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.

Diagnosis is not very advanced and is based on the telltale nodding seizures of the victims. When stunted growth and mental disability are also present, probability of nodding syndrome is high. In the future, neurological scans may also be used in diagnosis. As there is no known cure for the disease, treatment has been directed at symptoms, and has included the use of anticonvulsants such as sodium valproate and phenobarbitol. Anti-malaria drugs have also been administered, to unknown effect.

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.

"F. oxysporum" is a major wilt pathogen of many economically important crop plants. It is a soil-borne pathogen, which can live in the soil for long periods of time, so rotational cropping is not a useful control method. It can also spread through infected dead plant material, so cleaning up at the end of the season is important.

One control method is to improve soil conditions because "F. oxysporum" spreads faster through soils that have high moisture and bad drainage. Other control methods include planting resistant varieties, removing infected plant tissue to prevent overwintering of the disease, using soil and systemic fungicides to eradicate the disease from the soil, flood fallowing, and using clean seeds each year. Applying fungicides depends on the field environment. It is difficult to find a biological control method because research in a greenhouse can have different effects than testing in the field. The best control method found for "F. oxysporum" is planting resistant varieties, although not all have been bred for every forma specialis.

"F. oxysporum" f. sp. "batatas" can be controlled by using clean seed, cleaning up infected leaf and plant material and breeding for resistance. Fungicides can also be used, but are not as effective as the other two because of field conditions during application. Fungicides can be used effectively by dip treating propagation material.

Different races of "F. oxysporum" f. sp. "cubense", Panama disease on banana, can be susceptible, resistant and partially resistant. It can be controlled by breeding for resistance and through eradication and quarantine of the pathogen by improving soil conditions and using clean plant material. Biological control can work using antagonists. Systemic and soil fungicides can also be used.

The main control method for "F. oxysporum" f. sp. "lycopersici", vascular wilt on tomato, is resistance. Other effective control methods are fumigating the infected soil and raising the soil pH to 6.5-7.

The most effective way to control "F. oxysporum" f. sp. "melonis" is to graft a susceptible variety of melon to a resistant root-stock. Resistant cultivars, liming the soil to change soil pH to 6-7, and reducing soil nitrogen levels also help control "F. oxysporum" f. sp. "melonis".

The fungus "Trichoderma viride" is a proven biocontrol agent to control this disease in an environment friendly way.

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.

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.

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.

Three main things are needed to reduce stunting:

- a kind of environment where political commitment can thrive (also called an "enabling environment")

- applying several nutritional modifications or changes in a population on a large scale which have a high benefit and a low cost

- a strong foundation that can drive change (food security, empowerment of women and a supportive health environment through increasing access to safe water and sanitation).

To prevent stunting, it is not just a matter of providing better nutrition but also access to clean water, improved sanitation (hygienic toilets) and hand washing at critical times (summarised as "WASH"). Without provision of toilets, prevention of tropical intestinal diseases, which may affect almost all children in the developing world and lead to stunting will not be possible.

Studies have looked at ranking the underlying determinants in terms of their potency in reducing child stunting and found in the order of potency:

- percent of dietary energy from non-staples (greatest impact)

- access to sanitation and women's education

- access to safe water

- women's empowerment as measured by the female-to-male life expectancy ratio

- per capita dietary energy supply

Three of these determinants should receive attention in particular: access to sanitation, diversity of calorie sources from food supplies, and women's empowerment. A study by the Institute of Development Studies has stressed that: "The first two should be prioritized because they have strong impacts yet are farthest below their desired levels".

The goal of UN agencies, governments and NGO is now to optimise nutrition during the first 1000 days of a child's life, from pregnancy to the child's second birthday, in order to reduce the prevalence of stunting. The first 1000 days in a child's life are a crucial "window of opportunity" because the brain develops rapidly, laying the foundation for future cognitive and social ability. Furthermore, it is also the time when young children are the most at risk of infections that lead to diarrhoea. It is the time when they stop breast feeding (weaning process), begin to crawl, put things in their mouths and become exposed to faecal matter from open defecation and environmental enteropathies.

Ensuring proper nutrition of pregnant and lactating mothers is essential. Achieving so by helping women of reproductive age be in good nutritional status at conception is an excellent preventive measure. A focus on the pre-conception period has recently been introduced as a complement to the key phase of the 1000 days of pregnancy and first two years of life. An example of this is are attempts to control anemia in women of reproductive age. A well-nourished mother is the first step of stunting prevention, decreasing chances of the baby being born of low birth-weight, which is the first risk factor for future malnutrition.

After birth, in terms of interventions for the child, early initiation of breastfeeding, together with exclusive breastfeeding for the first 6 months, are pillars of stunting prevention. Introducing proper complementary feeding after 6 months of age together with breastfeeding until age 2 is the next step.

"Verticillium" wilt begins as a mild, local infection, which over a few years will grow in strength as more virile strains of the fungus develop. If left unchecked the disease will become so widespread that the crop will need to be replaced with resistant varieties, or a new crop will need to be planted altogether.

Control of "Verticilium" can be achieved by planting disease free plants in uncontaminated soil, planting resistant varieties, and refraining from planting susceptible crops in areas that have been used repeatedly for solanaceous crops. Soil fumigation can also be used, but is generally too expensive over large areas.

In tomato plants, the presence of ethylene during the initial stages of infection inhibits disease development, while in later stages of disease development the same hormone will cause greater wilt. Tomato plants are available that have been engineered with resistant genes that will tolerate the fungus while showing significantly lower signs of wilting.

"Verticillium albo-altrum", "Verticilium dahliae" and "V. longisporum" can overwinter as melanized mycelium or microsclerotia within live vegetation or plant debris. As a result, it can be important to clear plant debris to lower the spread of disease. "Verticilium dahliae" and "V. longisporum" are able to survive as microsclerotia in soil for up to 15 years.

Susceptible tomato seedlings inoculated with arbuscular mycorrhizal fungi and "Trichoderma Harzianum" show increased resistance towards "Verticillium" wilt.

No specific treatment is available, but antibiotics can be used to prevent secondary infections.

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

Biosecurity protocols including adequate isolation, disinfection are important in controlling the spread of the disease.

Prevention focuses on improving sanitation of water and food sources.

Treatment focuses on addressing the central components of intestinal inflammation, bacterial overgrowth and nutritional supplementation.

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 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.

There are multiple large-field, multi-country research initiatives focusing on strategies to prevent and treat EE.

- The MAL-ED project

- The Alive and Thrive nutrition project

- The Sanitation, Hygiene and Infant Nutrition Efficacy (SHINE) Trial (ClinicalTrials.gov identifier: NCT01824940)

- The WASH Benefits Study

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.

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.

Marshall–Smith syndrome is not to be confused with:

- Marshall syndrome (aka.Periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA syndrome, see also: Periodic fever syndrome)

- Sotos (like) syndrome

- Weaver-Smith syndrome (WSS)

Measures have been taken to reduce child malnutrition. Studies for the World Bank found that, from 1970 to 2000, the number of malnourished children decreased by 20 percent in developing countries. Iodine supplement trials in pregnant women have been shown to reduce offspring deaths during infancy and early childhood by 29 percent. However, universal salt iodization has largely replaced this intervention.

The Progresa program in Mexico combined conditional cash transfers with nutritional education and micronutrient-fortified food supplements; this resulted in a 10 percent reduction the prevalence of stunting in children 12–36 months old. Milk fortified with zinc and iron reduced the incidence of diarrhea by 18 percent in a study in India.

Breastfeeding can reduce rates of malnutrition and dehydration caused by diarrhea, but mothers are sometimes wrongly advised to not breastfeed their children. Breastfeeding has been shown to reduce mortality in infants and young children. Since only 38 percent of children worldwide under 6 months are exclusively breastfed, education programs could have large impacts on children malnutrition rates. However, breastfeeding cannot fully prevent PEM if not enough nutrients are consumed.

Although infection of avian reovirus is spread worldwide, it is rarely the sole cause of a disease. For chickens, the most common manifestation of the disease is joint/limb lameness. Confirming infection of avian reovirus can be detected through an ELISA test by using and observing the expression of σC and σB proteins. However, isolating and identifying reoviruses from tissue samples is very time consuming. Isolation is most successfully attained through inoculation of material into chick embryo cultures or fertile chicken eggs. Inoculation of embryonic eggs through the yolk sac has shown that the virus usually kills the embryos within 5 or 6 days post inoculation. Analyzing the samples, the embryos appeared hemorrhagic and necrotic lesions on the liver were present. (Jones, Onunkwo, 1978). There have also been approaches to identify avian reoviruses molecularly by observing infected tissues with dot-blot hybridization, PCR, and a combination of PCR and RFLP. This combination allows for the reovirus strain to be typed.

"E. histolytica" infections occur in both the intestine and (in people with symptoms) in tissue of the intestine and/or liver. As a result, two different classes of drugs are needed to treat the infection, one for each location. Such anti-amoebic drugs are known as amoebicides.

First reported from Saudi Arabia in 1988, Sanjad-Sakati syndrome, also known as "Hypoparathyroidism-Retardation-Dysmorphism (HRD) syndrome", or less commonly as the "Middle East syndrome", is a very rare genetically inherited disorder seen in the Middle East and children of Middle Eastern origin elsewhere in the world.The condition is named after Sami A. Sanjad and Nadia Awni Sakati.