MicrobiologyBytes

Rotaviruses were discovered in 1972 when the virus was seen by direct electron microscopy visualization in the intestinal biopsies of children with acute diarrhoea. The authors of a new review discuss the most relevant information in the field of rotavirus vaccines published from October 2007 to June 2009; new information on the virus, host response and disease burden that relate to our understanding of vaccine mechanisms and impact are discussed. The review focusses on the role of the vaccines for the developing world but this does not preclude the relevance of these vaccines for children living in the industrialized world.

Immune mechanisms involved in rotavirus-associated immunity potentially relevant for vaccine-associated immunity continue to be identified including anti-NSP4 antibodies, cellular and mucosal mechanisms. Rotavirus-associated disease burden is high, causing approximately 40% of diarrhea-associated hospitalizations in children less than 5 years of age worldwide; G12, G8 and P[6] antigenic types emerging in developing countries are increasing in prevalence and may share worldwide circulation with the other five more common serotypes. The two currently available vaccines, based on different immune concepts, (VP7/VP4 homotypic specificity for RotaTeq vs. homotypic and heterotypic specificity for Rotarix) have demonstrated high and sustained efficacy in middle and high-income countries. Recent efficacy and effectiveness studies demonstrate acceptable protection levels in the poorest countries of the world against most antigenic types, leading to universal vaccine recommendation. Postlicensure surveillance has not detected any signal of increased risk for intussusception in children vaccinated with any of the two vaccines.

Rotavirus vaccines are well tolerated and provide adequate protection against moderate to severe disease in high, middle and low-income regions. Partnerships between governments, industry, and funding agencies will now be urgently needed to promote vaccine use, especially in the less privileged countries of the world.

Rotavirus vaccines for the developing world. 2009 Current Opinion in Infectious Diseases 22 (5): 483-489

Related:

• Rotavirus Infection: A Systemic Illness?

Two-thirds of chicken on sale in the UK is contaminated with a bacterium which can cause severe food poisoning. Campylobacter, which can cause diarrhoea, cramping and abdominal pain, causes 55,000 cases of food poisoning a year in the UK. Cooking the meat properly kills the bug. The Food Standards Agency said the poultry industry should take action. Levels of Campylobacter in chicken were the same as when a similar survey was last carried out in 2001.

BBC News

Related:

• Campylobacter jejuni
• Understanding Campylobacter jejuni genomic diversity
• Animals farmed for meat are the main source of Campylobacter infections
• How Campylobacter jejuni survives within cells
• Protein promotes antibiotic resistance in Campylobacter

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Prions are transmissible, proteinaceous agents that cause fatal neurodegenerative diseases. In deer elk moose prions cause chronic wasting disease (CWD). The incidence of CWD can be remarkably high both in captive and wild herds and epidemiological data suggest that efficient horizontal transmission drives epidemic dynamics. Although deer can be infected orally and seem to be able to contract CWD from contaminated environments, precisely how and when CWD prions are shed into the environment have not been described. Previous studies have identified CWD prions in saliva, blood, urine, antler velvet, and muscle, lymphoid and other tissues of symptomatic cervids with late-stage disease. These sources of CWD prions may contribute to the spread of CWD, but none explains natural CWD transmission both within and between species in the deer family. To fit observed patterns, a natural CWD transmission mechanism must be effected within biologically realistic limits of the carrier medium, cannot require cannibalism and should be indirect to explain both environmental persistence and spread among multiple host species. Because empirical data and modelling suggested faecal excretion of prions throughout much of the disease course as potentially important to CWD transmission, researchers investigated whether prions are shed in faeces from mule deer during the course of CWD infection.

Asymptomatic deer excrete infectious prions in faeces. 2009 Nature 461: 529-532 doi:10.1038/nature08289
Infectious prion diseases – scrapie of sheep and chronic wasting disease (CWD) of several species in the deer family – are transmitted naturally within affected host populations. Although several possible sources of contagion have been identified in excretions and secretions from symptomatic animals, the biological importance of these sources in sustaining epidemics remains unclear. Here we show that asymptomatic CWD-infected mule deer (Odocoileus hemionus) excrete CWD prions in their faeces long before they develop clinical signs of prion disease. Intracerebral inoculation of irradiated deer faeces into transgenic mice overexpressing cervid prion protein (PrP) revealed infectivity in 14 of 15 faecal samples collected from five deer at 7–11 months before the onset of neurological disease. Although prion concentrations in deer faeces were considerably lower than in brain tissue from the same deer collected at the end of the disease, the estimated total infectious dose excreted in faeces by an infected deer over the disease course may approximate the total contained in a brain. Prolonged faecal prion excretion by infected deer provides a plausible natural mechanism that might explain the high incidence and efficient horizontal transmission of CWD within deer herds, as well as prion transmission among other susceptible cervids.

Why should we care?
Apart from the impact on wildlife, vCJD is a prion infection transmitted from infected cows to humans. People eat deer. Although there is no evidence that the CWN prion causes diseae in humans, this is definitely one to keep an eye on.

Related:

• A General Model of Prion Strains and Their Pathogenicity
• Prions, Proteasomes, and Mad Cows
• Oral transmission of prions is enhanced by binding to soil
• Prions and Cheetah Conservation

Malaria is a major contributor to the global disease burden, and disproportionately affects low-income countries with climates suitable for transmission. Vector control strategies have proven effective in reducing malaria transmission and prevalence, and are a key element of current malaria control initiatives. Indoor residual spraying and insecticide-treated bednets (ITNs) have been and remain the dominant methods of controlling malaria vectors, but problems of public health and insecticide resistance associated with chemical insecticides have increased interest in alternate methods, including novel biological methods. Because the incubation period of the malaria parasite is relatively long in comparison to the average adult mosquito lifespan, biological methods of vector control that have sublethal and lethal effects at different points in the mosquito life cycle may substantially reduce the potential for malaria transmission.

Biopesticides containing a fungus that is pathogenic to mosquitoes may be an effective means of reducing malaria transmission, particularly if used in combination with insecticide-treated ITNs. Results of a new study show that incorporating this novel vector control technique into existing vector management programmes may substantially reduce malaria transmission rates and help manage insecticide resistance. Using data from laboratory and field studies, the model estimates the impact of different vector control interventions on the mosquito life cycle and the average numbers of mosquitoes that survive to transmit malaria.  The results indicate that in order to successfully control malaria transmission, single intervention strategies must be widely used across the community, whether the strategy involves fungal biopesticides or ITNs.  If used in combination, the model shows that the interventions can interact to produce greater-than-expected reductions in malaria transmission rates.

This outcome is achieved because the presence of ITNs can increase mosquito exposure to biopesticide-sprayed surfaces.  Efficient combinations of interventions may allow each to be used at lower levels, and slow the development of resistance in the mosquito population.  The results suggest that combining fungal biopesticides and ITNs may be an efficient and effective strategy for malaria vector control. Malaria is a major contributor to the global disease burden, and disproportionately affects low income countries with climates suitable for transmission.  Mosquito control relies heavily on chemical insecticides, but growing problems of insecticide resistance have led to increased interest in novel methods, including biocontrol.  The Global Strategy for Integrated Vector Management, developed by the World Health Organisation, encourages the use of multiple vector control technologies in combination.  This research has used computer modelling to identify ways in which interventions can be combined to maximise the impact on malaria transmission, given the resources available.

Combining Fungal Biopesticides and Insecticide-Treated Bednets to Enhance Malaria Control. 2009 PLoS Comput Biol 5(10): e1000525 doi:10.1371/journal.pcbi.1000525
In developing strategies to control malaria vectors, there is increased interest in biological methods that do not cause instant vector mortality, but have sublethal and lethal effects at different ages and stages in the mosquito life cycle. These techniques, particularly if integrated with other vector control interventions, may produce substantial reductions in malaria transmission due to the total effect of alterations to multiple life history parameters at relevant points in the life-cycle and transmission-cycle of the vector. To quantify this effect, an analytically tractable gonotrophic cycle model of mosquitomalaria interactions is developed that unites existing continuous and discrete feeding cycle approaches. As a case study, the combined use of fungal biopesticides and insecticide treated bednets (ITNs) is considered. Low values of the equilibrium EIR and human prevalence were obtained when fungal biopesticides and ITNs were combined, even for scenarios where each intervention acting alone had relatively little impact. The effect of the combined interventions on the equilibrium EIR was at least as strong as the multiplicative effect of both interventions. For scenarios representing difficult conditions for malaria control, due to high transmission intensity and widespread insecticide resistance, the effect of the combined interventions on the equilibrium EIR was greater than the multiplicative effect, as a result of synergistic interactions between the interventions. Fungal biopesticide application was found to be most effective when ITN coverage was high, producing significant reductions in equilibrium prevalence for low levels of biopesticide coverage. By incorporating biological mechanisms relevant to vectorial capacity, continuous-time vector population models can increase their applicability to integrated vector management.

Related:

• Evolution-Proof Insecticides Against Malaria
• Malaria, mosquitoes and the legacy of Ronald Ross
• Malaria is a continuing danger to UK travellers
• Tough Choices – DDT or Malaria?
• New target for anti-malaria drugs

What Are Microsporidia?
Microsporidia are a diverse group of obligate intracellular eukaryotic parasites. There are approximately 1,300 species in 160 genera, but this certainly represents a tiny fraction of the real diversity because most potential hosts have been poorly studied. Nearly all microsporidia are known to infect animals, and some are responsible for a number of human diseases, predominantly associated with immune suppression. They also infect several commercially important animal species such as bees, silk worms, and salmon, and various domesticated mammals.

Are They Protists, Fungi, or What?
There has been considerable debate about the origin of microsporidia. Aside from their elaborate infection mechanism, they have few distinguishing features, and have thus been difficult to compare to other eukaryotes. When microsporidia were discovered in 1857, they were considered to be fungi. Eventually, because of the absence of many eukaryotic features in microsporidia, they were collectively called “Archezoa” and were thus proposed to be ancient, primitive lineages of great importance to understanding the origin of eukaryotes. Molecular data originally supported this hypothesis [7], but as the sampling of genes increased, another hypothesis emerged: that microsporidia are related to fungi. Thus our view of the origin of microsporidia has thus come full circle.

Are They Really Amitochondriate?
The Archezoa hypothesis (that microsporidia were an ancient, primitive lineage) was based on the absence of mitochondria in microscopy studies. Do they still have mitochondria, or did they lose them? Direct evidence for the retention of mitochondria came from the immuno-localisation of HSP70 which reveled multiple, tiny (50×90 nm) organelles bounded by two membranes, but lacking any other distinguishing structural features. This derived and reduced mitochondrion was named a mitosome.

What Are Microsporidian Genomes Like?
Microsporidian genomes are made up of multiple linear chromosomes much like that of other eukaryotes, but they are otherwise quite reduced and unusual. For a start, many microsporidian genomes are quite small. At the extreme, the Encephalitozoon intestinalis genome is only 2.3 Mbp, smaller than many bacterial genomes. The complete genome of E. cuniculi is only 2.9 Mbp, and only encodes about 2,000 protein-coding genes. The genome is highly compacted, with short intergenic regions, almost no repeats, and little evidence of selfish elements, altogether leading to a gene density approximately twice that of Saccharomyces.

How Do Microsporidia Depend On Their Host?
Microsporidia cannot grow or divide outside their host cell, but exactly how they interact and use resources from their host is only partially known. It has long been known that infection induces changes in the host that appear to be related to metabolic dependency. For example, infection by several species leads the host to surround the parasite with mitochondria, presumably supplying the parasite with energy.

Five Questions about Microsporidia. 2009 PLoS Pathog 5(9): e1000489 doi:10.1371/journal.ppat.1000489

Related:
Bee-Killing Parasite Genome Sequenced
Nematode provides new animal model for emerging pathogen