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It seems like when we observe animals in the wild, the occurrence of noticeable disease in adult individuals is much lower than in humans. Why?
There are a number of reasons that this could happen, but I want to know which reasons contribute the most, or what other reasons I haven't thought of could be involved. So, here's my list of theories:
1) Animals that are prone to disease usually die when very young, while humans in developed countries are given vaccinations/medical attention and have a much greater chance to live to adulthood and advanced age. However, even taking this into consideration, it seems like human populations in third-world countries with little or no access to medicine are much, much more riddled with disease than animal populations appear to be. (Or do they only look that way because that's what we see the most of in the news?)
2) The animals that we see in documentaries are generally purposely selected for viewing as being healthy individuals or a mostly healthy group. This doesn't account for YouTube's many amateur safari videos and pictures, however, where it still seems like animals die much more from territorial disputes or preying than of disease. Safari-goers aren't likely to sit around filming diseased animals, but it still seems like animals 'in the background' and in herds appear to generally be very healthy when it'd be pretty easy to notice a somehow diseased or disabled person in an equivalently large group on the sidewalk.
3) Most humans don't know what common wildlife diseases look or sound like, and at a distance they all appear healthy to us even if there is a roughly equivalent percentage of disease among adult animals as among adult humans.
3a) Animals are much better at concealing the symptoms of their common diseases than the average human, as a defense mechanism from predators. (I know that cats are particularly good at not showing that they're in pain, but I'm not sure how many other animals behave this way.)
4) While most modern humans go out of their way to do every possible thing they can to make sure an infant survives, animal parents purposely kill, abandon or even eat young that they can sense are diseased or disabled in some way. I saw an example of this on a youtube video where a lion cub was gored by a cape buffalo and its back legs were paralyzed. After numerous failed attempts to nudge the cub into standing or walking properly, the mother purposely killed the cub with a suffocating bite and ate it. (Did/do humans practice this to any significant extent? I once read about a culture, can't remember which, that didn't consider an infant viable enough to even name until it was at least 3 months old. I also read that either the ancient Greeks or the Romans would bathe a newborn in wine, and if it survived, it was deemed strong enough to deserve a chance at life. I don't know how true either of these claims are, though. But that's kind of a different question, so consider it optional 'bonus points' to answer.)
5) Diseased and disabled animals are killed off by predators or rivals quickly enough that the populations we see are filled with healthy animals just because the infirm are constantly weeded out. This doesn't address animals that have few/no natural predators or rivals, such as in the case of areas that have so many deer with no natural predators that human hunters must cull them to keep them from reproducing out of control. Are these populations more prone to adulthood diseases than populations that have natural predators?
6) At about seven billion, humans are easily the most populous species that is the size of humans. Other animals with larger populations are much smaller than humans. Compared to other animals of our size or larger, we are intensely overcrowded, leading to lots of people coming in contact with lots of other people all the time, frequently on an international scale as thousands of planes and ships travel around the world on a daily basis. This only covers contagious diseases, though. Even the most isolated hermit could die from a genetic condition that he had since before he was born.
7) Stress. Animals live what we would consider to be a very high-stress life, but they experience their stress in short, intense bursts. Humans, even (especially!) those who live in first-world countries with lots of information to learn and lots of things to do, often get to the point where they can't figure out where the 'off' switch for their stress is. Stress is a silent, gradual killer, and it's possible that minor genetic conditions that may have otherwise been fairly benign or unnoticed turn ugly as a person ages through a life where stress is constant.
8) Diet. It's no secret that there's a lot of heart disease and other diet-related issues in the modern world, but I don't know if that covers ancient humans, and there seems to have been plenty of disease to go around in the olden days even when people ate purely natural foods.
I can't think of any other theories at the moment. One way I thought of to possibly help answer this question was to take into consideration domestic animals - how many diseases do veterinarians have to treat compared to how many diseases human doctors have to treat? This line of thought is rather tainted by the fact that domestic animals are often given vaccinations of their own, though, but it doesn't seem like they receive nearly as many as humans do.
This is my first time asking a question on stackexchange, so I hope I've given you plenty of meat to chew on with this post. I look forward to the replies!
Many examples of animals which have more difficulty maintaining their population size than humans exist. This is partially why some species go extinct. The Tasmanian Devil is at high risk for extinction from a genetic predisposition for cancer onset by infection. Your premise that humans are unhealthy is not sound. Humans are long lived, genetically diverse animals which reproduce exceptionally. We are among the most successful species.
Why Do Gay Men Have an Increased Risk of HIV?
Latesha Elopre, MD, is a board-certified internist specializing in HIV. She is an assistant professor of infectious diseases at the University of Alabama at Birmingham.
In the United States, gay men are at a disproportionately high risk of getting HIV and AIDS. In 2016, 68% of all HIV infections in the U.S. affected men who have sex with men. The risk is even higher for gay black men. Why are gay men more likely to get HIV?
There are several reasons why gay and bisexual men are at higher risk of HIV than their straight counterparts. Some of the reasons are based on certain types of sex that result in greater risk of infection due to how HIV is biologically transmitted. Other reasons reflect social realities about how men who have sex with men (MSM) live in the world and are treated by society.
Why Animal-Borne Diseases Matter
Diseases passed to humans from animals are called zoonoses. What makes one of these diseases important? Two things, says zoonosis expert Lawrence T. Glickman, VMD, DrPH, professor of veterinary epidemiology and environmental health at Purdue University School of Veterinary Medicine, West Lafayette, Ind.
"If you ask Americans in general what is the most important zoonosis, most would say rabies," Glickman tells WebMD. "It is something they fear, it is in the news. But in terms of risk, there are only zero to two human cases a year in the U.S. It's one of those zoonoses that are important because of their seriousness, but not their frequency: rabies, tularemia, plague, monkeypox, listeria, anthrax. These are diseases that are very serious if one gets them but which are relatively uncommon."
On the flip side, Glickman notes, are animal-borne diseases that are important because they are fairly common even if not often fatal. Cat-scratch fever, for example, infects as many as 20,000 Americans a year. And an estimated 4%-20% of U.S. kids get roundworm from dogs and cats.
"Even these diseases can be quite serious," Glickman says. Here's a roundup of a few important zoonoses:
Watching the “epigenetic clock”
But it’s not just the genes themselves that suffer as animals age — so does their pattern of activation. An important way that cells turn genes on and off at the right time and place is by attaching chemical tags called methyl groups to sites that control gene activity. But these tags — also known as epigenetic marks — tend to get more random over time, leading gene activity to become less precise. In fact, geneticist Steve Horvath of UCLA and his colleagues have found that by assessing the status of a set of almost 800 methylation sites scattered around the genome, they can reliably estimate an individual’s age relative to the maximum lifespan of its species. This “epigenetic clock” holds for all the 192 species of mammals that Horvath’s team has looked at so far.
Notably, the epigenetic marks of longer-lived mammals take longer to degrade, which presumably means that their genes maintain youthful activity longer. In bats, for example, the longest-lived bats often have the slowest rate of change in methylations, while shorter-lived species change more quickly (see diagram).
Species of bats that do a better job of regulating the activity of their genes also tend to live longer lives. For 26 bat species of varying longevity, researchers compared DNA methylation rate—an indicator of how quickly the animals’ gene activity becomes perturbed—to their longevity quotient, which indicates how long each species lives relative to a typical mammal of its body size. (G.S. Wilkinson et al. / Nature Communications 2021)
As he digs deeper, Horvath is finding that certain methylation sites may predict a species’ lifespan regardless of the age at which he samples them. “To me, this is a miracle,” he says. “Let’s say you go into the jungle and find a new species — could be a new bat or any other mammal. I can tell you pretty accurately the maximum lifespan of the species.” The methylation clues also predict maximum lifespan for dog breeds, which may emerge as an important study organism for aging (see sidebar: “What Rover knows”). These lifespan-related methylations tend to be associated with genes related to development, Horvath finds, though more detailed connections have yet to be worked out. He hopes that this work, which is not yet published, can eventually point the researchers toward genes that are key for regulating lifespan and aging.
Improvements in molecular techniques are already giving researchers more powerful tools to tease out the ways in which extraordinarily long-lived organisms may differ from the ordinary. One promising technique involves sequencing not the DNA in cells, but the messenger RNA. Individual genes are copied into mRNA as the first step in producing proteins, so mRNA sequencing reveals which genes in the genome are active at any given moment. This profile — referred to as the transcriptome — gives a more dynamic view of a cell’s activity than just listing the genes in the genome.
Gladyshev’s team, for example, sequenced the transcriptomes of cells from the liver, kidney and brain of 33 species of mammals, then looked for patterns that correlated with lifespan. They found plenty, including differences in activity levels of many genes involved in cellular maintenance functions such as DNA repair, antioxidant defense and detoxification.
Black Americans and Diabetes
Black Americans -- and Mexican-Americans -- have twice the risk of diabetes as white Americans. In addition, blacks with diabetes have more serious complications -- such as loss of vision, loss of limbs, and kidney failure -- than whites, notes Maudene Nelson, RD, certified diabetes educator at Naomi Barry Diabetes Center at Columbia University.
"The theory is that maybe it is access to health care, or maybe a cultural fatalism -- thinking, 'It is God's will,' or, 'My family had it so I have it' -- not a sense of something I can have an impact on so it won't hurt me," Nelson tells WebMD. "But more and more there is thinking it is something that makes blacks genetically more susceptible. It is hard to tell how much of it is what."
Database and Conclusions
Database. Supplementary Table S1 lists 10 characteristics for each of 25 important ‘temperate’ (15) and ‘tropical’ (10) diseases (see Supplementary Note S3 for details of this distinction). Our aim was to select well-defined diseases causing the highest mortality and/or morbidity and hence of the highest historical and evolutionary significance (see Supplementary Note S1 for details of our selection criteria). Of the 25 diseases, we selected 17 because they are the ones assessed by Lopez et al. (2005) as imposing the heaviest world burdens today (they have the highest disability-adjusted life years (DALY) scores). Of the 17 diseases, 8 are temperate (hepatitis B, influenza A, measles, pertussis, rotavirus A, syphilis, tetanus and tuberculosis), and 9 are tropical (acquired immune deficiency syndrome (AIDS), Chagas' disease, cholera, dengue haemorrhagic fever, East and West African sleeping sicknesses, falciparum and vivax malarias, and visceral leishmaniasis).
We selected eight others (temperate diphtheria, mumps, plague, rubella, smallpox, typhoid and typhus, plus tropical yellow fever) because they imposed heavy burdens in the past, although modern medicine and public health have either eradicated them (smallpox) or reduced their burden. Except for AIDS, dengue fever, and cholera, which have spread and attained global impact in modern times, most of these 25 diseases have been important for more than two centuries.
Are our conclusions robust to variations in these selection criteria? For about a dozen diseases with the highest modern or historical burdens (for example, AIDS, malaria, plague, smallpox), there can be little doubt that they must be included, but one could debate some of the next choices. Hence we drew up three alternative sets of diseases sharing a first list of 16 indisputable major diseases but differing in the next choices, and we performed all 10 analyses described below on all three sets. It turned out that, with one minor exception, the three sets yielded qualitatively the same conclusions for all 10 analyses, although differing in their levels of statistical significance (see Supplementary Note S4). Thus, our conclusions do seem to be robust.
Temperate/tropical differences. Comparisons of these temperate and tropical diseases yield the following conclusions:
Most (10/15) of the temperate diseases, but none of the tropical diseases (P < 0.005), are so-called 𠆌rowd epidemic diseases’ (asterisked in Supplementary Table S1), defined as ones occurring locally as a brief epidemic and capable of persisting regionally only in large human populations. This difference is an immediate consequence of the differences enumerated in the preceding five paragraphs. If a disease is acute, efficiently transmitted, and quickly leaves its victim either dead or else recovering and immune to re-infection, the epidemic soon exhausts the local pool of susceptible potential victims. If in addition the disease is confined to humans and lacks significant animal and environmental reservoirs, depletion of the local pool of potential victims in a small, sparse human population results in local termination of the epidemic. If, however, the human population is large and dense, the disease can persist by spreading to infect people in adjacent areas, and then returning to the original area in a later year, when births and growth have regenerated a new crop of previously unexposed non-immune potential victims. Empirical epidemiological studies of disease persistence or disappearance in isolated human populations of various sizes have yielded estimates of the population required to sustain a crowd disease: at least several hundred thousand people in the cases of measles, rubella and pertussis (Anderson and May, 1991 Dobson and Carper, 1996). But human populations of that size did not exist anywhere in the world until the steep rise in human numbers that began around 11,000 years ago with the development of agriculture (Bellwood, 2005 Diamond, 1997). Hence the crowd epidemic diseases of the temperate zones must have evolved since then.
Of course, this does not mean that human hunter/gatherer communities lacked infectious diseases. Instead, like the sparse populations of our primate relatives, they suffered from infectious diseases with characteristics permitting them to persist in small populations, unlike crowd epidemic diseases. Those characteristics include: occurrence in animal reservoirs as well as in humans (such as yellow fever) incomplete and/or non-lasting immunity, enabling recovered patients to remain in the pool of potential victims (such as malaria) and a slow or chronic course, enabling individual patients to continue to infect new victims over years, rather than for just a week or two (such as Chagas' disease).
Pathogen origins. (See details for each disease in Supplementary Note S10). Current information suggests that 8 of the 15 temperate diseases probably or possibly reached humans from domestic animals (diphtheria, influenza A, measles, mumps, pertussis, rotavirus, smallpox, tuberculosis) three more probably reached us from apes (hepatitis B) or rodents (plague, typhus) and the other four (rubella, syphilis, tetanus, typhoid) came from still-unknown sources (see Supplementary Note S6). Thus, the rise of agriculture starting 11,000 years ago played multiple roles in the evolution of animal pathogens into human pathogens (Diamond, 1997 Diamond, 2002 McNeill, 1976). Those roles included both generation of the large human populations necessary for the evolution and persistence of human crowd diseases, and generation of large populations of domestic animals, with which farmers came into much closer and more frequent contact than hunter/gatherers had with wild animals. Moreover, as illustrated by influenza A, these domestic animal herds served as efficient conduits for pathogen transfers from wild animals to humans, and in the process may have evolved specialized crowd diseases of their own.
It is interesting that fewer tropical than temperate pathogens originated from domestic animals: not more than three of the ten tropical diseases of Supplementary Table S1, and possibly none (see Supplementary Note S7). Why do temperate and tropical human diseases differ so markedly in their animal origins? Many (4/10) tropical diseases (AIDS, dengue fever, vivax malaria, yellow fever) but only 1/15 temperate diseases (hepatitis B) have wild non-human primate origins (P < 0.04). This is because although non-human primates are the animals most closely related to humans and hence pose the weakest species barriers to pathogen transfer, the vast majority of primate species is tropical rather than temperate. Conversely, few tropical but many temperate diseases arose from domestic animals, and this is because domestic animals live mainly in the temperate zones, and their concentration there was formerly even more lop-sided (see Supplementary Note S8).
A final noteworthy point about animal-derived human pathogens is that virtually all arose from pathogens of other warm-blooded vertebrates, primarily mammals plus in two cases (influenza A and ultimately falciparum malaria) birds. This comes as no surprise, considering the species barrier to pathogen transfer posed by phylogenetic distance (Box A16-2). An expression of this barrier is that primates constitute only 0.5% of all vertebrate species but have contributed about 20% of our major human diseases. Expressed in another way, the number of major human diseases contributed, divided by the number of animal species in the taxonomic group contributing those diseases, is approximately 0.2 for apes, 0.017 for non-human primates other than apes, 0.003 for mammals other than primates, 0.00006 for vertebrates other than mammals, and either 0 or else 0.000003 (if cholera really came from aquatic invertebrates) for animals other than vertebrates (see Supplementary Note S9).
Geographic origins. To an overwhelming degree, the 25 major human pathogens analysed here originated in the Old World. That proved to be of great historical importance, because it facilitated the European conquest of the New World (the Americas). Far more Native Americans resisting European colonists died of newly introduced Old World diseases than of sword and bullet wounds. Those invisible agents of New World conquest were Old World microbes to which Europeans had both some acquired immunity based on individual exposure and some genetic resistance based on population exposure over time, but to which previously unexposed Native American populations had no immunity or resistance (Crosby, 1986 Diamond, 1997 McNeill, 1976 Ramenofsky, 1987). In contrast, no comparably devastating diseases awaited Europeans in the New World, which proved to be a relatively healthy environment for Europeans until yellow fever and malaria of Old World origins arrived (McNeill, 2006).
Why was pathogen exchange between Old and New Worlds so unequal? Of the 25 major human diseases analysed, Chagas' disease is the only one that clearly originated in the New World. For two others, syphilis and tuberculosis, the debate is unresolved: it remains uncertain in which hemisphere syphilis originated, and whether tuberculosis originated independently in both hemispheres or was brought to the Americas by Europeans. Nothing is known about the geographic origins of rotavirus, rubella, tetanus and typhus. For all of the other 18 major pathogens, Old World origins are certain or probable.
Our preceding discussion of the animal origins of human pathogens may help explain this asymmetry. More temperate diseases arose in the Old World than New World because far more animals that could furnish ancestral pathogens were domesticated in the Old World. Of the world's 14 major species of domestic mammalian livestock, 13, including the five most abundant species with which we come into closest contact (cow, sheep, goat, pig and horse), originated in the Old World (Diamond, 1997). The sole livestock species domesticated in the New World was the llama, but it is not known to have infected us with any pathogens (Diamond, 1997 Dobson, 1996)—perhaps because its traditional geographic range was confined to the Andes, it was not milked or ridden or hitched to ploughs, and it was not cuddled or kept indoors (as are some calves, lambs and piglets). Among the reasons why far more tropical diseases (nine versus one) arose in the Old World than the New World are that the genetic distance between humans and New World monkeys is almost double that between humans and Old World monkeys, and is many times that between humans and Old World apes and that much more evolutionary time was available for transfers from animals to humans in the Old World (about 5 million years) than in the New World (about 14,000 years).
Definitions of EID vary, including: a disease which incidence in humans has been increasing a disease which has a tendency to spread geographically, cause an increased incidence, or infect a new species or new populations or, a disease spreading within any host population (24). Pathogens may also be considered emerging, for example, antimicrobial resistant bacteria. These definitions can be similarly applied to wildlife and plant diseases (27, 28), in both terrestrial and marine ecosystems (29). There can also be an apparent emergence of newly discovered or previously underdiagnosed diseases (24, 26, 30).
Taylor et al. (31) found that viruses and protozoa had the highest proportions of emerging pathogens. Zoonotic pathogens were found twice as likely to be emerging as non-zoonotic, but this was only seen in some taxa (bacteria and fungi). The host jump occurring in zoonotic infection can either cause an establishment of the pathogen in the new population with subsequent spread, or there may be recurrent events of transmission from a reservoir to the new host, after which no further transmission occurs, or there is a limited small outbreak (32). The dominance of zoonotic infections among emerging health threats has also been demonstrated among recent events of public health importance in the Americas, where 70% of the events were caused by zoonotic agents (33).
Some areas of the world, ‘hot spots’, have a tendency to have more events of EID (20, 34). These often have a rapid intensification of agricultural systems, especially of livestock keeping, and increasing interactions between animals, humans, and ecosystems, often caused by rapidly changing habits and practices within societies (18, 35). Equally important from a public health point of view may be the 𠆌old spots’, neglected locations where public health measurements are non-effective and diseases which are controlled elsewhere still flourish (18) and may constitute a disease reservoir for future re-emergence.
Especially small-scale or backyard farmers may be disproportionally affected by the negative impacts of EID (36). Emerging diseases, such as highly pathogenic avian influenza, can lead to industry decline or restructuring with negative effects on small-scale producers and value chain actors (37).
McMichael (38) proposed five categories of promoters for emerging infections: land use and environmental changes demographic changes host conditions human consumption behaviour and other behaviours such as social and cultural interaction, sexual habits, and drug use. Apart from these, factors within the pathogen, such as the capacity to evolve through mutations, are important for disease emergence (39).
The EID that have received most publicity during the last decades have been viruses. Notable examples have been HIV, SARS, and Ebola. It is estimated that 44% of the diseases considered emerging in humans are viral (31).
RNA viruses are prone to emergence because of their rapid replication and high mutation rates, with around one misreading per replication, and large viral populations (40, 41). However, the increased evolutionary pressure of having to adapt to both invertebrate and vertebrate hosts creates a lower rate of mutation in vector-borne viruses, and most of their mutations are synonymous (42).
Apart from point mutations, viruses can evolve through recombination events, especially among segmented viruses. The reassortment that occurs in influenza viruses is one example of this whereby influenza viruses create new combinations of genes. Single-stranded viruses may also recombine when different viral strains circulate in the same area, and occasionally infect the same cell, as in the example of Japanese encephalitis virus (43, 44). However, in spite of the increased tendency for recombinations among segmented viruses, single-stranded RNA viruses seem to be overrepresented among emerging pathogens (32).
Bacteria and rickettsia constitute 38% of human pathogens, and 30% of the emerging pathogens in humans (31). Because of public health breakdown or complacency, many bacterial diseases have been re-emerging, such as cholera and plague in India (45). One of the most alarming phenomena in bacteria is the spread of antibiotic resistance. Although bacteria have a continuous evolution with mutations, they also have means of spreading their genetic material laterally between species through interchange of plasmids or integrons (46). This capacity to share genetic material is not a phenomenon restricted to antibiotic resistance but an efficient way of handling different adverse environmental circumstances in nature as well (49, 50). In the same manner, lateral transfer may occur of virulence genes (48), and integration of toxin gene elements from phages seems to commonly occur in Escherichia coli, although the toxins are not always expressed to the same amount (26).
Most studies seem to show that the acquisition of antimicrobial resistance genes in bacteria do cause a comparative disadvantage compared with non-resistant bacteria in the absence of antibiotics, but studies of some genes have shown no difference, or even the opposite. A longer evolution together with a resistance gene may lower the costs for the bacteria (51).
Fungal infections are emerging not only among plants, where they have long been an important cause of losses, but also among fishes, corals, amphibians, bats, and humans (52). In fact, fungal infections are contributing to the majority of extinction events that are known to have been caused by infectious diseases (52, 53). This may be because fungi may effectively infect 100% of a population, before it is killed by the high mortality. Many fungi further have the possibility to persist as free-living spores (52).
In addition to the fungi that directly infect humans and animals, fungi that produce toxins can cause disease indirectly. Fumonisins and aflatoxins are toxins produced by different moulds, mainly Fusarium and Aspergillus species, and the growth of these fungi is promoted by climatic circumstances and bad storage conditions (54, 55). The toxins have severe health impacts on humans and animals, and the costs of diseases and of the condemned crops are high (56, 57). Climate changes are likely to affect the impact further (58).
Even though part of the increased reports of parasitic disease may be due to previous underreporting, the incidence does seem to be increasing. Large parts of the industrialized countries have managed to reduce the burden of many parasites, whereas in many countries multiple chronic infections are common (59). Most helminthic infections (95%) are zoonotic, and protozoal infections in humans, both zoonotic and non-zoonotic, are likely to be emerging (31). An emerging problem in parasites is increasing resistance, which cause many drugs to be ineffective (60).
In the analysis by Taylor et al. (31) on human pathogens, the causal agent of bovine spongiform encephalopathy was the only listed prion, classified as both zoonotic and emerging. There are, however, other infections of importance among animals. Chronic wasting disease in cervids is spreading in North America and affects cervid populations, but is believed to have low zoonotic potential (61). New strains of atypical scrapie in sheep and the detection of other new transmissible spongiform encephalopathies have also caused increased concerns, both for emergence within animal populations as well as for their possible zoonotic implications (62).
Routes of transmission
Infections transmitted directly between individuals are dependent on the contact rate between susceptible and infectious people, and thus subsequently on the population density and the mixing of populations. Direct transmission of zoonotic diseases requires contact between animal hosts and humans, as in the case of rabies transmission, but transmission can also occur in the other direction. Close contact increases risk of transmission from pets or livestock to their owners, and the growing demands for exotic pets (63) with subsequent increased trade further increases risk for introduction of new pathogens. Food- and water-borne pathogens are the major contribution to the billions of annual diarrhoea cases that occur (18). Increases in food-borne transmission may be an effect of the difficulties in handling the manure from animal production safely, as this can be a source of many zoonotic pathogens (64). This is an issue both for small-scale farming where there may be no systems to handle manure at all, and in industrialized systems where the sheer amount of manure produced daily causes management problems. In addition, increasing water scarcity and water pollution in the future (65) may cause increased risks for decreased food safety.
Vector-borne diseases constitute around 23% of the infections considered emerging (20). Although arboviruses can be transmitted by a wide range of arthropods, mosquitoes are the most important from a veterinary and medical point of view and may have been parasitizing on mammalian blood for 100 million years (66). Disease from vector-borne pathogens often occurs as spillover events, as the pathogens generally circulate between reservoir hosts and the invertebrate vectors without causing apparent disease. However, many vectors are not specific in their requirements of their feeding hosts and may feed on other animals. These opportunistic, oligophilic vectors can thus transfer a pathogen from a reservoir host to animals or humans where disease occurs. Often these new incidental hosts are less capable of amplifying the pathogen and are epidemiological dead ends.
The complex nature of vector-borne transmission makes it difficult to predict how changes will affect the incidence. Temperature affects both the longevity, the incubation period within the vector, abundance, behaviour, and the reproduction cycles of the mosquito and thus warmer climates may lead both to increased transmission as well as reduced, when the lifespan of the mosquito is reduced below the time required for the virus to replicate (67). The essence is that any factors that contribute to shorter incubation periods, increased mosquito abundance, increased proportion of suitable hosts, or increased vector survival will increase the disease transmission.
The opportunistic behaviour of many vectors can cause them to change their feeding according to the host availability, and even mosquitoes with a strong preferences for humans will feed on other hosts if they are abundant enough (68). Presence of multiple species can, in theory, have both a diluting effect, where the feeding on other species decreases the proportion of vectors feeding on the target species for a disease, and an amplifying effect where the access to multiple feeding hosts cause an increased abundance of vectors (69). The dilution effect of other animals has been used in zooprophylaxis, when a species, often cattle, is used to divert mosquitoes away from another species, but this does not work if the vector abundance is increased (68).
The concept of Susceptible-Infected–Removed (SIR) has been used to model infectious diseases since it was proposed in the 1920s. The model is, however, simplified, and for more appropriate modelling it may be necessary to include a category of exposed and latently infected (70).
Generally, the spread of infectious diseases is promoted by all factors that increase the contact rate, especially between susceptible and infected individuals create more susceptible individuals and increase the time of infectiousness (71). Actions causing the opposite will thus reduce the spread. Often there are multiple steps before an action taken by humans converts into increased risk for disease, which may cause a delayed increase of incidence ( Fig. 1 ). Because the disease dynamics of SIR is essential and basic to epidemiology of humans, animals, and plants, all factors proposed by the literature are listed here according to their effect on these categories. Thus, for the purpose of this framework, the factors: 1) increasing the number of susceptible individuals, 2) increasing the risks of exposure, and 3) increasing how infectious the infected individual is, are considered factors increasing the risks for disease emergence.
Do humans have high natural miscarriage rates among animals? If so, why?
The perception I have of human birth is that compared to other animals, it's complicated and highly error-prone. This site said that 15% of pregnancies are miscarriages is this especially high in the animal kingdom? Do humans have an especially hard/volatile reproductive cycle? If so, how would that have happened evolutionarily?
As a layman, I think you need to restrict your question to comparing us to other animals (other mammals?) that have single, live births as the norm. Comparing us to, say, mice or rats isn't really useful because their strategy is completely different: have a bunch of pups, and hope that at least X% of them survive to reproduce.
See, that may be a major factor in it right there: human gestation is complicated, lengthy and costly -- add in a decade of childhood care and suddenly it's only worthwhile (evolutionarily) for pretty healthy, well-formed young to be carried to term.
As people mentioned below, primates and elephants are probably good comparisons. What about whales? If I remember correctly, their tendency for single birth is very, very high as well, and they're similarly complicated. They might not be a good comparison for the birthing process, because they're in water and probably have it much easier, but the internal gestation would seem to be similarly complicated and error prone.
"Whale miscarriage rate" doesn't return squat, though.
The fact that humans are bipedal means that the legs attach at the bottom of the pelvis whereas in four legged animals the hind legs attach more lateral to the pelvis making a wider opening.
Bipedal-ism comes with an evolutionary cost: a complicated and expensive child birth. The reason this has persisted is because by virtue of being bipedal, we freed up our hands to make and use tools which catalyzed the long evolutionary reaction that would eventually allow us to develop cognitive ability to deal with such a complicated childbirth as well as aid us in our survival in the changing environment -- making bipedal-ism a net positive in our attempts at survival.
As has been mentioned, this is why humans are born so premature compared to other mammals and even primates. If the fetus stayed inside any longer, it would grow too large and inflexible to make it through the birth canal.
TLDR: It is bipedal-ism that makes human childbirth so complicated, but the trait carries enough positives to make it persist among us.
I also hear that we are all born prematurely because of the size of our brains. This is why a lot of other animals know how to walk and do other basic things as soon as they are born, while we take an extra year or two to learn.
The prematurity is an interesting thing. I hadn't really realized that, but it makes sense, given how utterly helpless babies are compared to all other animals.
As well as freeing our ancestors' hands for tool-making, bipedalism is a more calorie-effective method of locomotion than knuckle-dragging. source
It is bipedal-ism that makes human childbirth so complicated, but the trait carries enough positives to make it persist among us.
While this may be true, that would only be associated with perinatal mortality, not miscarriages, which are generally defined, in humans, to be limited to the first 20 weeks of pregnancy. Furthermore, at least 15% of pregnancies end in miscarriage, put the perinatal mortality rate is less than 3%.
Most miscarriages occur early in the first trimester and are caused by chromosomal abnormalities.
Apparently the human miscarriage rate is higher than other species.
My wife had 5 miscarriages, we have 2 perfect kids. We started late though, in our mid 30s. It's not uncommon to have greater risk of miscarriage as a woman ages. We did a karyotype for I think 3 or 4 of those. I remember three of them. One was a Trisomy 9 defect, one was a Trisomy 16, and one was a Trisomy 18. The Trisomy 18 also had anencephaly and we figured this out early enough to term before the 12th week.
Anways, I'm wondering if it's because couples are putting off baby-making until women are older and egg divisions are more prone to defects? The younger a women is the less chance. It's not socially acceptable to get knocked up at 16.
My wife and I have been through this also and I asked our genetic counselor the same question. She said age didnt start playing a significant role until your 40s.
I also wonder if older men (thus older sperm) has any affect as well? I assume since baby-making is a two person game, it's not just the woman's eggs that are compromised with age.
It's not socially acceptable to get knocked up at 16, but puberty happens so early in girls that it would be natural for them to have babies even younger.
It is also true that the age of the man plays a significant role. While spermatozoa are constantly refreshed, the cells in the gonads that produce them are not. Genetic damage accumulates over time in them as well.
That it is not socially acceptable to start a family until later, unfortunately, is entirely unrelated to our biology. That's related entirely to the willingness of employers at the onset of the Industrial Age not being willing to pay adolescents enough for them to support a family on, and society permitting that. Parenting a child also produces substantial brain development in the parents. It is most likely that we evolved so that our brains rely on this development occurring at the beginning of adolescence while plasticity is still high. But, we're unlikely to find out if that is true or not until there is much more progress in the field of neuroscience. Until then, we live with whatever consequences our social customs produce as they diverge from the lifestyles we evolved with. They very well might be positive changes, we just don't have any objective reason to believe one way or the other since such things were never even considered in the formation of our culture.
Determining infant mortality rates may be difficult in other animals as there are lots of differences between us and them- not all animals use doctors, though domesticated ones do, some have larger litters and expect some mortality, etc. However, some animals have fairly well defined infant mortality rates. Cows, for example, are very well studied due to the dairy industry. From that we know calves that are well cared for can have a mortality rate of 3.5% or as high as 30% if not well cared for. That number is for calves from birth to reproduction age, however. At birth mortality is going to be even lower. When I worked on a farm for a few years and birthed goats, the number varied. The first year there was a disease running through the herd that caused premature births and at birth mortality was high, though still under 20%. By my third year, the mortality rate for goat kids from birth to weaning was less than 2%. I'm having a hard time finding proper documentation of this, but this website indicates typical abortion rates in goats range from 2-5%. Goats usually have 1-3 kids while cows almost always have 1 calf at a time. I think the largest difference between these rates and human rates is that almost all humans have the right to have children, while not all animals have equal rights to give birth. Domesticated animals unfit for breeding will be culled or sold off, and wild animals that are unfit for breeding will likely be removed from the breeding population because they wont survive through childbirth. I don't think our reproduction is really all that different, but we expect even those unfit for reproduction will give birth (such as those who are overweight, underweight, chronically ill, etc).
Why Are We Eating so Much More Than We Used to?
Starting in the mid 1890’s, American insurance companies began recording the heights and weights of men and women seeking life insurance. From that time to the mid-1970’s, the weights of typical American men and women remained remarkably constant. Over these 80 years, the average middle-aged woman weighed 145-150 pounds, and the average man, 165-170 pounds. But starting in the mid-1970’s our weights suddenly began to shoot up so that the average man or woman today weighs 25 pounds more. As we all participate in the American obesity epidemic, almost everyone is heavier today than their counterparts of 40 years earlier. Why?
In one sense, the answer is easy: We are heavier because we are eating more. The average number of calories per person in the American food supply was actually lower in 1965 (3100 calories) than it was in 1909 (3500), but then began to go up and is now more than 3900, an increase of 25%. The increase is the same when allowances are made for waste and spoiling, and there is a similar jump in the number of calories based on peoples’ reports of what they have eaten. So why are we eating many more calories than we used to?
Some experts say we are eating more because we are so addicted to fat and sugar that we cannot stop ourselves from eating too much when our foods our laced with these tempting, tasty ingredients. But if we look at the share of calories in our food supply from sugars, it fell during the time we were gaining weight, and the share from all fat also fell until 1997 when it started to rise again. Others blame all carbohydrates, but their percentage has not changed either.
And there was no reason we could not have been eating more forty or fifty years ago if we had wanted to. Sugar was just as sweet, and there was no lack of appealing foods and sugary creamy desserts. In fact, for those who remember, food tasted even better when it was prepared with plenty of animal fat. People could have easily afforded to buy more food, and to eat more cookies, cakes, ice cream, and drink more sugar-sweetened sodas, but they didn’t. Those with higher incomes—and even better access—weighed less, not more. Men and women would usually add some pounds between their late teens and middle age, but much less than they do now, and most people seemed to be content with their weight. There were hardly any books about dieting, and no weight loss programs, joggers, or fitness clubs.
To better understand why we are eating more today, we need to consider how our brains control our desire for food. Our appetite and weight are carefully regulated by an ancient part of the brain, the hypothalamus. This almond-sized bundle of nerve tissue makes sure that animals eat enough to maintain their body functions and activities, but not enough to get fat. (Most animals have no more than five percent of their weight in fat.) In regulating our hunger, the hypothalamus monitors the levels of the sugars, amino acids, and fatty acids in our blood which are the end products of our digestion. And it pays particular attention to fat. Not only is fat the best source of calories, but it makes up about a fifth of the cells in our bodies not counting water, and half of our brain cells. And there are two “essential” types of polyunsaturated fat in our cells, omega-3 and omega-6, that can only come from our diets.
If we compare the current American diet with our diets forty years ago, we find similar levels of sugars, amino acids, and total fats, but the amounts of the two types of omega fats have changed very dramatically. In a natural diet of grains, meat, dairy foods, fruits, and vegetables, there is a bit more omega-6 than omega-3, but today there is more than twenty-times more omega-6 than omega-3. This shift in the proportion of these different fats is by far the biggest change in our diets over the past forty years.
One reason for this shift is a three-fold increase in our consumption of processed vegetable oils made from corn and soybeans these oils are now the major source of fat in the American diet, and they are ubiquitous. They are used to make processed foods, including fried foods, fast foods, snack foods, and baked goods. Since most vegetables and grains have only a small amount of fat, there would be no way we could consume this much vegetable oil without the industrialized chemical processing of corn and soybeans.
The other reason for the remarkable change in the omega balance of our diets is the decision to increase meat production by feeding corn and soybeans to immobilized cattle, pigs, and poultry instead of letting them graze on the grass that has been their natural diet for fifty million years. While grass has much more omega-3 than omega-6, corn is almost all omega-6. An analysis of a hair from CNN’s medical correspondent in 2007 showed that 69% of the carbon atoms in his body came from corn!
To make matters worse, vegetable oils high in omega-6 interfere with our getting the omega-3 which is naturally present in food. While fish and seafood are especially rich in the active forms of omega-3, when they are fried or cooked with vegetable oils, the omega-3 they contain is no longer available to us.
But is it possible that this dramatic change in the balance between omega-3 and omega-6 fats could be making us eat more? There is good reason to think so. They are much more in balance in the western European diet, and people there weigh much less. American men and women who have high levels in their blood of the most active forms of omega-3 and low levels of active omega-6 weigh forty pounds less than those with high omega-6 and low omega-3. The average ratio of omega-6 to omega-3 in Americans is more than five to one, while in the Japanese, who have very little obesity, there is more omega-3 than omega-6. There is also another clue from an unusual form of vitamin E that is especially abundant in corn and soybean oils. The level of this odd vitamin in our blood tells how much corn and soybean oil we are eating and the higher the level, the more we weigh.
We are also learning more about how omega fats influence the appetite-regulating cells in the hypothalamus. These cells are rich in receptors for endocannabinoids, our body’s form of the ingredient in marijuana that increases appetite. Because these are made from the active form of omega-6, arachidonic acid, more omega-6 in the diet means more munchy-promoting endocannibinoids. Arachidonic acid is also the source of inflammatory types of signaling molecules called eicosanoids which are also linked to increased weights. Omega-3-based eicosanoids have the opposite effect.
The most active form of omega-3, DHA, is critically important for the growth, development, and functioning of our brain, and the hypothalamus may also be able to sense how much is in the blood. Those with higher levels of DHA in their blood tend to have lower levels of arachidonic. People are hungrier after meals high in omega-6 than meals high in omega-3, even if the total amount of fat is the same.
Ours is the only country in the world that has transformed its diet so radically. This change was actually thought to be beneficial because of the mistaken belief that increasing omega-6 would reduce the risk of heart disease. The western European diet today is much closer to the diet we had forty years ago, with 41% more animal than vegetable fat, and, not surprisingly, their weights are very similar to our weights back then. And their death rates from heart disease are also much lower than ours.
While our highly industrialized methods of food production have temporarily lowered the cost of calories in our food supply, we know that they cannot be sustained in the future. And, unfortunately, the unprecedented shift in our diets from a natural pattern that has been maintained for tens of thousands of years to a sudden and unnatural dependence on corn, soybeans, and their oils has now made us the fattest people on the planet. There is more on diet and weight in our book, Why Women Need Fat.
COVID-19 has taken over world headlines since it first emerged in December of 2019. As the disease spread into a pandemic, scientists have scrambled to learn as much about it as quickly as possible. An early bright spot in the overwhelmingly negative news about COVID-19 was that it was believed pets could not get or carry the virus. However, recently a tiger at the Bronx Zoo tested positive for COVID-19, which opened the questions: Can I infect my pet or another animal? And can an infected animal infect me?
What is a virus?
COVID-19 is the name of the disease caused by the virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A virus is any of a large group of microscopic infectious agents. Viruses are composed of genetic material, RNA or DNA, surrounded by a protein coat called a capsid. The capsid keeps the genetic material safe. Some viruses also have greasy coat called an envelope. A virus is a parasite and needs a cell to replicate. Like some animal species, viruses are grouped into families and types with other genetically related viruses. Coronaviruses are a large family of viruses that usually use cells in the respiratory tract of a human or non-human animal to replicate. They often cause mild to moderate upper-respiratory tract illnesses.
Corona means “crown” in Latin. Corona viruses are named for the spikes on their surface that look like the points on a crown. NIAID-RM
What is zoonotic disease transmission?
The virus causing COVID-19 was passed to humans through zoonotic disease transmission. Zoonotic disease transmission is when a disease passes from non-human animals to humans. Zoonotic diseases can be caused by viruses, bacteria, parasites, and fungi. Coronaviruses are common in humans as well as many different species of animals, including camels, cattle, cats, and bats. Sometimes, coronaviruses can transfer from animal species to humans and cause diseases. We have seen this happen with SARS-1 in 2002-2003 and MERS 2012-present, but how does this happen? Dr. Don Neiffer, Chief Veterinarian at Smithsonian National Zoo and Conservation Biology Institute says, "Viruses are as variable as other forms of life and take lots of strategies to survive and pass along genetic material. Some viruses have evolved in humans and others in animal species. Primates (including us), bats, and rodents are much more related genetically than many people realize. Consequently, it is not surprising that viruses carried in bats and rodents can take advantage of our cells and DNA/RNA and cause problems."
The CDC estimates that more than six out of every 10 known infectious diseases in people can be spread from animals, and three out of every four new or emerging infectious diseases in people come from animals. mauribo/iStock/Getty Images Plus
What is reverse zoonoses?
Similar to how animals can pass disease to humans, we can pass disease to them. Reverse zoonoses is when humans spread diseases to other animal species. According to Dr. Neiffer, "Some viruses evolved in humans but are related enough to some viruses in other species that we pose a risk to them." Diseases spread from humans to other animals do not always have the same symptoms. A virus called Herpes Simplex-1 causes blisters on the lips known as cold sores in humans, but it can kill gibbons, marmosets, and tamarins. COVID-19 presents in humans with mild to severe respiratory symptoms including fever and shortness of breath. The tiger who tested positive for COVID-19, however, presented with decreased activity, decreased appetite, and a dry cough with no fever or shortness of breath.
A Malayan tiger like this one was diagnosed with COVID-19 at the Bronx Zoo. alexmatamata/iStock/Getty Images Plus
Why do some viruses exhibit reverse zoonoses and some don't?
Not all viruses can be passed from humans to animals. And not all viruses that can be passed from humans can infect all or even many different animal species. Dr. Neiffer explains the reason why some viruses exhibit reverse zoonoses and some don't "has to do with not only the ability of the animal to become infected but the ability for the virus to replicate in the new host. So in case of COVID-19, the virus entered humans and was able to replicate and be shed." Dogs and cats have also been exposed to COVID-19. Dogs have shown no clinical signs of infection, and there is no evidence of virus replication. In the case of the cats, however, the tiger that tested positive showed clinical symptoms and was infected. Dr. Neiffer says, "There is then the potential for those felids to transfer disease to same or other species."
Great Apes like this orangutan may be susceptible to COVID-19. COVID-19 is an abbreviation—CO stands for corona, VI for virus, D for disease, and 19 for the year. Jessie Cohen, Smithsonian's National Zoo
Should we be concerned about COVID-19 transmission to other animals?
The short answer is "yes," but Dr. Neiffer states, "The results of disease transmission will be variable depending on the species affected. While the news of a COVID-19 infected tiger may be disheartening, it is not surprising. In the previous coronavirus outbreak of SARS-1, carnivores such as ferrets and civets were susceptible to the disease." For other animals Dr. Neiffer states, "We have made assumptions based on relatedness to us that non-human primates, particularly great apes, are susceptible to COVID-19." We also know that other coronaviruses that affect humans can affect at least some other primates. Where the Bronx cats are concerned, all six symptomatic animals including the tiger who tested positive for COVID-19 are recovering from mild symptoms. While there is no evidence at this time that infected cats would be a risk for humans, caution must be exercised. Staff at the Bronx Zoo have started wearing personal protective equipment when working with felids in addition to primates. The Smithsonian National Zoo and Conservation Biology Institute staff have started wear personal protective equipment when working with their large cats and were already wearing personal protective equipment to protect great apes and other primates.
We thank Dr. Don Neiffer for his expertise and the entire Smithsonian National Zoo and Conservation Biology Institute staff for caring for the animals during this challenging time.