Decomposition is the process by which organic substances are broken down into simpler matter. The process is a part of nutrient cycle and is essential for recycling the finite matter that occupies physical space in the biosphere. Bodies of living organisms begin to decompose shortly after death. Animals, such as worms, also help decompose the organic materials. Organisms that do this are known as decomposers. Although no two organisms decompose in the same way, they all undergo the same sequential stages of decomposition. The science which studies decomposition is generally referred to as "taphonomy" from the Greek word "taphos", meaning tomb.

One can differentiate abiotic from biotic decomposition (biodegradation). The former means "degradation of a substance by chemical or physical processes, e.g., hydrolysis. The latter means "the metabolic breakdown of materials into simpler components by living organisms", typically by microorganisms.

Age of Death: Stillborn fetuses and infants putrefy slowly due to their sterility. Generally, younger people putrefy more quickly than older people.

Condition of the Body: A body with a greater fat percentage and less lean body mass will have a faster rate of putrefaction, as fat retains more heat and it carries a larger amount of fluid in the tissues.

Cause of Death: The cause of death has a direct relationship to putrefaction speed, with bodies that died from acute violence or accident generally putrefying slower than those that died from infectious diseases. Certain poisons, such as potassium cyanide or strychnine may also delay putrefaction, while chronic alcoholism will speed it.

External Injuries: Antemortem or postmortem injuries can speed putrefaction as injured areas can be more susceptible to invasion by bacteria.

Certain poisonous substances to the body can delay the process of putrefaction. They include:

- Carbolic acid (Phenol)

- Arsenic and antimony

- Strychnine

- Nux Vomica (Plant)

- Zinc chloride, ZnCl

Biodegradation is the disintegration of materials by bacteria, fungi, or other biological means.

The term is often used in relation to: biomedicine, waste management, ecology, and the bioremediation of the natural environment. It is now commonly associated with environmentally-friendly products, capable of decomposing back into natural elements.

Although often conflated, "biodegradable" is distinct in meaning from: "compostable". While biodegradable simply means "can be consumed by microorganisms", "compostable" makes the further specific demand that the object break down under composting conditions.

Organic material can be degraded aerobically (with oxygen) or anaerobically (without oxygen). Decomposition of biodegradable substances may include both biological and abiotic steps.

Biodegradable matter is generally organic material that provides a nutrient for microorganisms. These are so numerous and diverse that a huge range of compounds can be biodegraded, including hydrocarbons (oils), polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs) and pharmaceutical substances.

Microorganisms secrete biosurfactant, an extracellular surfactant, to enhance this process.

A body buried in a sufficiently dry environment may be well preserved for decades. This was observed in the case for murdered civil rights activist Medgar Evers, who was found to be almost perfectly preserved over 30 years after his death, permitting an accurate autopsy when the case of his murder was re-opened in the 1990s.

Bodies submerged in a peat bog may become naturally "embalmed", arresting decomposition and resulting in a preserved specimen known as a bog body. The time for an embalmed body to be reduced to a skeleton varies greatly. Even when a body is decomposed, embalming treatment can still be achieved (the arterial system decays more slowly) but would not restore a natural appearance without extensive reconstruction and cosmetic work, and is largely used to control the foul odors due to decomposition.

An animal can be preserved almost perfectly, for millions of years in a resin such as amber.

There are some examples where bodies have been inexplicably preserved (with no human intervention) for decades or centuries and appear almost the same as when they died. In some religious groups, this is known as incorruptibility. It is not known whether or for how long a body can stay free of decay without artificial preservation.

Citrus Black Spot is a fungal disease caused by Guignardia citricarpa. This Ascomycete fungus affects citrus plants throughout subtropical climates, causing a reduction in both fruit quantity and quality. Symptoms include both fruit and leaf lesions, the latter being critical to inter-tree dispersal. Strict regulation and management is necessary to control this disease since there are currently no citrus varieties that are resistant.

In practice, almost all chemical compounds and materials are subject to biodegradation processes. The significance, however, is in the relative rates of such processes, such as days, weeks, years or centuries. A number of factors determine the rate at which this degradation of organic compounds occurs. Salient factors include light, water and oxygen. Temperature is also important because chemical reactions proceed more quickly at higher temperatures. The degradation rate of many organic compounds is limited by their bioavailability. Compounds must be released into solution before organisms can degrade them.

Biodegradability can be measured in a number of ways. Respirometry tests can be used for aerobic microbes. First one places a solid waste sample in a container with microorganisms and soil, and then aerates the mixture. Over the course of several days, microorganisms digest the sample bit by bit and produce carbon dioxide – the resulting amount of CO serves as an indicator of degradation. Biodegradability can also be measured by anaerobic microbes and the amount of methane or alloy that they are able to produce. In formal scientific literature, the process is termed bioremediation.

There is no resistance to Citrus Black Spot and once a tree has been infected there is no known cure causing tree removal to be the best option. Both Federal and State governments have recommended the following preventative measures.

To control "Guignardia citriparpa" fungicides like copper and/or strobilurins should be applied monthly from early May to the middle of September (in the northern hemisphere). Applications of the fungicides are recommended in early April (northern hemisphere) if that month has experienced more rainfall than usual resulting in the ideal conditions for citrus black spot to form.

Table 1. Recommended Chemical Controls for Citrus Black Spot

1)Lower rates can be used on smaller trees. Do not use less than minimum label rate.

2)Mode of action class for citrus pesticides from the Fungicide Resistance Action Committee (FRAC) 20111. Refer to ENY-624, "Pesticide Resistance and Resistance Management," in the 2012 Florida Citrus Pest Management Guide for more details.

3)Do not use more than 4 applications of strobilurin fungicides/season. Do not make more than 2 sequential applications of strobilurin fungicides.

Another method of control is to accelerate the leaf litter decomposition under the trees in citrus groves. Accelerating this decomposition reduces the chance for ascospore inoculation which generally takes place in the middle of March. There are three possible methods to hasten this decomposition. One method is the increase the mircrosprinkler irrigation in the grove to half an hour for at least five days of the week. This form of control should continue for about a month and a half. The second method is to apply urea or ammonium to the leaf litter. The last and final method to accelerate leaf decomposition is to apply lime or calcium carbonate to the litter. Urea, lime, and calcium carbonate reduce the number of fungal structures and spore production. Since the fungus requires wet conditions to thrive, air flow in the citrus grove should be maximized to reduce leaf wetness.

Along with these methods it is also important to get rid of debris such as fallen fruit or twigs in a manner that reduces the chances of infecting other plants. Citrus Black Spot can colonize and reproduce on dead twigs. To dispose of citrus debris it should either be heated to a minimum of 180℉ for two hours, incinerated, buried in a landfill, or fed to livestock. Plant trash should be moved with caution if at all to avoid spreading the infectious ascospores. Any trees that are infected with citrus black spot should be removed from the grove and disposed of. These trees must be removed because those that are declining and stressed will often have off season bloom. If there is more than one age of fruit present on the tree, it is possible for the asexual spores on the fruit to be transferred to new fruit, intensifying the disease. This off season blooming is often more problematic with Valencia oranges when old and new crops overlap.

The degree of rigor mortis may be used in forensic pathology, to determine the approximate time of death. A dead body holds its position as rigor mortis sets in. If the body is moved after death, but before rigor mortis begins, forensic techniques such as livor mortis can be applied. If the position in which a body is found does not match the location where it is found (for example, if it is flat on its back with one arm sticking straight up), that could mean someone moved it.

Several factors also affect the progression of rigor mortis, and investigators take these into account when estimating the time of death. One such factor is the ambient temperature. When conditions are warm, the onset and pace of rigor mortis are sped up by providing a conducive environment for the metabolic processes that cause decay. Low temperatures, however, slow them down. Therefore, for a person who dies outside in frozen conditions rigor mortis may last several days more than normal, so investigators may have to abandon it as a tool for determining time of death.

Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect. Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.

Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly suppresses the rate of fluid motion" in dentin.

The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.

Exposure of children to secondhand tobacco smoke is associated with tooth decay.

Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,

such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.

Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.

Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the identification of high-risk individuals can lead to more effective long-term patient management that prevents caries initiation and arrests or reverses the progression of lesions.

Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

Iron (Fe) deficiency is a plant disorder also known as "lime-induced chlorosis". It can be confused with manganese deficiency. A deficiency in the soil is rare but iron can be unavailable for absorption if soil pH is not between about 5 and 6.5. A common problem is excessive alkalinity of the soil (the pH is above 6.5). Also, iron deficiency can develop if the soil is too waterlogged or has been overfertilised. Elements like calcium, zinc, manganese, phosphorus, or copper can tie up iron if they are present in high amounts.

Iron is needed to produce chlorophyll, hence its deficiency causes chlorosis. For example, iron is used in the active site of glutamyl-tRNA reductase, an enzyme needed for the formation of 5-Aminolevulinic acid which is a precursor of heme and chlorophyll.

Symptoms include leaves turning yellow or brown in the margins between the veins which may remain green, while young leaves may appear to be bleached. Fruit would be of poor quality and quantity. Any plant may be affected, but raspberries and pears are particularly susceptible, as well as most acid-loving plants such as azaleas and camellias.

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities.

Molar incisor hypomineralization, which seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mother’s milk, premature birth and oxygen deprivation at birth, and certain disorders during the child’s first 3 years such as such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypovitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms.

Amelogenesis imperfecta, which occurs in between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.

The evidence for linking malocclusion and/or crowding to dental caries is weak; however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries is more likely to develop (see next section). Also, caries is more likely to develop when food is trapped between teeth.

The term alimentary mycotoxicoses refers to the effect of poisoning by Mycotoxins (The term 'mycotoxin' is usually reserved for the toxic chemical products produced by fungi that readily colonize crops) through food consumption. Mycotoxins sometimes have important effects on human and animal health. For example, an outbreak which occurred in the UK in 1960 caused the death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal. In the USSR in World War II, 5,000 people died due to Alimentary Toxic Aleukia (ALA). The common foodborne Mycotoxins include:

- Aflatoxins – originated from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of Aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result in necrosis, cirrhosis, and carcinoma. In the US, the acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5 μg/kg. The official document can be found at FDA's website.

- Altertoxins – are those of Alternariol (AOH), Alternariol methyl ether (AME), Altenuene (ALT), Altertoxin-1 (ATX-1), Tenuazonic acid (TeA) and Radicinin (RAD), originated from Alternaria spp. Some of the toxins can be present in sorghum, ragi, wheat and tomatoes. Some research has shown that the toxins can be easily cross-contaminated between grain commodities, suggesting that manufacturing and storage of grain commodities is a critical practice.

- Citrinin

- Citreoviridin

- Cyclopiazonic acid

- Cytochalasins

- Ergot alkaloids / Ergopeptine alkaloids – Ergotamine

- Fumonisins – Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and Esophageal cancer in humans. For human and animal health, both the FDA and the EC have regulated the content levels of toxins in food and animal feed.

- Fusaric acid

- Fusarochromanone

- Kojic acid

- Lolitrem alkaloids

- Moniliformin

- 3-Nitropropionic acid

- Nivalenol

- Ochratoxins – In Australia, The Limit of Reporting (LOR) level for Ochratoxin A (OTA) analyses in 20th Australian Total Diet Survey was 1 µg/kg, whereas the EC restricts the content of OTA to 5 µg/kg in cereal commodities, 3 µg/kg in processed products and 10 µg/kg in dried vine fruits.

- Oosporeine

- Patulin – Currently, this toxin has been advisably regulated on fruit products. The EC and the FDA have limited it to under 50 µg/kg for fruit juice and fruit nectar, while limits of 25 µg/kg for solid-contained fruit products and 10 µg/kg for baby foods were specified by the EC.

- Phomopsins

- Sporidesmin A

- Sterigmatocystin

- Tremorgenic mycotoxins – Five of them have been reported to be associated with molds found in fermented meats. These are Fumitremorgen B, Paxilline, Penitrem A, Verrucosidin, and Verruculogen.

- Trichothecenes – sourced from Cephalosporium, Fusarium, Myrothecium, Stachybotrys and Trichoderma. The toxins are usually found in molded maize, wheat, corn, peanuts and rice, or animal feed of hay and straw. Four trichothecenes, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and deoxynivalenol (DON) have been most commonly encountered by humans and animals. The consequences of oral intake of, or dermal exposure to, the toxins will result in Alimentary toxic aleukia, neutropenia, aplastic anemia, thrombocytopenia and/or skin irritation. In 1993, the FDA issued a document for the content limits of DON in food and animal feed at an advisory level. In 2003, US published a patent that is very promising for farmers to produce a trichothecene-resistant crop.

- Zearalenone

- Zearalenols

Globally, infants are a population that are especially vulnerable to foodborne disease. The World Health Organization has issued recommendations for the preparation, use and storage of prepared formulas. Breastfeeding remains the best preventative measure for protection of foodborne infections in infants.

Rigor mortis (Latin: "rigor" "stiffness", "mortis" "of death"), the third stage of death, is one of the recognizable signs of death, caused by chemical changes in the muscles post mortem, which cause the limbs of the corpse to stiffen. In humans, rigor mortis can occur as soon as 4 hours post mortem.

Populations groups at risk:

- In the US:

- Children and young adults: Drowning rates are highest for children under 5 years of age and persons 15–24 years of age.

- Males: Nearly 80% of people who die from drowning are male.

- Minorities: The fatal unintentional drowning rate for African Americans between 2005 and 2009 was significantly higher than that of whites across all ages. The fatal drowning rate of African American children of ages from 5 to 14 is almost three times that of white children in the same age range, and 5.5 times higher in swimming pools. These disparities might be associated with lack of basic swimming skills in some minority populations.

Behavioral and physical factors:

- In the US:

- Use of alcohol increases the risk of drowning. Among adolescents and adults, alcohol use is involved in almost a quarter of emergency department visits for drowning.

- Inability to swim: Participation in formal swimming lessons can reduce the risk of drowning among children aged 1 to 4 years.

- Free access to water: Effective barriers prevent young children from gaining access to the water

- Ineffective supervision: Drowning can occur anywhere there is water, and even in the presence of lifeguards.

- Risk can vary with location depending on age. Children between 1 and 4 usually drown in home swimming pools. Drownings in natural water settings increase with age. More than half of drownings among those 15 years and older occurred in natural water environments.

- Failure to wear life jackets or personal flotation devices was implicated in 88% of the boating related drownings in the US during 2010.

- For persons with seizure disorders, drowning is the most common cause of death by unintentional injury, largely in the bathtub.

Drowning is a major worldwide cause of death and injury in children. Long term neurological outcomes of drowning cannot be predicted accurately during the early stages of treatment and although survival after long submersion times, mostly by young children, has been reported, many survivors will remain severely and permanently neurologically compromised after much shorter submersion times. Factors affecting probability of long term recovery with mild deficits or full function in young children include the duration of submersion, whether advanced life support was needed at the accident site, the duration of cardiopulmonary resuscitation, and whether spontaneous breathing and circulation are present on arrival at the emergency room.

Data on long-term outcome are scarce and unreliable. Neurological examination at the time of discharge from hospital does not accurately predict long term outcomes. Some victims who suffered from severe brain injury and were transferred to other institutions died months or years after the drowning and are recorded as survivors. Non-fatal drownings have been estimated as two to four times more frequent than fatal drownings.

Sepsis causes millions of deaths globally each year and is the most common cause of death in people who have been hospitalized. The worldwide incidence of sepsis is estimated to be 18 million cases per year. In the United States sepsis affects approximately 3 in 1,000 people, and severe sepsis contributes to more than 200,000 deaths per year.

Sepsis occurs in 1–2% of all hospitalizations and accounts for as much as 25% of ICU bed utilization. Due to it rarely being reported as a primary diagnosis (often being a complication of cancer or other illness), the incidence, mortality, and morbidity rates of sepsis are likely underestimated. A study by the Agency for Healthcare Research and Quality (AHRQ) of selected States found that there were approximately 651 hospital stays per 100,000 population with a sepsis diagnosis in 2010. It is the second-leading cause of death in non-coronary intensive care unit (ICU) and the tenth-most-common cause of death overall (the first being heart disease). Children under 12 months of age and elderly people have the highest incidence of severe sepsis. Among U.S. patients who had multiple sepsis hospital admissions in 2010, those who were discharged to a skilled nursing facility or long term care following the initial hospitalization were more likely to be readmitted than those discharged to another form of care. A study of 18 U.S. States found that, amongst Medicare patients in 2011, sepsis was the second most common principal reason for readmission within 30 days.

Several medical conditions increase a person's susceptibility to infection and developing sepsis. Common sepsis risk factors include age (especially the very young and old); conditions that weaken the immune system such as cancer, diabetes, or the absence of a spleen; and major trauma and burns.

Approximately 20–35% of people with severe sepsis and 30–70% of people with septic shock die. Lactate is a useful method of determining prognosis with those who have a level greater than 4 mmol/L having a mortality of 40% and those with a level of less than 2 mmol/L have a mortality of less than 15%.

There are a number of prognostic stratification systems such as APACHE II and Mortality in Emergency Department Sepsis. APACHE II factors in the person's age, underlying condition, and various physiologic variables to yield estimates of the risk of dying of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly influences the risk of death. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis. The Mortality in Emergency Department Sepsis (MEDS) score is simpler and useful in the emergency department environment.

Some people may experience severe long-term cognitive decline following an episode of severe sepsis, but the absence of baseline neuropsychological data in most people with sepsis makes the incidence of this difficult to quantify or to study.

The cause of postmortem fetal extrusion is not completely understood, as the event is neither predictable nor replicable under experimental conditions. Evidence has accumulated opportunistically and direct observation is serendipitous. While it is possible that more than one cause can produce the same result, there is an accepted hypothesis, based on established research in the fields of biochemistry and forensic taphonomy, and further supported by observational research, that accounts for the taphonomic mechanisms that would result in the most often encountered cases of postmortem extrusion of a non-viable fetus.

Typically, as a dead body decomposes, body tissues become depleted of oxygen and the body begins to putrefy; anaerobic bacteria in the gastrointestinal tract proliferate and as a result of increased metabolic activity, release gases such as carbon dioxide, methane, and hydrogen sulfide. These bacteria secrete exoenzymes to break down body cells and proteins for ingestion which thus weakens organ tissues. Increasing pressure forces the diffusion of excessive gases into the weakened tissues where they enter the circulatory system and spread to other parts of the body, causing both torso and limbs to become bloated. These decompositional processes weaken the structural integrity of organs by separating necrotizing tissue layers. Bloating usually begins from two to five days after death, depending on external temperature, humidity, and other environmental conditions. As the volume of gas increases, the pressure begins to force various body fluids to exude from all natural orifices. It is at this point during the decomposition of a pregnant body that amniotic membranes become stretched and separated, and intraabdominal gas pressure may force the and prolapse of the uterus, which would result in the expulsion of the fetus through the vaginal canal. It has been observed that the bodies of multiparous women are more likely to spontaneously expel the fetus during decomposition than those who died during their first pregnancy, because of the more elastic nature of the cervix.

Coffin birth, also known as postmortem fetal extrusion, is the expulsion of a nonviable fetus through the vaginal opening of the decomposing body of a deceased pregnant woman as a result of the increasing pressure of intra-abdominal gases. This kind of postmortem delivery occurs very rarely during the decomposition of a body. The practice of chemical preservation, whereby chemical preservatives and disinfectant solutions are pumped into a body to replace natural body fluids (and the bacteria that reside therein), have made the occurrence of "coffin birth" so rare that the topic is rarely mentioned in international medical discourse.

Typically during the decomposition of a human body, naturally occurring bacteria in the organs of the abdominal cavity (such as the stomach and intestines) generate gases as by-products of metabolism, which causes the body to swell. In some cases, the confined pressure of the gases can squeeze the uterus (the womb), even forcing it downward, and it may and be forced out of the body through the vaginal opening (a process called "prolapse"). If a fetus is contained within the uterus, it could therefore be expelled from the mother's body through the vaginal opening when the uterus turns inside-out, in a process that, to outward appearances, mimics childbirth. The main differences lie in the state of the mother and fetus and the mechanism of delivery: in the event of natural, live childbirth, the mother's contractions encourage the infant to emerge from the womb; in a case of coffin birth, built-up gas pressure within the putrefied body of a pregnant woman pushes the dead fetus from the body of the mother.

Cases have been recorded by medical authorities since the 16th century, though some archaeological cases provide evidence for its occurrence in many periods of human history. While cases of postmortem fetal expulsion have always been rare, the phenomenon has been recorded under disparate circumstances and is occasionally seen in a modern forensic context when the body of a pregnant woman lies undisturbed and undiscovered for some time following death. There are also cases whereby a fetus may become separated from the body of the pregnant woman about the time of death or during decomposition, though because those cases are not consistent with the processes described here, they are not considered true cases of postmortem fetal extrusion.

The origin and mode of transmission of the prions causing CWD is unknown, but recent research indicates that prions can be excreted by deer and elk, and are transmitted by eating grass growing in contaminated soil. Animals born in captivity and those born in the wild have been affected with the disease. Based on epidemiology, transmission of CWD is thought to be lateral (from animal to animal). Maternal transmission may occur, although it appears to be relatively unimportant in maintaining epidemics. An infected deer's saliva is able to spread the CWD prions. Exposure between animals is associated with sharing food and water sources contaminated with CWD prions shed by diseased deer.

The disease was first identified in 1967 in a closed herd of captive mule deer in contiguous portions of northeastern Colorado. In 1980, the disease was determined to be a TSE. It was first identified in wild elk and mules in 1981 in Colorado and Wyoming, and in farmed elk in 1997.

In May 2001, CWD was also found in free-ranging deer in the southwestern corner of Nebraska (adjacent to Colorado and Wyoming) and later in additional areas in western Nebraska. The limited area of northern Colorado, southern Wyoming, and western Nebraska in which free-ranging deer, moose, and/or elk positive for CWD have been found is referred to as the endemic area. The area in 2006 has expanded to six states, including parts of eastern Utah, southwestern South Dakota, and northwestern Kansas. Also, areas not contiguous (to the endemic area) areas in central Utah and central Nebraska have been found. The limits of the affected areas are not well defined, since the disease is at a low incidence and the amount of sampling may not be adequate to detect it. In 2002, CWD was detected in wild deer in south-central Wisconsin and northern Illinois and in an isolated area of southern New Mexico. In 2005, it was found in wild white-tailed deer in New York and in Hampshire County, West Virginia. In 2008, the first confirmed case of CWD in Michigan was discovered in an infected deer on an enclosed deer-breeding facility. It is also found in the Canadian provinces of Alberta and Saskatchewan. In February 2011, the Maryland Department of Natural Resources reported the first confirmed case of the disease in that state. The affected animal was a white-tailed deer killed by a hunter.

CWD has also been diagnosed in farmed elk and deer herds in a number of states and in two Canadian provinces. The first positive farmed elk herd in the United States was detected in 1997 in South Dakota.

Since then, additional positive elk herds and farmed white-tailed deer herds have been found in South Dakota (7), Nebraska (4), Colorado (10), Oklahoma (1), Kansas (1), Minnesota (3), Montana (1), Wisconsin (6) and New York (2). As of fall of 2006, four positive elk herds in Colorado and a positive white-tailed deer herd in Wisconsin remain under state quarantine. All of the other herds have been depopulated or have been slaughtered and tested, and the quarantine has been lifted from one herd that underwent rigorous surveillance with no further evidence of disease. CWD also has been found in farmed elk in the Canadian provinces of Saskatchewan and Alberta. A retrospective study also showed mule deer exported from Denver to the Toronto Zoo in the 1980s were affected. In June 2015, the disease was detected in a male white-tailed deer on a breeding ranch in Medina County, Texas. State officials euthanized 34 deer in an effort to contain a possible outbreak.

Species that have been affected with CWD include elk, mule deer, white-tailed deer, black-tailed deer, and moose. Other ruminant species, including wild ruminants and domestic cattle, sheep, and goats, have been housed in wildlife facilities in direct or indirect contact with CWD-affected deer and elk, with no evidence of disease transmission. However, experimental transmission of CWD into other ruminants by intracranial inoculation does result in disease, suggesting only a weak molecular species barrier exists. Research is ongoing to further explore the possibility of transmission of CWD to other species.

By April 2016 CWD had been found in captive animals in South Korea; the disease arrived there with live elk that were imported for farming in the late 1990s.

Fear of being buried alive is the fear of being placed in a grave while still alive as a result of being incorrectly pronounced dead. The abnormal, psychopathological version of this fear is referred to as taphophobia (from Greek τάφος - "taphos", "grave, tomb" and φόβος - "phobos", "fear"), which is translated as "fear of graves".

Before the advent of modern medicine, the fear was not entirely irrational. Throughout history, there have been numerous cases of people being buried alive by accident. In 1905, the English reformer William Tebb collected accounts of premature burial. He found 219 cases of near live burial, 149 actual live burials, 10 cases of live dissection and 2 cases of awakening while being embalmed.

The 18th century had seen the development of mouth-to-mouth resuscitation and crude defibrillation techniques to revive persons considered dead, and the Royal Humane Society had been formed as the Society for the Recovery of Persons Apparently Drowned. In 1896, an American funeral director, T. M. Montgomery, reported that "nearly 2% of those exhumed were no doubt victims of suspended animation", although folklorist Paul Barber has argued that the incidence of burial alive has been overestimated, and that the normal effects of decomposition are mistaken for signs of life.

There have been many urban legends of people being accidentally buried alive. Legends included elements such as someone entering into the state of sopor or coma, only to wake up years later and die a horrible death. Other legends tell of coffins opened to find a corpse with a long beard or corpses with the hands raised and palms turned upward. Of note is a legend about the premature burial of Ann Hill Carter Lee, the wife of Henry Lee III. On his deathbed in 1799, George Washington made his attendants promise not to bury him for two days.

Literature found fertile ground in exploring the natural fear of being buried alive. One of Edgar Allan Poe's horror stories, "The Premature Burial", is about a person suffering from taphophobia. Other Poe stories about premature burial are "The Fall of the House of Usher" and "The Cask of Amontillado"—and to a lesser extent, “The Black Cat”.

Fear of being buried alive was elaborated to the extent that those who could afford it would make all sorts of arrangements for the construction of a safety coffin to ensure this would be avoided (e.g., glass lids for observation, ropes to bells for signaling, and breathing pipes for survival until rescued).

An urban legend states that the sayings "Saved by the bell" and "Dead ringer" are both derived from the notion of having a rope attached to a bell outside the coffin that could alert people that the recently buried person is not yet deceased; these theories have been proven a hoax.

CWD may be directly transmitted via contact with infected animals, their bodily tissues, and their bodily fluids. Transmission may result from contact with both clinically affected and infected, but asymptomatic, cervids.

Recent research on Rocky Mountain elk found that with CWD-infected dams, many sub-clinical, there was a high rate (80%) of maternal-to-offspring transmission of CWD prions, regardless of gestational period. While not dispositive relative to disease development in the fetus, this does suggest that maternal transmission may be yet another important route of direct CWD transmission.