The Irish potato famine pathogen Phytophthora infestans originated in central Mexico rather than the Andes

Phytophthora infestans is a destructive plant pathogen best known for causing the disease that triggered the Irish potato famine and remains the most costly potato pathogen to manage worldwide. Identification of P. infestan’s elusive center of origin is critical to understanding the mechanisms of repeated global emergence of this pathogen. There are two competing theories, placing the origin in either South America or in central Mexico, both of which are centers of diversity of Solanum host plants. To test these competing hypotheses, we conducted detailed phylogeographic and approximate Bayesian computation analyses, which are suitable approaches to unraveling complex demographic histories. Our analyses used microsatellite markers and sequences of four nuclear genes sampled from populations in the Andes, Mexico, and elsewhere. To infer the ancestral state, we included the closest known relatives Phytophthora phaseoli, Phytophthora mirabilis, and Phytophthora ipomoeae, as well as the interspecific hybrid Phytophthora andina. We did not find support for an Andean origin of P. infestans; rather, the sequence data suggest a Mexican origin. Our findings support the hypothesis that populations found in the Andes are descendants of the Mexican populations and reconcile previous findings of ancestral variation in the Andes. Although centers of origin are well documented as centers of evolution and diversity for numerous crop plants, the number of plant pathogens with a known geographic origin are limited. This work has important implications for our understanding of the coevolution of hosts and pathogens, as well as the harnessing of plant disease resistance to manage late blight.The potato pathogen Phytophthora infestans, the causal agent of potato late blight, is the plant pathogen that has most greatly impacted humanity to date. This pathogen is best known for its causal involvement in the Irish potato famine after introduction of the HERB-1 strain to Ireland from the Americas in the 19th century (1). To this day, potato late blight remains a major threat to food security and carries a global cost conservatively estimated at more than $6 billion per year (2). In the 1980s, a single asexual lineage named US-1, possibly derived from the same metapopulation as HERB-1 (1), dominated global populations, whereas a genetically diverse and sexual population of P. infestans in central Mexico led to formulation of the hypothesis identifying Mexico as this pathogen’s center of origin (3, 4). A competing hypothesis argues that the center of origin of the potato, the South American Andes, is the center of origin of P. infestans (5). This hypothesis recently gained prominence after an analysis demonstrated ancestral variation in Andean lineages of P. infestans (5). Other evidence supporting this hypothesis includes infection of native Solanum hosts and an Andean distribution for Phytophthora andina, a phylogenetic relative of P. infestans (6).Evidence supporting a Mexican center of origin is substantial, but inconclusive (4). Two close relatives of P. infestans, Phytophthora ipomoeae and Phytophthora mirabilis, are endemic to central Mexico (7, 8). P. ipomoeae and P. mirabilis cause disease on two endemic plant host groups, Ipomoea spp. and Mirabilis jalapa, respectively. Populations of P. infestans in the Toluca Valley, southwest of Mexico City, are genetically diverse, are in Hardy–Weinberg equilibrium, and contain mating types A1 and A2 in the expected 1:1 ratio for sexual populations (9, 10). Before a migration event from Mexico to Europe in the 1970s (11, 12), only A1 mating types of P. infestans were found worldwide outside of central Mexico, limiting other populations to asexual reproduction (13). Tuber-bearing native Solanum species occur throughout the Toluca Valley (14). Of the R genes that have been used to confer resistance to strains of P. infestans in potato, the majority described to date originated from Solanum demissum or Solanum edinense in the Toluca Valley, with some discovered in South America (15).Support for the alternate hypothesis that P. infestans originated in the Andes is based on a coalescent analysis conducted by Gómez-Alpizar et al. (5). This analysis used the nuclear RAS locus and the mitochondrial P3 and P4 regions to infer rooted gene genealogies that showed ancestral lineages rooted in the Andes. Furthermore, the Mexico sample harbored less nucleotide diversity than the Andean population. P. andina was identified as the ancestral lineage for the mitochondrial genealogy; however, P. mirabilis and P. ipomoeae were not included in that study. P. andina has since been shown to be a hybrid species derived from P. infestans and a Phytophthora sp. unknown to science (16). Surprisingly, populations of P. infestans and P. andina are clonal in South America and are not in Hardy–Weinberg equilibrium (6, 17–19). Thus, the question of whether P. infestans originated in the Andes or central Mexico remained unresolved.Powerful approaches for determining the demographic and evolutionary history of organisms are now available (20). Many of these approaches rely on the power of coalescent theory for inferring the genealogical history of a species based on a representative population sample (21–23). Bayesian phylogeography uses geographic information in light of phylogenetic uncertainty to provide model-based inference of geographic locations of ancestral strains (24). The isolation with migration (IM) model and associated software uses likelihood-based inference to infer divergence time between evolutionary lineages (25). Approximate Bayesian computation (ABC) makes use of coalescent simulations and likelihood-free inference to contrast complex demographic scenarios. Each of these methods has proven useful in reconstructing the demography of pests and pathogens (24, 26–29).The objective of the present study was to reconcile the two competing hypotheses on the origin of P. infestans using Bayesian phylogenetics and ABC. We sampled key populations of P. infestans from central Mexico and the Andes and expanded on the analysis of Gómez-Alpizar et al. (5) by sequencing additional nuclear loci to assess support for the center of origin across multiple loci. To determine ancestral state, we added sequences from the sister taxa P. andina, P. mirabilis, P. ipomoeae, and Phytophthora phaseoli, all of which belong to Phytophthora clade 1c (30, 31). Finally, we aimed to reconcile the biology of P. infestans in Mexico with the findings of Gómez-Alpizar et al. (5) of ancestral variation in the Andes.     

Nodding syndrome in Mundri county,South Sudan: environmental,nutritional and infectious factors

Background

Nodding Syndrome is a seizure disorder of children in Mundri County, Western Equatoria, South Sudan. The disorder is reported to be spreading in South Sudan and northern Uganda.

Objective

To describe environmental, nutritional, infectious, and other factors that existed before and during the de novo 1991 appearance and subsequent increase in cases through 2001.

Methods

Household surveys, informant interviews, and case-control studies conducted in Lui town and Amadi village in 2001–2002 were supplemented in 2012 by informant interviews in Lui and Juba, South Sudan.

Results

Nodding Syndrome was associated with Onchocerca volvulus and Mansonella perstans infections, with food use of a variety of sorghum (serena) introduced as part of an emergency relief program, and was inversely associated with a history of measles infection. There was no evidence to suggest exposure to a manmade neurotoxic pollutant or chemical agent, other than chemically dressed seed intended for planting but used for food. Food use of cyanogenic plants was documented, and exposure to fungal contaminants could not be excluded.

Conclusion

Nodding Syndrome in South Sudan has an unknown etiology. Further research is recommended on the association of Nodding Syndrome with onchocerciasis/mansonelliasis and neurotoxins in plant materials used for food.     

Reduced influenza antiviral treatment among children and adults hospitalized with laboratory-confirmed influenza infection in the year after the 2009 pandemic

Influenza antiviral treatment is recommended for all persons hospitalized with influenza virus infection. During the 2010-2011 influenza season, antiviral treatment of children and adults hospitalized with laboratory-confirmed influenza declined significantly compared with treatment during the 2009 pandemic (children, 56% vs 77%; adults, 77% vs 82%; both P < .01).     

Charlson Co‐morbidity Index and albumin significantly associated with fracture risk in peritoneal dialysis patients

Published literature on fracture in dialysis patients seldom addressed the effect of co‐morbidity and malnutrition. In this study, we reported the incidence and risk factors for fracture in peritoneal dialysis patients. Peritoneal dialysis patients who had fractures between 2006 and 2011 were recruited. Demographic data, details of fracture, Charlson Co‐morbidity Index (CCI) and biochemical parameters were also collected. Non‐fracture controls, matched for age, gender and duration of dialysis, were also recruited at ratio 1:1 for fracture risk analysis. The incidence of fracture was 1 in 37 patient‐years. The commonest site of fracture was neck of femur (n = 16, 55.2%). Twenty‐four patients (82.8%) developed fracture after slip and fall injury. Eight out of 17 self‐ambulatory patients (47.1%) became non‐ambulatory after fracture. Infection was the commonest complication during hospitalization. Univariant analysis demonstrated high CCI (P = 0.001), hypoalbuminaemia (P < 0.001), loss of self autonomy (P = 0.006) and non‐ambulatory state (P = 0.011) significantly associated with increased fracture risk. However, only CCI (odds ratio (OR) 1.373, P = 0.028) and albumin (OR 0.893, P = 0.025) increased fracture risk significantly on multivariant analysis. Bone profile and parathyroid hormone were not significant risk factors. To conclude, fracture associated with adverse outcome in peritoneal dialysis patients. High CCI score and hypoalbuminaemia significantly increase risk of fracture.     

The Pregnancy,Arsenic, and Immune Response (PAIR) Study in rural northern Bangladesh

Background

Arsenic exposure and micronutrient deficiencies may alter immune reactivity to influenza vaccination in pregnant women, transplacental transfer of maternal antibodies to the foetus, and maternal and infant acute morbidity.

Objectives

The Pregnancy, Arsenic, and Immune Response (PAIR) Study was designed to assess whether arsenic exposure and micronutrient deficiencies alter maternal and newborn immunity and acute morbidity following maternal seasonal influenza vaccination during pregnancy.

Population

The PAIR Study recruited pregnant women across a large rural study area in Gaibandha District, northern Bangladesh, 2018–2019.

Design

Prospective, longitudinal pregnancy and birth cohort.

Methods

We conducted home visits to enrol pregnant women in the late first or early second trimester (11–17 weeks of gestational age). Women received a quadrivalent seasonal inactivated influenza vaccine at enrolment. Follow-up included up to 13 visits between enrolment and 3 months postpartum. Arsenic was measured in drinking water and maternal urine. Micronutrient deficiencies were assessed using plasma biomarkers. Vaccine-specific antibody titres were measured in maternal and infant serum. Weekly telephone surveillance ascertained acute morbidity symptoms in women and infants.

Preliminary Results

We enrolled 784 pregnant women between October 2018 and March 2019. Of 784 women who enrolled, 736 (93.9%) delivered live births and 551 (70.3%) completed follow-up visits to 3 months postpartum. Arsenic was detected (≥0.02 μg/L) in 99.7% of water specimens collected from participants at enrolment. The medians (interquartile ranges) of water and urinary arsenic at enrolment were 5.1 (0.5, 25.1) μg/L and 33.1 (19.6, 56.5) μg/L, respectively. Water and urinary arsenic were strongly correlated (Spearman's ⍴ = 0.72) among women with water arsenic ≥ median but weakly correlated (⍴ = 0.17) among women with water arsenic < median.

Conclusions

The PAIR Study is well positioned to examine the effects of low-moderate arsenic exposure and micronutrient deficiencies on immune outcomes in women and infants. Registration : NCT03930017.