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Wednesday, March 11, 2020

Foodborne illness

From Wikipedia, the free encyclopedia
 
Foodborne illness (also foodborne disease and colloquially referred to as food poisoning) is any illness resulting from the spoilage of contaminated food, pathogenic bacteria, viruses, or parasites that contaminate food, as well as toxins such as poisonous mushrooms and various species of beans that have not been boiled for at least 10 minutes.

Symptoms vary depending on the cause, and are described below in this article. A few broad generalizations can be made. For contaminants requiring an incubation period, symptoms may not manifest for hours to days, depending on the cause and on quantity of consumption. Longer incubation periods tend to cause sufferers to not associate the symptoms with the item consumed, so they may misattribute the symptoms to gastroenteritis, for example.

Symptoms often include vomiting, fever, and aches, and may include diarrhea. Bouts of vomiting can be repeated with an extended delay in between, because even if infected food was eliminated from the stomach in the first bout, microbes, like bacteria, (if applicable) can pass through the stomach into the intestine and begin to multiply. Some types of microbes stay in the intestine, some produce a toxin that is absorbed into the bloodstream, and some can directly invade deeper body tissues.

Causes

Poorly stored food in a refrigerator

Foodborne illness usually arises from improper handling, preparation, or food storage. Good hygiene practices before, during, and after food preparation can reduce the chances of contracting an illness. There is a consensus in the public health community that regular hand-washing is one of the most effective defenses against the spread of foodborne illness. The action of monitoring food to ensure that it will not cause foodborne illness is known as food safety. Foodborne disease can also be caused by a large variety of toxins that affect the environment.

Furthermore, foodborne illness can be caused by pesticides or medicines in food and natural toxic substances such as poisonous mushrooms or reef fish.

Bacteria

Bacteria are a common cause of foodborne illness. The United Kingdom, in 2000, reported the individual bacteria involved as the following: Campylobacter jejuni 77.3%, Salmonella 20.9%, Escherichia coli O157:H7 1.4%, and all others less than 0.56%. In the past, bacterial infections were thought to be more prevalent because few places had the capability to test for norovirus and no active surveillance was being done for this particular agent. Toxins from bacterial infections are delayed because the bacteria need time to multiply. As a result, symptoms associated with intoxication are usually not seen until 12–72 hours or more after eating contaminated food. However, in some cases, such as Staphylococcal food poisoning, the onset of illness can be as soon as 30 minutes after ingesting contaminated food.

Salmonella

Most common bacterial foodborne pathogens are:
Other common bacterial foodborne pathogens are:
Less common bacterial agents:

Enterotoxins

In addition to disease caused by direct bacterial infection, some foodborne illnesses are caused by enterotoxins (exotoxins targeting the intestines). Enterotoxins can produce illness even when the microbes that produced them have been killed. Symptom appearance varies with the toxin but may be rapid in onset, as in the case of enterotoxins of Staphylococcus aureus in which symptoms appear in one to six hours. This causes intense vomiting including or not including diarrhea (resulting in staphylococcal enteritis), and staphylococcal enterotoxins (most commonly staphylococcal enterotoxin A but also including staphylococcal enterotoxin B) are the most commonly reported enterotoxins although cases of poisoning are likely underestimated. It occurs mainly in cooked and processed foods due to competition with other biota in raw foods, and humans are the main cause of contamination as a substantial percentage of humans are persistent carriers of S. aureus. The CDC has estimated about 240,000 cases per year in the United States.
The rare but potentially deadly disease botulism occurs when the anaerobic bacterium Clostridium botulinum grows in improperly canned low-acid foods and produces botulin, a powerful paralytic toxin. 

Pseudoalteromonas tetraodonis, certain species of Pseudomonas and Vibrio, and some other bacteria, produce the lethal tetrodotoxin, which is present in the tissues of some living animal species rather than being a product of decomposition.

Emerging foodborne pathogens

Many foodborne illnesses remain poorly understood.

Preventing bacterial food poisoning

Proper storage and refrigeration of food help in the prevention of food poisoning

Prevention is mainly the role of the state, through the definition of strict rules of hygiene and a public services of veterinary surveying of animal products in the food chain, from farming to the transformation industry and delivery (shops and restaurants). This regulation includes:
  • traceability: in a final product, it must be possible to know the origin of the ingredients (originating farm, identification of the harvesting or of the animal) and where and when it was processed; the origin of the illness can thus be tracked and solved (and possibly penalized), and the final products can be removed from the sale if a problem is detected;
  • enforcement of hygiene procedures such as HACCP and the "cold chain";
  • power of control and of law enforcement of veterinarians.
In August 2006, the United States Food and Drug Administration approved Phage therapy which involves spraying meat with viruses that infect bacteria, and thus preventing infection. This has raised concerns, because without mandatory labelling consumers would not be aware that meat and poultry products have been treated with the spray.

At home, prevention mainly consists of good food safety practices. Many forms of bacterial poisoning can be prevented by cooking it sufficiently, and either eating it quickly or refrigerating it effectively. Many toxins, however, are not destroyed by heat treatment.

Techniques that help prevent food borne illness in the kitchen are hand washing, rinsing produce, preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between 40 and 140 °F (4 and 60 °C), called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containers for quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of 165 °F (74 °C) or until hot or steaming to kill bacteria.

Mycotoxins and alimentary mycotoxicoses

The term alimentary mycotoxicosis refers to the effect of poisoning by mycotoxins through food consumption. The term mycotoxin is usually reserved for the toxic chemical products produced by fungi that readily colonize crops. 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:

Viruses

Viral infections make up perhaps one third of cases of food poisoning in developed countries. In the US, more than 50% of cases are viral and noroviruses are the most common foodborne illness, causing 57% of outbreaks in 2004. Foodborne viral infection are usually of intermediate (1–3 days) incubation period, causing illnesses which are self-limited in otherwise healthy individuals; they are similar to the bacterial forms described above.
  • Enterovirus
  • Hepatitis A is distinguished from other viral causes by its prolonged (2–6 week) incubation period and its ability to spread beyond the stomach and intestines into the liver. It often results in jaundice, or yellowing of the skin, but rarely leads to chronic liver dysfunction. The virus has been found to cause infection due to the consumption of fresh-cut produce which has fecal contamination.
  • Hepatitis E
  • Norovirus
  • Rotavirus
  • Rotavirus

Parasites

Most foodborne parasites are zoonoses.

Natural toxins

Several foods can naturally contain toxins, many of which are not produced by bacteria. Plants in particular may be toxic; animals which are naturally poisonous to eat are rare. In evolutionary terms, animals can escape being eaten by fleeing; plants can use only passive defenses such as poisons and distasteful substances, for example capsaicin in chili peppers and pungent sulfur compounds in garlic and onions. Most animal poisons are not synthesised by the animal, but acquired by eating poisonous plants to which the animal is immune, or by bacterial action.
Some plants contain substances which are toxic in large doses, but have therapeutic properties in appropriate dosages.

Other pathogenic agents

"Ptomaine poisoning"

In 1883, the Italian, Professor Salmi, of Bologna, introduced the generic name ptomaine (from Greek ptōma, "fall, fallen body, corpse") for alkaloids found in decaying animal and vegetable matter, especially (as reflected in their names) putrescine and cadaverine. The 1892 Merck's Bulletin stated, "We name such products of bacterial origin ptomaines; and the special alkaloid produced by the comma bacillus is variously named Cadaverine, Putrescine, etc." While The Lancet stated, "The chemical ferments produced in the system, the... ptomaines which may exercise so disastrous an influence." It is now known that the "disastrous... influence" is due to the direct action of bacteria and only slightly to the alkaloids. Thus, the use of the phrase "ptomaine poisoning" is now obsolete.

Tainted potato salad sickening hundreds at a Communist political convention in Massillon, Ohio, and aboard a Washington DC cruise boat in separate incidents during a single week in 1932 drew national attention to the dangers of so-called "ptomaine poisoning" in the pages of the American news weekly, Time. Another newspaper article from 1944 told of more than 150 persons being hospitalized in Chicago with ptomaine poisoning apparently from rice pudding served by a chain of restaurants.

Mechanism

Incubation period

The delay between the consumption of contaminated food and the appearance of the first symptoms of illness is called the incubation period. This ranges from hours to days (and rarely months or even years, such as in the case of listeriosis or bovine spongiform encephalopathy), depending on the agent, and on how much was consumed. If symptoms occur within one to six hours after eating the food, it suggests that it is caused by a bacterial toxin or a chemical rather than live bacteria.

The long incubation period of many foodborne illnesses tends to cause sufferers to attribute their symptoms to gastroenteritis. 

During the incubation period, microbes pass through the stomach into the intestine, attach to the cells lining the intestinal walls, and begin to multiply there. Some types of microbes stay in the intestine, some produce a toxin that is absorbed into the bloodstream, and some can directly invade the deeper body tissues. The symptoms produced depend on the type of microbe.

Infectious dose

The infectious dose is the amount of agent that must be consumed to give rise to symptoms of foodborne illness, and varies according to the agent and the consumer's age and overall health. Pathogens vary in minimum infectious dose; for example, Shigella sonnei has a low estimated minimum dose of < 500 colony-forming units (CFU) while Staphylococcus aureus has a relatively high estimate.

In the case of Salmonella a relatively large inoculum of 1 million to 1 billion organisms is necessary to produce symptoms in healthy human volunteers, as Salmonellae are very sensitive to acid. An unusually high stomach pH level (low acidity) greatly reduces the number of bacteria required to cause symptoms by a factor of between 10 and 100.

Epidemiology

Asymptomatic subclinical infection may help spread these diseases, particularly Staphylococcus aureus, Campylobacter, Salmonella, Shigella, Enterobacter, V. cholerae, and Yersinia. For example, as of 1984 it was estimated that in the United States, 200,000 people were asymptomatic carriers of Salmonella.

Infants

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.

United States

In the United States, using FoodNet data from 2000–2007, the CDC estimated there were 47.8 million foodborne illnesses per year (16,000 cases for 100,000 inhabitants) with 9.4 million of these caused by 31 known identified pathogens.
  • 127,839 were hospitalized (43 per 100,000 inhabitants per year).
  • 3,037 people died (1.0 per 100,000 inhabitants per year).
Causes of foodborne illness in US

Cause Annual cases Rate
(per 100,000 inhabitants)
1 Norovirus 5,461,731 cases X
2 Salmonella 1,027,561 cases X
3 Clostridium perfringens 965,958 cases X
4 Campylobacter 845,024 cases X

Causes of death by foodborne illness in US

Cause Annual deaths Rate
(per 100,000 inhabitants)
1 Salmonella 378 cases 0.126
2 Toxoplasma gondii 327 cases 0.109
3 Listeria 255 cases 0.085
4 Norovirus 149 cases 0.050

United Kingdom

According to a 2012 report from the Food Standards Agency, there are around a million cases of foodborne illness per year (1,580 cases for 100,000 inhabitants).
  • 20,000 were hospitalized (32 per 100,000 inhabitants);
  • 500 people died (0.80 per 100,000 inhabitants).

France

This data pertains to reported medical cases of 23 specific pathogens in the 1990s, as opposed to total population estimates of all food-borne illness for the United States.

In France, for 750,000 cases (1210 per 100,000 inhabitants):
  • 70,000 people consulted in the emergency department of a hospital (113 per 100,000 inhabitants);
  • 113,000 people were hospitalized (182 per 100,000 inhabitants);
  • 460 people died (0.75 per 100,000 inhabitants).

Australia

A study by the Australian National University, published in November 2014, found in 2010 that there were an estimated 4.1 million cases of foodborne gastroenteritis acquired in Australia on average each year, along with 5,140 cases of non-gastrointestinal illness. The study was funded by the Australian Department of Health, Food Standards Australia New Zealand and the NSW Food Authority.

The main causes were Norovirus, pathogenic Escherichia coli, Campylobacter spp. and non-typhoidal Salmonella spp., although the causes of approximately 80% of illnesses were unknown. Approximately 25% (90% CrI: 13%–42%) of the 15.9 million episodes of gastroenteritis that occur in Australia were estimated to be transmitted by contaminated food. This equates to an average of approximately one episode of foodborne gastroenteritis every five years per person. Data on the number of hospitalisations and deaths represent the occurrence of serious foodborne illness. Including gastroenteritis, non-gastroenteritis and sequelae, there were an estimated annual 31,920 (90% CrI: 29,500–35,500) hospitalisations due to foodborne illness and 86 (90% CrI: 70–105) deaths due to foodborne illness circa 2010. This study concludes that these rates are similar to recent estimates in the US and Canada.

A main aim of this study was to compare if foodborne illness incidence had increased over time. In this study, similar methods of assessment were applied to data from circa 2000, which showed that the rate of foodborne gastroenteritis had not changed significantly over time. Two key estimates were the total number of gastroenteritis episodes each year, and the proportion considered foodborne. In circa 2010, it was estimated that 25% of all episodes of gastroenteritis were foodborne. By applying this proportion of episodes due to food to the incidence of gastroenteritis circa 2000, there were an estimated 4.3 million (90% CrI: 2.2–7.3 million) episodes of foodborne gastroenteritis circa 2000, although credible intervals overlap with 2010. Taking into account changes in population size, applying these equivalent methods suggests a 17% decrease in the rate of foodborne gastroenteritis between 2000 and 2010, with considerable overlap of the 90% credible intervals.

This study replaces a previous estimate of 5.4 million cases of food-borne illness in Australia every year, causing:
  • 18,000 hospitalizations
  • 120 deaths (0.5 deaths per 100,000 inhabitants)
  • 2.1 million lost days off work
  • 1.2 million doctor consultations
  • 300,000 prescriptions for antibiotics.
Most foodborne disease outbreaks in Australia have been linked to raw or minimally cooked eggs or poultry. The Australian Food Safety Information Council estimates that one third of cases of food poisoning occur in the home

Outbreaks

The vast majority of reported cases of foodborne illness occur as individual or sporadic cases. The origin of most sporadic cases is undetermined. In the United States, where people eat outside the home frequently, 58% of cases originate from commercial food facilities (2004 FoodNet data). An outbreak is defined as occurring when two or more people experience similar illness after consuming food from a common source.

Often, a combination of events contributes to an outbreak, for example, food might be left at room temperature for many hours, allowing bacteria to multiply which is compounded by inadequate cooking which results in a failure to kill the dangerously elevated bacterial levels.

Outbreaks are usually identified when those affected know each other. However, more and more, outbreaks are identified by public health staff from unexpected increases in laboratory results for certain strains of bacteria. Outbreak detection and investigation in the United States is primarily handled by local health jurisdictions and is inconsistent from district to district. It is estimated that 1–2% of outbreaks are detected.

Society and culture

United Kingdom

In postwar Aberdeen (1964) a large-scale (>400 cases) outbreak of typhoid occurred, caused by contaminated corned beef which had been imported from Argentina. The corned beef was placed in cans and because the cooling plant had failed, cold river water from the Plate estuary was used to cool the cans. One of the cans had a defect and the meat inside was contaminated. This meat was then sliced using a meat slicer in a shop in Aberdeen, and a lack of cleaning the machinery led to spreading the contamination to other meats cut in the slicer. These meats were then eaten by the people of Aberdeen who then became ill.

Serious outbreaks of foodborne illness since the 1970s prompted key changes in UK food safety law. These included the death of 19 patients in the Stanley Royd Hospital outbreak and the bovine spongiform encephalopathy (BSE, mad cow disease) outbreak identified in the 1980s. The death of 21 people in the 1996 Wishaw outbreak of E. coli O157[76][77] was a precursor to the establishment of the Food Standards Agency which, according to Tony Blair in the 1998 white paper A Force for Change Cm 3830, "would be powerful, open and dedicated to the interests of consumers".

In May 2015, for the second year running, England’s Food Standards Agency devoted its annual Food Safety Week to – “The Chicken Challenge”. The focus was on the handling of raw chicken in the home and in catering facilities in a drive to reduce the worryingly high levels of food poisoning from the campylobacter bacterium. Anne Hardy argues that widespread public education of food hygiene can be useful, particularly through media (T.V cookery programmes) and advertisement. She points to the examples set by Scandinavian societies.

United States

In 2001, the Center for Science in the Public Interest petitioned the United States Department of Agriculture to require meat packers to remove spinal cords before processing cattle carcasses for human consumption, a measure designed to lessen the risk of infection by variant Creutzfeldt–Jakob disease. The petition was supported by the American Public Health Association, the Consumer Federation of America, the Government Accountability Project, the National Consumers League, and Safe Tables Our Priority.

None of the US Department of Health and Human Services targets regarding incidence of foodborne infections were reached in 2007.

A report issued in June 2018 by NBC's Minneapolis station using research by both the CDC and the Minnesota Department of Health concluded that foodborne illness is on the rise in the U.S. The CDC has reported approximately four thousand cases of food poisoning annually in the last few years. Experts cite increased handling of food by humans as a major contributor, leading to outbreaks of parasites such as E. coli and cyclospora which can only come from human fecal matter.

Organizations

The World Health Organization Department of Food Safety and Zoonoses (FOS) provides scientific advice for organizations and the public on issues concerning the safety of food. Its mission is to lower the burden of foodborne disease, thereby strengthening the health security and sustainable development of Member States. Foodborne and waterborne diarrhoeal diseases kill an estimated 2.2 million people annually, most of whom are children. WHO works closely with the Food and Agriculture Organization of the United Nations (FAO) to address food safety issues along the entire food production chain—from production to consumption—using new methods of risk analysis. These methods provide efficient, science-based tools to improve food safety, thereby benefiting both public health and economic development.

International Food Safety Authorities Network (INFOSAN)

The International Food Safety Authorities Network (INFOSAN) is a joint program of the WHO and FAO. INFOSAN has been connecting national authorities from around the globe since 2004, with the goal of preventing the international spread of contaminated food and foodborne disease and strengthening food safety systems globally. This is done by:
  1. Promoting the rapid exchange of information during food safety events;
  2. Sharing information on important food safety issues of global interest;
  3. Promoting partnership and collaboration between countries; and
  4. Helping countries strengthen their capacity to manage food safety risks.
Membership to INFOSAN is voluntary, but is restricted to representatives from national and regional government authorities and requires an official letter of designation. INFOSAN seeks to reflect the multidisciplinary nature of food safety and promote intersectoral collaboration by requesting the designation of Focal Points in each of the respective national authorities with a stake in food safety, and a single Emergency Contact Point in the national authority with the responsibility for coordinating national food safety emergencies; countries choosing to be members of INFOSAN are committed to sharing information between their respective food safety authorities and other INFOSAN members. The operational definition of a food safety authority includes those authorities involved in: food policy; risk assessment; food control and management; food inspection services; foodborne disease surveillance and response; laboratory services for monitoring and surveillance of foods and foodborne diseases; and food safety information, education and communication across the farm-to-table continuum.

Prioritisation of food-borne pathogens

Food and Agriculture Organization of the United Nations and The World Health Organization published have made a global ranking of food-borne parasites using a multicriteria ranking tool concluding that Taen.
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Tuesday, March 10, 2020

Cross-species transmission

From Wikipedia, the free encyclopedia
 
Cross-species transmission (CST), also called interspecies transmission, host jump, or spillover, is the ability for a foreign virus, once introduced into an individual of a new host species, to infect that individual and spread throughout a new host population. Steps involved in the transfer of viruses to new hosts include contact between the virus and the host, infection of an initial individual leading to amplification and an outbreak, and the generation within the original or new host of viral variants that have the ability to spread efficiently between individuals in populations of the new host Often seen in emerging viruses where one species transfers to another, which in turn transfers to humans. Examples include HIV-AIDS, SARS, ebola, swine flu, rabies, and avian influenza. Bacterial pathogens can also be associated with CST.

The exact mechanism that facilitates transfer is unknown, however, it is believed that viruses with a rapid mutation rate are able to overcome host-specific immunological defenses. This can occur between species that have high contact rates. It can also occur between species with low contact rates but usually through an intermediary species. Bats, for example, are mammals and can directly transfer rabies to humans through bite and also through aerosolization of bat saliva and urine which are then absorbed by human mucous membranes in the nose, mouth and eyes. Note: the document used as a reference does not use the words urine or saliva so this citation is questionable. A host shifting event is defined as a strain that was previously zoonotic and now circulates exclusively among humans.

Similarity between species, for example, transfer between mammals, is believed to be facilitated by similar immunological defenses. Other factors include geographic area, intraspecies behaviours, and phylogenetic relatedness. Virus emergence relies on two factors: initial infection and sustained transmission.

Prevalence

Cross-species transmission is the most significant cause of disease emergence in humans and other species. Wildlife zoonotic diseases of microbial origin are also the most common group of human emerging diseases, and CST between wildlife and livestock has appreciable economic impacts in agriculture by reducing livestock productivity and imposing export restrictions. This makes CST of major concern for public health, agriculture, and wildlife management. 

A large proportion of viral pathogens that have emerged recently in humans are considered to have originated from various animal species. This is shown by several recent epidemics such as, avian flu, Ebola, monkey pox, and Hanta viruses. There is evidence to suggest that some diseases can potentially be re-introduced to human populations through animal hosts after they have been eradicated in humans. There is a risk of this phenomenon occurring with morbilliviruses as they can readily cross species barriers. CST can also have a significant effect on produce industries. Genotype VI-Avian paramyxovirus serotype 1 (GVI-PMV1) is a virus that arose through cross-species transmission events from Galliformes (i.e. chicken) to Columbiformes, and has become prevalent in the poultry industry. CST of rabies virus variants between many different species populations is a major wildlife management concern. Introduction of these variants into non-reservoir animals increases the risk of human exposures and threatens current advances toward rabies control.

Many pathogens are thought to have host specialization, which explains the maintenance of distinct strains in host species. Pathogens would have to overcome their host specificity to cross to a new host species. Some studies have argued that host specializations may be exaggerated, and pathogens are more likely to exhibit CST than previously thought. Original hosts usually have low death rates when infected with a pathogen, with fatality rates tending to be much higher in new hosts.

Cross-Species Transmission between Humans and Nonhuman Primates

Due to the close relation of humans and nonhuman primates (NHP), disease transmission between NHP and humans is relatively common and can become a major public health concern. Diseases, such as HIV and human adenoviruses have been associated with NHP interactions. In places where contact between humans and NHPs is frequent, precautions are often taken to prevent disease transmission. Simian foamy viruses (SFV) is an enzootic retrovirus that has high rates of cross-species transmission and has been known to affect humans bitten by infected NHPs. It has caused health concerns in places like Indonesia where visitors at monkey temples can contract SFV from temple macaques (Macaca fascicularis). TMAdV (titi monkey adenovirus) is a highly divergent, sharing <57 a="" href="https://en.wikipedia.org/wiki/Pairwise_comparison" title="Pairwise comparison">pairwise
nucleotide identity with other adenoviruses, NHP virus that had a high fatality rate (83%) in monkeys and is capable of spreading through human hosts.

Predicting and Preventing Transmission between Species

Prediction and monitoring are important for the study of CSTs and their effects. However, factors that determine the origin and fate of cross-species transmission events remain unclear for the majority of human pathogens. This has resulted in the use of different statistical models for the analyzation of CST. Some of these include risk-analysis models, single rate dated tip (SRDT) models, and phylogenetic diffusion models. The study of the genomes of pathogens involved in CST events is very useful in determining their origin and fate. This is because a pathogens genetic diversity and mutation rate are key factors in determining if it is able to transmit across multiple hosts. This makes it important for the genomes of transmission species to be partially or completely sequenced. A change in genomic structure could cause a pathogen that has narrow host range to become capable of exploiting a wider host range. Genetic distance between different species, geographical range, and other interaction barriers will also influence cross-species transmission.

One approach to risk assessment analysis of CST is to develop risk-analysis models that break the ‘‘process’’ of disease transmission into component parts. Processes and interactions that could lead to cross-species disease transmission are explicitly described as a hypothetical infection chain. Data from laboratory and field experiments is used to estimate the probability of each component, expected natural variation, and margins of error.

Different types of CST research would require different analysis pathways to meet their needs. A study on identification of viruses in bats that could spread to other mammals used the workflow: sequencing of genomic samples → “cleaning” of raw reads → elimination of host reads and eukaryotic contaminants → de novo assembly of the remaining reads → annotation of viral contigs → molecular detection of specific viruses → phylogenetic analysis → interpretation of data.

Detecting CST and estimating its rate based on prevalence data is challenging. Due to these difficulties computational methods are used to analyse CST events and the pathogens associated with them. The explosive development of molecular techniques has opened new possibilities for using phylogenetic analysis of pathogen genetics to infer epidemiological parameters. This provides some insight into the origins of these events and how they could be addressed. Methods of CST prevention are currently using both biological and computational data. An example of this is using both cellular assays and phylogenetic comparisons to support a role for TRIM5α, the product of the TRIM5 gene, in suppressing interspecies transmission and emergence of retroviruses in nature.

Cross-Species Transmission Analyzation

Phylogeny

The comparison of genomic data is very important for the study of cross-species transmission. Phylogenetic analysis is used to compare genetic variation in both pathogens associated with CST and the host species that they infect. Taken together, it is possible to infer what allowed a pathogen to crossover to a new host (i.e. mutation in a pathogen, change in host susceptibility) and how this can be prevented in the future. If the mechanisms a pathogens uses to initially enter a new species are well characterized and understood a certain level of risk control and prevention can be obtained. In contact, a poor understanding of pathogens, and their associated diseases, makes it harder for preventive measures to be taken.

Alternative hosts can also potentially have a critical role in the evolution and diffusion of a pathogen. When a pathogen crosses species it often acquires new characteristics that allow it to breach host barriers. Different pathogen variants can have very different effects on host species. Thus it can be beneficial to CST analysis to compare the same pathogens occurring in different host species. Phylogenetic analysis can be used to track a pathogens history through different species populations. Even if a pathogen is new and highly divergent, phylogenetic comparison can be very insightful. A useful strategy for investigating the history of epidemics caused by pathogen transmission combines molecular clock analysis, to estimate the timescale of the epidemic, and coalescent theory, to infer the demographic history of the pathogen. When constructing phylogenies, computer databases and tools are often used. Programs, such as BLAST, are used to annotate pathogen sequences, while databases like GenBank provide information about functions based on the pathogens genomic structure. Trees are constructed using computational methods such as MPR or Bayesian Inference, and models are created depending on the needs of the study. Single rate dated tip (SRDT) models, for example, allows for estimates of timescale under a phylogenetic tree. Models for CST prediction will vary depending on what parameters need to be accounted for when constructing the model.

Most Parsimonious Reconstruction (MPR)

Parsimony is the principle in which one chooses the simplest scientific explanation that fits the evidence. In terms of building phylogenetic trees, the best hypothesis is the one that requires the fewest evolutionary changes. Using parsimony to reconstruct ancestral character states on a phylogenetic tree is a method for testing ecological and evolutionary hypotheses. This method can be used in CST studies to estimate the number of character changes that exist between pathogens in relation to their host. This makes MPR useful for tracking a CST pathogen to its origins. MPR can also be used to the compare traits of host species populations. Traits and behaviours within a population could make them more susceptible to CST. For example, species which migrate regionally are important for spreading viruses through population networks.

Despite the success of parsimony reconstructions, research suggests they are often sensitive and can sometimes be prone to bias in complex models. This can cause problems for CST models that have to consider many variables. Alternatives methods, such as maximum likelihood, have been developed as an alternative to parsimony reconstruction.

Using Genetic Markers

Two methods of measuring genetic variation, variable number tandem repeats (VNTRs) and single nucleotide polymorphisms (SNPs), have been very beneficial to the study of bacterial transmission. VNTRs, due to the low cost and high mutation rates, make them particularly useful to detect genetic differences in recent outbreaks, and while SNPs have a lower mutation rate per locus than VNTRs, they deliver more stable and reliable genetic relationships between isolates. Both methods are used to construct phylogenies for genetic analysis, however, SNPs are more suitable for studies on phylogenies contraction. However, it can be difficult for these methods accurately simulate CSTs everts. Estimates of CST based on phylogenys made using VNTR marker can be biased towards detecting CST events across a wide range of the parameters. SNPs tend to be less biased and variable in estimates of CST when estimations of CST rates are low and low number of SNPs is used. In general, CST rate estimates using these methods are most reliable in systems with more mutations, more markers, and high genetic differences between introduced strains. CST is very complex and models need to account for a lot of parameters to accurately represent the phenomena. Models that oversimplify reality can result in biased data. Multiple parameters such as number of mutations accumulated since introduction, stochasticity, the genetic difference of strains introduced, and the sampling effort can make unbiased estimates of CST difficult even with whole-genome sequences, especially if sampling is limited, mutation rates are low, or if pathogens were recently introduced. More information on the factors that influence CST rates is needed for the contraction of more appropriate models to study these events.

The process of using genetic markers to estimate CST rates should take into account several important factors to reduce bias. One, is that the phylogenetic tree constructed in the analysis needs to capture the underlying epidemiological process generating the tree. The models need to account for how the genetic variability of a pathogen influences a disease in a species, not just general differences in genomic structure. Two, the strength of the analysis will depend on the amount of mutation accumulated since the pathogen was introduced in the system. This is due to many models using amount of mutations as an indicator of CST frequency. Therefore, efforts are focused on estimating either time since introduction or the substitution rate of the marker (from laboratory experiments or genomic comparative analysis). This is important not only when using the MPR method but also for Likelihood approaches that require an estimation of the mutation rate. Three, CST will also affect disease prevalence in the potential host, so combining both epidemiological time series data with genetic data may be an excellent approach to CST study

Bayesian Analysis

Bayesian frameworks are a form of maximum likelihood-based analyses and can be very effective in cross-species transmission studies. Bayesian inference of character evolution methods can account for phylogenetic tree uncertainty and more complex scenarios, with models such as the character diffusion model currently being developed for the study of CST in RNA viruses. A Bayesian statistical approach presents advantages over other analyses for tracking CST origins. Computational techniques allow integration over an unknown phylogeny, which cannot be directly observed, and unknown migration process, which is usually poorly understood.

The Bayesian frameworks are also wellsuited to bring together different kinds of information. The BEAST software, which has a strong focus on calibrated phylogenies and genealogies, illustrates this by offering a large number of complementary evolutionary models including substitution models, demographic and relaxed clock models that can be combined into a full probabilistic model. By adding spatial reconstruction, these models create the probability of biogeographical history reconstruction from genetic data. This could be useful for determining origins of cross-species transmissions. The high effectiveness of Bayesian statistical methods has made them instrumental in evolutionary studies. Bayesian ancestral host reconstruction under discrete diffusion models can be used to infer the origin and effects of pathogens associated with CST. One study on Human adenoviruses using Bayesian supported a gorilla and chimpanzee origin for the viral species, aiding prevention efforts. Despite presumably rare direct contact between sympatric populations of the two species, CST events can occur between them. The study also determined that two independent HAdV-B transmission events to humans occurred and that the HAdV-Bs circulating in humans are of zoonotic origin and have probably affected global health for most of our species lifetime.

Phylogenetic diffusion models are frequently used for phylogeographic analyses, with the inference of host jumping becoming of increasing interest. The Bayesian inference approach enables model averaging over a number of potential diffusion predictors and estimates the support and contribution of each predictor while marginalizing over phylogenetic history. For studying viral CST, the flexibility of the Bayesian statistical framework allows for the reconstruction of virus transmission between different host species while simultaneously testing and quantifying the contribution of multiple ecological and evolutionary influences of both CST spillover and host shifting. One study on rabies in bats showed geographical range overlap is a modest predictor for CST, but not for host shifts.[3] This highlights how Bayesian inferences in models can be used for CST analysis.
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Virome

From Wikipedia, the free encyclopedia
https://en.wikipedia.org/wiki/Virome

Virome refers to the collection of nucleic acids, both RNA and DNA, that make up the viral community associated with a particular ecosystem or holobiont. The word is derived from virus and genome and first used by Forest Rohwer and colleagues to describe viral shotgun metagenomes. All macro-organisms have viromes that include bacteriophage and viruses. Viromes are important in the nutrient and energy cycling, development of immunity, and a major source of genes through lysogenic conversion.

History

Viromes were the first examples of shotgun community sequence, which is now known as metagenomics. In the 2000s, the Rohwer lab sequenced viromes from seawater, marine sediments, adult human stool, infant human stool, soil, and blood. This group also performed the first RNA virome with collaborators from the Genomic Institute of Singapore. From these early works, it was concluded that most of the genomic diversity is contained in the global virome and that most of this diversity remains uncharacterized. This view was supported by individual genomic sequencing project, particularly the mycobacterium phage.

Methods of study

In order to study the virome, virus-like particles are separated from cellular components, usually using a combination of filtration, density centrifugation, and enzymatic treatments to get rid of free nucleic acids. The nucleic acids are then sequenced and analyzed using metagenomic methods. Alternatively, there are recent computational methods that use directly metagenomic assembled sequences to discover viruses.

The Global Ocean Viromes (GOV) is a dataset consisting of deep sequencing from over 150 samples collected across the world's oceans in two survey periods by an international team.

Virus hosts

We can determine the metagenome host from prophage identity sequence.

Viruses are the most abundant biological entities on Earth, but challenges in detecting, isolating, and classifying unknown viruses have prevented exhaustive surveys of the global virome. Over 5 Tb of metagenomic sequence data were used from 3,042 geographically diverse samples to assess the global distribution, phylogenetic diversity, and host specificity of viruses.

Proportion of 18,470 viral connected with predicted hosts at various taxonomic levels.

In August 2016, over 125,000 partial DNA viral genomes, including the largest phage yet identified, increased the number of known viral genes by 16-fold. A suite of computational methods was used to identify putative host virus connections. The isolate viral host information was projected onto a group, resulting in host assignments for 2.4% of viral groups.

Then the CRISPR–Cas prokaryotic immune system which holds a "library" of genome fragments from phages (proto-spacers) that have previously infected the host. Spacers from isolate microbial genomes with matches to metagenomic viral contigs (mVCs) were identified for 4.4% of the viral groups and 1.7% of singletons. The hypothesis was explored that viral transfer RNA (tRNA) genes originate from their host.

Viral tRNAs identified in 7.6% of the mVCs were matched to isolate genomes from a single species or genus. The specificity of tRNA-based host viral assignment was confirmed by CRISPR–Cas spacer matches showing a 94% agreement at the genus level. These approaches identified 9,992 putative host–virus associations enabling host assignment to 7.7% of mVCs. The majority of these connections were previously unknown, and include hosts from 16 prokaryotic phyla for which no viruses have previously been identified.

Three proto-spacers encoded on mVCs identified in human oral metagenomic samples that were linked to CRISPR spacers from hosts from distinct phyla, Actinomycetes sp. oral taxon 180 (Actinobacteria) and Streptococcus plurextorum DSM 22810 (Firmicutes).
 
Many viruses specialize in infecting related hosts. Viral generalists that infect hosts across taxonomic orders may exist. Most CRISPR spacer matches were from viral sequences to hosts within one species or genus. Some mVCs were linked to multiple hosts from higher taxa. A viral group composed of macs from human oral samples contained three distinct photo-spacers with nearly exact matches to spacers in Actionbacteria and Firmicutes.

In January 2017, the IMG/VR system -- the largest interactive public virus database contained 265,000 metagenomic viral sequences and isolate viruses. This number scaled up to over 760,000 in November 2018 (IMG/VR v.2.0). The IMG/VR systems serve as a starting point for the sequence analysis of viral fragments derived from metagenomic samples.
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