In 2000, rates of child malnutrition were much higher in low income countries (36 percent) compared to middle income countries (12 percent) and the United States (1 percent).

Studies in Bangladesh in 2009 found that the mother’s literacy, low household income, higher number of siblings, less access to mass media, less supplementation of diets, unhygienic water and sanitation are associated with chronic and severe malnutrition in children.

Wasting can be caused by an extremely low energy intake (e.g., caused by famine), nutrient losses due to infection, or a combination of low intake and high loss. Infections and conditions associated with wasting include tuberculosis, chronic diarrhea, AIDS, and superior mesenteric artery syndrome. The mechanism may involve cachectin – also called tumor necrosis factor, a macrophage-secreted cytokine. Caretakers and health providers can sometimes contribute to wasting if the patient is placed on an improper diet. Voluntary weight loss and eating disorders are excluded as causes of wasting.

Respiratory complications are often cause of death in early infancy.

After the first discovery and description of Marshall–Smith syndrome in 1971, research to this rare syndrome has been carried out.

- Adam, M., Hennekam, R.C.M., Butler, M.G., Raf, M., Keppen, L., Bull, M., Clericuzio, C., Burke, L., Guttacher, A., Ormond, K., & Hoyme, H.E. (2002). Marshall–Smith syndrome: An osteochondrodysplasia with connective tissue abnormalities. 23rd Annual David W. Smith Workshop on Malformations and Morphogenesis, August 7, Clemson, SC.

- Adam MP, Hennekam RC, Keppen LD, Bull MJ, Clericuzio CL, Burke LW, Guttmacher AE, Ormond KE and Hoyme HE: Marshall-Smith Syndrome: Natural history and evidence of an osteochondrodysplasia with connective tissue abnormalities. American Journal of Medical Genetics 137A:117–124, 2005.

- Baldellou Vazquez A, Ruiz-Echarri Zelaya MP, Loris Pablo C, Ferr#{225}ndez Longas A, Tamparillas Salvador M. El sIndrome de Marshall-Smith: a prop#{243}sito de una observad#{243}n personal. An Esp Pediatr 1983; 18:45-50.

- Butler, M.G. (2003). Marshall–Smith syndrome. In: The NORD Guide to Rare Disorders. (pp219–220) Lippincott, Williams & Wilkins, Philadelphia, PA.

- Charon A, Gillerot T, Van Maldergem L, Van Schaftingen MH, de Bont B, Koulischer L. The Marshall–Smith syndrome. Eur J Pediatr 1990; 150: 54-5.

- Dernedde, G., Pendeville, P., Veyckemans, F., Verellen, G. & Gillerot, Y. (1998). Anaesthetic management of a child with Marshall–Smith syndrome. Canadian Journal of Anesthesia. 45 (7): 660. Anaesthetic management of a child with Marshall-Smith syndrome

- Diab, M., Raff, M., Gunther, D.F. (2002). Osseous fragility in Marshall–Smith syndrome. Clinical Report: Osseous fragility in Marshall-Smith syndrome

- Ehresmann, T., Gillessen-Kaesbach G., Koenig R. (2005). Late diagnosis of Marshall Smith Syndrome (MSS). In: Medgen 17.

- Hassan M, Sutton T, Mage K, LimalJM, Rappaport R. The syndrome of accelerated bone maturation in the newborn infant with dysmorphism and congenital malformations: (the so-called Marshall–Smith syndrome). Pediatr Radiol 1976; 5:53-57.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. Western Society for Pediatric Research, Carmel, California, February, 1987. Clin Res 35:68A, 1987.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. David W. Smith Morphogenesis and Malformations Workshop. Greenville, SC, August, 1987. Proceedings of the Greenwood Genetics Center 7:152, 1988.

- Hoyme HE, Byers PH, Guttmacher AE: Marshall–Smith syndrome: Further evidence of an osteochondrodysplasia in long-term survivors. David W. Smith Morphogenesis and Malformations Workshop, Winston-Salem, NC, August, 1992. Proceedings of the Greenwood Genetic Center 12:70, 1993.

- .

- Tzu-Jou Wang (2002). Marshall–Smith syndrome in a Taiwanese patient with T-cell immunodeficiency. Am J Med Genet Part A;112 (1):107-108.

Antiretrovirals and anabolic steroids have been used to treat HIV wasting syndrome. Additionally, an increase in protein-rich foods such as peanut butter, eggs, and cheese can assist in controlling the loss of muscle mass.

Fusarium wilt is a common vascular wilt fungal disease, exhibiting symptoms similar to Verticillium wilt. The pathogen that causes Fusarium wilt is "Fusarium oxysporum" ("F. oxysporum"). The species is further divided into forma specialis based on host plant.

There are several diseases that are caused by avian reovirus, which includes, avian arthritis/tenosynovitis, runting-stunting syndrome, and blue wing disease in chickens. Blue wing disease affects young broiler chickens and has an average mortality rate of 10%. It causes intramuscular and subcutaneous hemorrhages and atrophy of the spleen, bursa of Fabricius, and thymus. When young chickens are experimentally infected with avian reovirus, it is spread rapidly throughout all tissues. This virus is spread most frequently in the skin and muscles, which is also the most obvious site for lesions. Avian arthritis causes significant lameness in joints, specifically the hock joints. In the most severe cases, viral arthritis has caused the tendon to rupture. Chickens that have contracted runting-stunting syndrome cause a number of individuals in a flock to appear noticeably small due to its delayed growth. Diseased chicks are typically pale, dirty, wet, and may have a distending abdomen. Some individuals may display “helicopter-like” feathers in their wings and other feather abnormalities. The virus has also been shown to cause osteoporosis.

Malnutrition and being underweight are more common in the elderly than in adults of other ages. If elderly people are healthy and active, the aging process alone does not usually cause malnutrition. However, changes in body composition, organ functions, adequate energy intake and ability to eat or access food are associated with aging, and may contribute to malnutrition. Sadness or depression can play a role, causing changes in appetite, digestion, energy level, weight, and well-being. A study on the relationship between malnutrition and other conditions in the elderly found that malnutrition in the elderly can result from gastrointestinal and endocrine system disorders, loss of taste and smell, decreased appetite and inadequate dietary intake. Poor dental health, ill-fitting dentures, or chewing and swallowing problems can make eating difficult. As a result of these factors, malnutrition is seen to develop more easily in the elderly.

Rates of malnutrition tend to increase with age with less than 10 percent of the "young" elderly (up to age 75) malnourished, while 30 to 65 percent of the elderly in home care, long-term care facilities, or acute hospitals are malnourished. Many elderly people require assistance in eating, which may contribute to malnutrition. Because of this, one of the main requirements of elderly care is to provide an adequate diet and all essential nutrients.

In Australia malnutrition or risk of malnutrition occurs in 80 percent of elderly people presented to hospitals for admission. Malnutrition and weight loss can contribute to sarcopenia with loss of lean body mass and muscle function. Abdominal obesity or weight loss coupled with sarcopenia lead to immobility, skeletal disorders, insulin resistance, hypertension, atherosclerosis, and metabolic disorders. A paper from the "Journal of the American Dietetic Association" noted that routine nutrition screenings represent one way to detect and therefore decrease the prevalence of malnutrition in the elderly.

During pregnancy and breastfeeding, women must ingest enough nutrients for themselves and their child, so they need significantly more protein and calories during these periods, as well as more vitamins and minerals (especially iron, iodine, calcium, folic acid, and vitamins A, C, and K). In 2001 the FAO of the UN reported that iron deficiency afflicted 43 percent of women in developing countries and increased the risk of death during childbirth. A 2008 review of interventions estimated that universal supplementation with calcium, iron, and folic acid during pregnancy could prevent 105,000 maternal deaths (23.6 percent of all maternal deaths).

Frequent pregnancies with short intervals between them and long periods of breastfeeding add an additional nutritional burden.

This disorder is caused by an abnormality of the TBCE gene, the locus for which is on Chromosome 1q42.3. The locus is a 230 kb region of gene with identified deletions and mutations in affected individuals. There are rare cases of the disorder not being due to a TBCE gene abnormality.

"Verticillium" spp. attack a very large host range including more than 350 species of vegetables, fruit trees, flowers, field crops, and shade or forest trees. Most vegetable species have some susceptibility, so it has a very wide host range. A list of known hosts is at the bottom of this page.

The symptoms are similar to most wilts with a few specifics to "Verticillium". Wilt itself is the most common symptom, with wilting of the stem and leaves occurring due to the blockage of the xylem vascular tissues and therefore reduced water and nutrient flow. In small plants and seedlings, "Verticillium" can quickly kill the plant while in larger, more developed plants the severity can vary. Some times only one side of the plant will appear infected because once in the vascular tissues, the disease migrates mostly upward and not as much radially in the stem. Other symptoms include stunting, chlorosis or yellowing of the leaves, necrosis or tissue death, and defoliation. Internal vascular tissue discoloration might be visible when the stem is cut.

In "Verticillium", the symptoms and effects will often only be on the lower or outer parts of plants or will be localized to only a few branches of a tree. In older plants, the infection can cause death, but often, especially with trees, the plant will be able to recover, or at least continue living with the infection. The severity of the infection plays a large role in how severe the symptoms are and how quickly they develop.

Environmental enteropathy is believed to result in chronic malnutrition and subsequent growth stunting (low height-for-age measurement) as well as other child development deficits.

Roberts syndrome is an extremely rare condition that only affects about 150 reported individuals. Although there have been only about 150 reported cases, the affected group is quite diverse and spread worldwide. Parental consanguinity (parents are closely related) is common with this genetic disorder. The frequency of Roberts syndrome carriers is unknown.

Vaccines are available (ATCvet codes: for the inactivated vaccine, for the live vaccine, plus various combinations).

Given that avian reovirus infections are widespread, the viruses are relatively resistant outside the host, and that vertical and horizontal transmission occurs, eradicating avian reovirus infection in commercial chicken flocks is very unlikely. In addition, absence of detectable seroconversion and failure to detect virus in cloacal swabs are unreliable indicators of resisting infection, or transmission via the egg. Thus, the most proactive and successful approach to controlling this disease is through vaccination. Since chicks are more prone to being detrimentally affected by the disease right after hatching, vaccine protocols that use live and killed vaccines are designed to provide protection during the very early stages of life. This approach has been accomplished through active immunity after early vaccination and a live vaccine or passive immunity from maternal antibodies followed with vaccination of the breeder hens. Currently, efforts toward administering inactivated or live vaccines to breeding stock to allow passive immunity to the offspring via the yolk are being taken.

In the 1960s, researchers reported a syndrome of non-specific histopathological and functional changes to the small intestine in individuals living in unsanitary conditions. This syndrome was observed predominantly in tropical regions across Latin America, sub-Saharan Africa and Asia. The geographic distribution of the syndrome lead to the original term of "tropical enteropathy" (sometimes also "tropical jejunopathy").

Following initial reports, further investigation revealed that these symptoms were not specific to tropical climates. For example, individuals in more wealthy tropical countries, such as Qatar and Singapore, did not exhibit these symptoms. Similarly, subsequent studies have shown this condition to be common across the developing world, closely associated with impoverished conditions but independent of climate or geography. As a result, the term "environmental enteropathy" was introduced to specify that this condition is not only found in tropical areas and is believed to be caused by environmental factors.