BBC News: At least 35,000 people have taken part in the latest mass protest in South Korea against the government’s decision to allow US beef imports to resume. South Korea used to be a big market for US beef, but suspended imports in 2003 after a BSE (”mad cow disease”) outbreak. The decision to lift the ban has led to weeks of protests based on health fears and discontent with the government. As a result, the South Korean government has sought extra safety assurances from the US authorities on American beef. Both governments insist the beef is safe.
A biologist and undergraduate student have discovered that what’s good for an area’s bird population is also good for people living nearby. The new research indicates that areas which have a more diverse bird population (biodiversity) show much lower incidences of West Nile virus infection in the human population. West Nile develops rapidly in bird populations, and then can be passed to humans or other animals through a vector mechanism, often a mosquito. This work research constitutes the largest-scale application to date of the “dilution effect”, a pattern whereby increased biodiversity in wildlife results in lower risks of humans becoming infected by animal diseases. The dilution effect was first reported in Lyme disease, but the authors are the first to demonstrate the dilution effect in a disease that has bird hosts. Other infectious diseases of concern, such as avian flu and bubonic plague, may fit the dilution effect as well. We don’t yet know the precise mechanism that drives this pattern, but it’s likely to be due to diverse areas having relatively few of the bird species that are particularly competent hosts and reservoirs for the virus. Host competence refers to the qualities that make a particular species of bird best able to contract the disease and pass it on through a vector. The highest levels of host competence are found in crows, jays, thrushes and sparrows - the very birds that tend to thrive when avian biodiversity is reduced. Very small changes in land management could attract more bird species, with the increase in biodiversity paying off in the form of lower human infection rates during outbreaks of West Nile or other diseases in the bird population. Biodiversity is a public health service that people have rarely considered and the value of this service should be considered when developing land and managing bird populations in the future.
Increased Avian Diversity Is Associated with Lower Incidence of Human West Nile Infection: Observation of the Dilution Effect. PLoS ONE 3(6): e2488
Recent infectious disease models illustrate a suite of mechanisms that can result in lower incidence of disease in areas of higher disease host diversity - the “dilution effect”. These models are particularly applicable to human zoonoses, which are infectious diseases of wildlife that spill over into human populations. As many recent emerging infectious diseases are zoonoses, the mechanisms that underlie the “dilution effect” are potentially widely applicable and could contribute greatly to our understanding of a suite of diseases. The dilution effect has largely been observed in the context of Lyme disease and the predictions of the underlying models have rarely been examined for other infectious diseases on a broad geographic scale. Here, we explored whether the dilution effect can be observed in the relationship between the incidence of human West Nile virus (WNV) infection and bird (host) diversity in the eastern US. We constructed a novel geospatial contrasts analysis that compares the small differences in avian diversity of neighboring US counties (where one county reported human cases of WNV and the other reported no cases) with associated between-county differences in human disease. We also controlled for confounding factors of climate, regional variation in mosquito vector type, urbanization, and human socioeconomic factors that are all likely to affect human disease incidence. We found there is lower incidence of human WNV in eastern US counties that have greater avian (viral host) diversity. This pattern exists when examining diversitydisease relationships both before WNV reached the US (in 1998) and once the epidemic was underway (in 2002). The robust disease-diversity relationships confirm that the dilution effect can be observed in another emerging infectious disease and illustrate an important ecosystem service provided by biodiversity, further supporting the growing view that protecting biodiversity should be considered in public health and safety plans.
Real-Time High Resolution 3D Imaging of the Lyme Disease Spirochete Adhering to and Escaping from the Vasculature of a Living Host. PLoS Pathog 2008 4(6): e1000090
Pathogenic spirochetes are bacteria that cause a number of emerging diseases worldwide, including Lyme disease. Spirochetes exhibit an unusual form of helical motility and can infect many different tissues. However, the mechanism by which they disseminate from the blood to target sites is unknown. Direct visualization of bacterial pathogens at the single cell level in living hosts is important, since this approach is likely to yield critical insight into disease processes. In a recent paper, researchers engineered a fluorescent strain of Borrelia burgdorferi, the Lyme disease pathogen, and used confocal microscopy to directly visualize these bacteria in real time and in 3D in living mice. They found that spirochete interaction with and dissemination out of the vasculature was a multi-stage process of unexpected complexity and that spirochete movement appeared to play an integral role in dissemination. This is the first report of high resolution 3D visualization of a bacterial pathogen in a living mammalian host, and provides the first direct insight into spirochete dissemination in vivo.
In the first section of this video you can see B. burgdorferi moving in the ear of a living mouse. The second section shows B. burgdorferi in a postcapillary venule in the skin of the mouse, and the third section shows the actual moment of escape from the blood vessel into the surrounding tissue.
Commercial hunting and habitat loss are major drivers of the rapid decline of great apes. Ecotourism and research have been widely promoted as a means of providing alternative value for apes and their habitats. However, close contact between humans and habituated apes during ape tourism and research has raised concerns that disease transmission risks might outweigh benefits. To date only bacterial and parasitic infections of typically low virulence have been shown to move from humans to wild apes. This paper presents the first direct evidence of virus transmission from humans to wild apes. Tissue samples from habituated chimpanzees that died during three respiratory-disease outbreaks at our research site, Côte d’Ivoire, contained two common human paramyxoviruses. Virus strains sampled from chimpanzees were closely related to strains circulating in contemporaneous, worldwide human epidemics. Twenty-four years of mortality data from observed chimpanzees reveal that such respiratory outbreaks could have a long history. In contrast, survey data show that research presence has had a strong positive effect in suppressing poaching around the research site. These observations illustrate the challenge of maximizing the benefit of research and tourism to great apes while minimizing the negative side effects.
Dengue is a mosquito-borne disease caused by four serotypes of dengue virus (DENV1–DENV4) and is currently the most common arbovirus (arthropod-transmitted) disease worldwide. Primary infection with any of the four DV serotypes typically results in dengue fever (DF), a relatively mild influenza-like illness which subsequently provides lifelong immunity to the infecting strain. However, the bad news is that secondary infection with different DV serotype is associated with an increased risk of developing more serious conditions such as dengue haemorrhagic fever (DHF) and the life-threatening dengue shock syndrome (DSS).
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The first well documented outbreaks of dengue occurred in the eighteenth century, although the disease may have been around in China eight hundred years earlier. Dengue virus was first isolated by Japanese and American scientists during World War II. Dengue is now a major public health problem, with approximately 50 million people infected each year (of whom around 20,000 die) and nearly half the world’s population, about 3.5 billion people, at risk of infection. Unfortunately, no dengue virus-specific therapies or vaccines are currently available. The incidence of dengue infection has increased dramatically in the past 50 years. This is due in part to population growth and urbanization in tropical and subtropical countries. Originally found in the jungles and rural areas of Southeast Asia, dengue virus is now maintained primarily in an urban cycle involving human hosts and Aedes aegypti and A. albopictus mosquitoes. Urban areas frequently contain many breeding sites for the mosquitoes that transmit the virus, such as rain-filled old tyres. Successful mosquito control has also been problematic. Dengue viruses have evolved rapidly as they have spread worldwide, and genotypes associated with increased virulence have expanded from South and Southeast Asia into the Pacific and the Americas.
The pathogenesis of dengue haemorrhagic fever and dengue shock syndrome remain unclear. The requirement for a second infection with a different serotype of the virus suggested that antibody-dependent enhancement is involved in these more serious conditions. After an initial period of protection, antibodies from the primary infection can cross-react with other dengue virus serotypes but have waned to non-neutralizing levels. These non-neutralizing antibodies could then mediate an increased uptake of virus into monocyte/macrophage cells via Fc receptors, leading to increased virus replication and immune activation including massive cytokine release (known as a “cytokine storm”). An alternative theory involves reactivation of cross-reactive memory T cells specific for the previous rather than the current virus strain, resulting in delayed virus clearance and/or increased cytokine secretion along with increased apoptosis of both infected and uninfected bystander cells (known as “original antigenic sin”).
With only around 65% homology based on amino acid sequence, the four dengue viruses could have been classified as separate virus groups but instead are treated as four serotypes belonging to a single group. It appears that there may be differences between the viruses, with DENV2 most commonly been associated with DHF/DSS and DENV4 the least likely to cause the more serious infections, but all serotypes can cause all of the conditions.
Because of the nature of dengue virus pathogenesis, a tetravalent vaccine effective against all four dengue virus serotypes is urgently needed. Vaccines which induce weak immune responses below protective levels over time are not acceptable because of the severe consequences of secondary DENV infections. Efforts to develop a dengue vaccine have encompassed live attenuated virus vaccines, inactivated virus vaccines, subunit vaccines and DNA vaccines. Vaccines of each type are currently or have been subjected to clinical trials, but none has yet been approved for use. Travelers to affected regions should take precautions against being bitten by mosquitos, use insect repellent day and night and check that hotels provide mosquito nets. Just another joy of those long-haul holidays.
Haemorrhagic disease, encephalitis, biphasic fever, flaccid paralysis, and jaundice are typical manifestations of diseases in human beings after infections by mosquito-borne or tick-borne flaviviruses such as yellow fever, dengue, West Nile, St Louis encephalitis, Japanese encephalitis, tick-borne encephalitis, Kyasanur Forest disease, and Omsk haemorrhagic fever. Although the characteristics of these viruses are well defined, they are still unpredictable with increases in disease severity, unusual clinical manifestations, unexpected methods of transmission, long-term persistence, and the discovery of new species. This paper compares the epidemiological and clinical features of the medically important flaviviruses, consider the effect of human activity on their evolution and dispersal, and draw attention to new findings and some of the unanswered questions, unresolved issues, and controversies that remain.
The amyloidoses are a group of protein misfolding disorders characterized by the accumulation of amyloid fibrils formed from a variety of proteins that, under normal physiological conditions, are harmless and soluble. Currently, 25 amyloid diseases have been identified, such as the prion diseases, Alzheimer’s disease, type 2 diabetes, and various systematic amyloidoses. Although the various proteins that can polymerize into amyloid fibrils have unrelated sequences, they can all form fibrils with a similar ultrastructural appearance. Among them, prion diseases such as transmissible spongiform encephalopathy (TSE), including scrapie in sheep, bovine spongiform encephalopathy (BSE), and chronic wasting disease (CWD) of deer and elk, are highly infectious. In these diseases, prion (PrPSc), an abnormal form of the host cellular prion protein (PrPC), induces the conformational change of PrPC to the PrPSc and causes a detectable phenotype or disease in the affected individual. AA amyloidosis is characterized by the systemic deposition of extracellular fibrils composed of amyloid A protein, primarily in the spleen; liver; and, to a lesser extent, in other organs. In most species, AA amyloidosis occurs sporadically and is typically secondary to chronic inflammation, infection, or neoplasia. Intriguing recent data suggest that AA amyloidosis could be transmitted by a prion-like infectious process through a seeding-nucleation mechanism.
The cheetah (Acinonyx jubatus) is in danger of extinction and is included on The World Conservation Union list of vulnerable species. Although efforts have been made in wildlife sanctuary parks and zoos worldwide to prevent extinction, a steady increase in the size of the cheetah population is hampered by the high prevalence of certain diseases in captive cheetahs. In particular, systemic AA amyloidosis is regarded as an increasingly important cause of morbidity and mortality in captive cheetahs as prevalence increased from 20% in pre-1990 reported necropsies to an unusual 70% of necropsied cheetahs in 1995. Despite much effort, the pathogenesis for AA amyloidosis in cheetahs is still only partially understood. However, environmental epidemiological studies indicate that breeding conditions have a prominent effect on the incidence of AA amyloidosis. A high rearing density is always associated with early age of onset, and with the high incidence and severity of AA amyloidosis, findings similar to sheep scrapie and cervid CWD. Thus, sustained epidemics of sheep scrapie and cervid CWD appear to be principally due to horizontal (animal to animal) transmission, although the routes of natural transmission remain to be clarified. The propagation of AA amyloidosis among captive cheetah populations may also depend on a horizontal transmission pathway. Identification of the mode of transmission is a prerequisite for disease control. This study shows that the faeces from a cheetah with AA amyloidosis can act as a possible transmission agent to accelerate the onset of AA amyloidosis.
Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease PNAS USA May 12, 2008
AA amyloidosis is one of the principal causes of morbidity and mortality in captive cheetahs (Acinonyx jubatus), which are in danger of extinction, but little is known about the underlying mechanisms. Given the transmissible characteristics of AA amyloidosis, transmission between captive cheetahs may be a possible mechanism involved in the high incidence of AA amyloidosis. In this study of animals with AA amyloidosis, we found that cheetah feces contained AA amyloid fibrils that were different from those of the liver with regard to molecular weight and shape and had greater transmissibility. The infectious activity of fecal AA amyloid fibrils was reduced or abolished by the protein denaturants 6M guanidine HCl and formic acid or by AA immunodepletion. Thus, we propose that feces are a vehicle of transmission that may accelerate AA amyloidosis in captive cheetah populations. These results provide a pathogenesis for AA amyloidosis and suggest possible measures for rescuing cheetahs from extinction.
It might seem like prions are always bad news, but if that were true, they would be an evolutionary disadvantage and would surely have been lost. So the truth must be more complicated, and in tomorrow’s post, we’ll see how.
Pathogenic microbes are emerging and re-emerging at an alarming rate. Of the 175 emerging infectious diseases of humans, 132 are zoonotic, residing in wildlife reservoir species and occasionally transmitted to humans either directly or via an intermediate vector. Zoonotic pathogens are not specialists on any single species, they can infect humans and at least one non-human animal. A robust understanding of the transmission cycle in nature that governs the distribution and abundance of pathogens, and thus contact with humans, is essential for the effective control of emerging infectious diseases. This paper investigates the degree to which the zoonotic pathogen that causes Lyme disease, Borrelia burgdorferi, is maintained and amplified by multiple reservoir host species.
Conspicuous impacts of inconspicuous hosts on the Lyme disease epidemic
Proc Biol Sci. 2008 275: 227-235
Emerging zoonotic pathogens are a constant threat to human health throughout the world. Control strategies to protect public health regularly fail, due in part to the tendency to focus on a single host species assumed to be the primary reservoir for a pathogen. Here, we present evidence that a diverse set of species can play an important role in determining disease risk to humans using Lyme disease as a model. Host-targeted public health strategies to control the Lyme disease epidemic in North America have focused on interrupting Borrelia burgdorferi transmission between blacklegged ticks and the putative dominant reservoir species, white-footed mice. However, B. burgdorferi infects more than a dozen vertebrate species, any of which could transmit the pathogen to feeding ticks and increase the density of infected ticks and Lyme disease risk. Using genetic and ecological data, we demonstrate that mice are neither the primary host for ticks nor the primary reservoir for B. burgdorferi, feeding 10% of all ticks and 25% of B. burgdorferi-infected ticks. Inconspicuous shrews feed 35% of all ticks and 55% of infected ticks. Because several important host species influence Lyme disease risk, interventions directed at a multiple host species will be required to control this epidemic.
Over the past week, international news stories have concentrated on the devastating cyclone in Burma (Myanmar), and the almost certain consequence of disease outbreaks in the aftermath. But at the same time, there’s another microbiology story unfolding in East Asia. Beginning in March, a large outbreak of hand, foot and mouth disease (HFMD) was reported from Fuyang city in Anhui Province in China. Note that HFMD is a human disease caused by enteroviruses belonging to the picornavirus family, but is not the same as the animal disease foot and mouth (FMD) caused by a different kind of picornavirus.
HFMD usually affects infants and children, is quite common worldwide and can be caused by a number of different enteroviruses. It is highly contagious and is spread through direct contact with the mucus, saliva, or faeces of an infected person. Like other enterovirus infections (including polio), HFMD typically occurs in small epidemics, usually during the summer and autumn months with an incubation period of 3-7 days.
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Enterovirus infections are common and occur worldwide. Although many infections show no symptoms and often go unnoticed, these viruses are also associated with occasional outbreaks in which a larger than usual number of patients develop clinical disease, sometimes with fatal consequences. The current outbreak is one of these. Initial testing for a variety of respiratory diseases did not reveal any conclusive results, but on April 23, the presence of Enterovirus (EV71) was confirmed. As of May 8th, at least 30 deaths had been reported and the disease had spread to 11 cities and several provinces across China. In all the fatal cases, which represent less than 1% of the thousands of children infected, the victims died with serious complications such as neurogenic pulmonary oedema (breathing difficulties reminiscent to those seen in polio victims).
Enterovirus replication begins in the gastrointestinal or respiratory tract but once the virus is present in the bloodstream may affect various tissues and organs, causing a variety of diseases. Clinically, it is difficult to distinguish the specific cause of most enterovirus infections. Diagnostic testing for non-polio enteroviruses requires specialized laboratory facilities. Diagnosis is made by detecting virus in the throat, in faecal samples or, more convincingly, from specimens collected from the affected part of the body, for example, cerebrospinal fluid (CSF) or biopsy material. A four-fold rise in the level of neutralizing antibody in specimens collected during the acute and convalescent phases of illness provides the best evidence for a recent infection. No specific antiviral agents are currently available for treatment of enterovirus infections, although intravenous administration of immune globulin may have a use in preventing severe disease in immunocompromised individuals or those with life-threatening disease.
EV71 was first isolated in an outbreak of neurological disease in California in 1969. One of the nastier enteroviruses, EV71 has been associated with several epidemics of severe neurological disease in children, mostly in East Asia. An outbreak in Taiwan in 1998 resulted in 129,106 reported cases, 405 children hospitalized and more than 80 deaths. EV71 appears to be emerging as an important virulent neurotropic enterovirus just as poliomyelitis is nearing eradication, but little is known about the molecular mechanisms of host response to EV71 infection.
Transmission of enterovirus infections is increased by poor hygiene and overcrowded living conditions. Improved sanitation and general hygiene are important preventive measures. Measures that can be taken to avoid getting infected with enteroviruses include frequent handwashing, especially after nappy (diaper) changes or going to the toilet, disinfection of contaminated surfaces with bleach, and washing soiled articles of clothing. Enteroviruses are quite resistant to many disinfectants so it is important to use chlorinated (bleach) or iodized disinfectants. During recognised epidemics, it may be advised to close institutions such as schools or child care facilities in order to reduce transmission among young children. Chinese public health experts currently predict that the number of cases will continue to increase and peak around June-July.
Both friendly and destructive bacteria live in our mouths, eyes, skin and elsewhere. Over millions of years, the body has come to an accommodation with those creatures, generally striking a balance ensuring survival. This balance has been severely offset in recent years, due to a “cleanliness” obsession that arose when it became clear that some germs were responsible for diseases. This idea was effectively demonstrated by UK researcher David Strachan, whose research led to what is now called the “hygiene hypothesis” - respiratory illnesses result from lack of cross-microbe activity to build immunities. In short, rich, small families were more prone to allergies than large, poorer ones. As Sachs points out, humans in our society overreacted to the new knowledge about disease-causing germs and sought to eliminate them all. The imbalance has led to many tragic situations, and initiated a guarantee that more, perhaps worse, situations are in the offing. What are we to do about it?
Jessica Sachs guides us through the findings of scores of scientists’ work that has revised the approach we were taught about “germs” in our childhood. Eating mud, something many of us were at least verbally chastised for, turns out to be a good thing, even a necessity. From birth, the introduction of certain microbes initiate processes the body needs to keep going. For most people today, it’s well known that microbes in our tummies are part of the process of digestion. Escherichia coli is known to be a true friend - in controlled numbers and certain strains. What’s less known is how many other bacteria the body relies on to get certain jobs done. One of those jobs is keeping the immune system properly tuned. A lazy immune system is unresponsive or unable to react to invasion. An overly ambitious one can turn on its own body and destroy it.
Publisher Hill & Wang, Oct 2007, ISBN-10: 0809050633
Both friendly and destructive bacteria live in our mouths, eyes, skin and elsewhere. Over millions of years, the body has come to an accommodation with those creatures, generally striking a balance ensuring survival. This balance has been severely offset in recent years, due to a “cleanliness” obsession that arose when it became clear that some germs were responsible for diseases. This idea was effectively demonstrated by UK researcher David Strachan, whose research led to what is now called the “hygiene hypothesis” - respiratory illnesses result from lack of cross-microbe activity to build immunities. In short, rich, small families were more prone to allergies than large, poorer ones. As Sachs points out, humans in our society overreacted to the new knowledge about disease-causing germs and sought to eliminate them all. The imbalance has led to many tragic situations, and initiated a guarantee that more, perhaps worse, situations are in the offing. What are we to do about it?