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Concept: Infection

213

Simon Hay and colleagues discuss the potential and challenges of producing continually updated infectious disease risk maps using diverse and large volume data sources such as social media.

Concepts: Epidemiology, Disease, Infectious disease, Infection, Clinical surveillance, Disease surveillance

210

There has not previously been a systematic comparison of awards for research funding in infectious diseases by sex. We investigated funding awards to UK institutions for all infectious disease research from 1997 to 2010, across disease categories and along the research and development continuum.

Concepts: Epidemiology, Disease, Infectious disease, Infection

198

Zika virus is an emerging mosquito-borne flavivirus that typically causes an asymptomatic infection or mild illness, although infection during pregnancy is a cause of microcephaly and other serious brain abnormalities. Guillain-Barré syndrome and other neurologic complications can occur in adults after Zika virus infection. However, there are few published reports describing postnatally acquired Zika virus disease among children. During January 2015-July 2016, a total of 158 cases of confirmed or probable postnatally acquired Zika virus disease among children aged <18 years were reported to CDC from U.S. states. The median age was 14 years (range = 1 month-17 years), and 88 (56%) were female. Two (1%) patients were hospitalized; none developed Guillain-Barré syndrome, and none died. All reported cases were travel-associated. Overall, 129 (82%) children had rash, 87 (55%) had fever, 45 (29%) had conjunctivitis, and 44 (28%) had arthralgia. Health care providers should consider a diagnosis of Zika virus disease in children who have an epidemiologic risk factor and clinically compatible illness, and should report cases to their state or local health department.

Concepts: Health care, Medicine, Health, Epidemiology, Infectious disease, Death, Infection, Illness

195

ABSTRACT A new human coronavirus (hCoV-EMC) has emerged very recently in the Middle East. The clinical presentation resembled that of the severe acute respiratory syndrome (SARS) as encountered during the epidemic in 2002/2003. In both cases, acute renal failure was observed in humans. HCoV-EMC is a member of the same virus genus as SARS-CoV but constitutes a sister species. Here we investigated whether it might utilize angiotensin-converting enzyme 2 (ACE2), the SARS-CoV receptor. Knowledge of the receptor is highly critical because the restriction of the SARS receptor to deep compartments of the human respiratory tract limited the spread of SARS. In baby hamster kidney (BHK) cells, lentiviral transduction of human ACE2 (hACE2) conferred permissiveness and replication for SARS-CoV but not for hCoV-EMC. Monkey and human kidney cells (LLC-MK2, Vero, and 769-P) and swine kidney cells were permissive for both viruses, but only SARS-CoV infection could be blocked by anti-hACE2 antibody and could be neutralized by preincubation of virus with soluble ACE2. Our data show that ACE2 is neither necessary nor sufficient for hCoV-EMC replication. Moreover, hCoV-EMC, but not SARS-CoV, replicated in cell lines from Rousettus, Rhinolophus, Pipistrellus, Myotis, and Carollia bats, representing four major chiropteran families from both suborders. As human CoV normally cannot replicate in bat cells from different families, this suggests that hCoV-EMC might use a receptor molecule that is conserved in bats, pigs, and humans, implicating a low barrier against cross-host transmission. IMPORTANCE  A new human coronavirus (hCoV) emerged recently in the Middle East. The disease resembled SARS (severe acute respiratory syndrome), causing a fatal epidemic in 2002/2003. Coronaviruses have a reservoir in bats and because this novel virus is related to SARS-CoV, we investigated whether it might replicate in bat cells and use the same receptor (angiotensin-converting enzyme 2 [ACE2]). This knowledge is highly critical, because the SARS-CoV receptor influenced pathology, and its localization in the deep respiratory tract is thought to have restricted the transmissibility of SARS. Our data show that hCoV-EMC does not need the SARS-CoV receptor to infect human cells. Moreover, the virus is capable of infecting human, pig, and bat cells. This is remarkable, as human CoVs normally cannot replicate in bat cells as a consequence of host adaptation. Our results implicate that the new virus might use a receptor that is conserved between bats, pigs and humans suggesting a low barrier against cross-host transmission.

Concepts: Protein, Virus, Infection, Severe acute respiratory syndrome, Mammal, Primate, Bat, Coronavirus

194

Simultaneous infection by multiple parasite species (viruses, bacteria, helminths, protozoa or fungi) is commonplace. Most reports show co-infected humans to have worse health than those with single infections. However, we have little understanding of how co-infecting parasites interact within human hosts. We used data from over 300 published studies to construct a network that offers the first broad indications of how groups of co-infecting parasites tend to interact. The network had three levels comprising parasites, the resources they consume and the immune responses they elicit, connected by potential, observed and experimentally proved links. Pairs of parasite species had most potential to interact indirectly through shared resources, rather than through immune responses or other parasites. In addition, the network comprised 10 tightly knit groups, eight of which were associated with particular body parts, and seven of which were dominated by parasite-resource links. Reported co-infection in humans is therefore structured by physical location within the body, with bottom-up, resource-mediated processes most often influencing how, where and which co-infecting parasites interact. The many indirect interactions show how treating an infection could affect other infections in co-infected patients, but the compartmentalized structure of the network will limit how far these indirect effects are likely to spread.

Concepts: Immune system, Inflammation, Infectious disease, Bacteria, Infection, Fungus, Parasitism, Antiseptic

193

On 9 June 2008, the UK’s largest mass stranding event (MSE) of short-beaked common dolphins (Delphinus delphis) occurred in Falmouth Bay, Cornwall. At least 26 dolphins died, and a similar number was refloated/herded back to sea. On necropsy, all dolphins were in good nutritive status with empty stomachs and no evidence of known infectious disease or acute physical injury. Auditory tissues were grossly normal (26/26) but had microscopic haemorrhages (5/5) and mild otitis media (1/5) in the freshest cases. Five lactating adult dolphins, one immature male, and one immature female tested were free of harmful algal toxins and had low chemical pollutant levels. Pathological evidence of mud/seawater inhalation (11/26), local tide cycle, and the relative lack of renal myoglobinuria (26/26) suggested MSE onset on a rising tide between 06∶30 and 08∶21 hrs (9 June). Potential causes excluded or considered highly unlikely included infectious disease, gas/fat embolism, boat strike, by-catch, predator attack, foraging unusually close to shore, chemical or algal toxin exposure, abnormal weather/climatic conditions, and high-intensity acoustic inputs from seismic airgun arrays or natural sources (e.g., earthquakes). International naval exercises did occur in close proximity to the MSE with the most intense part of the exercises (including mid-frequency sonars) occurring four days before the MSE and resuming with helicopter exercises on the morning of the MSE. The MSE may therefore have been a “two-stage process” where a group of normally pelagic dolphins entered Falmouth Bay and, after 3-4 days in/around the Bay, a second acoustic/disturbance event occurred causing them to strand en masse. This spatial and temporal association with the MSE, previous associations between naval activities and cetacean MSEs, and an absence of other identifiable factors known to cause cetacean MSEs, indicates naval activity to be the most probable cause of the Falmouth Bay MSE.

Concepts: Disease, Infectious disease, Causality, Pathology, Infection, Toxin, Dolphin, Porpoise

192

In the third millennium B.C., the Indus Civilization flourished in northwest India and Pakistan. The late mature phase (2200-1900 B.C.) was characterized by long-distance exchange networks, planned urban settlements, sanitation facilities, standardized weights and measures, and a sphere of influence over 1,000,000 square kilometers of territory. Recent paleoclimate reconstructions from the Beas River Valley demonstrate hydro-climatic stress due to a weakened monsoon system may have impacted urban centers like Harappa by the end of the third millennium B.C. the impact of environmental change was compounded by concurrent disruptions to the regional interaction sphere. Climate, economic, and social changes contributed to the disintegration of this civilization after 1900 B.C. We assess evidence for paleopathology to infer the biological consequences of climate change and socio-economic disruption in the post-urban period at Harappa, one of the largest urban centers in the Indus Civilization. Bioarchaeological evidence demonstrates the prevalence of infection and infectious disease increased through time. Furthermore, the risk for infection and disease was uneven among burial communities. Corresponding mortuary differences suggest that socially and economically marginalized communities were most vulnerable in the context of climate uncertainty at Harappa. Combined with prior evidence for increasing levels of interpersonal violence, our data support a growing pathology of power at Harappa after 2000 B.C. Observations of the intersection between climate change and social processes in proto-historic cities offer valuable lessons about vulnerability, insecurity, and the long-term consequences of short-term strategies for coping with climate change.

Concepts: Disease, Infectious disease, Infection, India, Pakistan, Indus River, Punjab, Indus Valley Civilization

191

Innate Defense Regulators (IDRs) are short synthetic peptides that target the host innate immune system via an intracellular adaptor protein which functions at key signaling nodes. In this work, further details of the mechanism of action of IDRs have been discovered. The studies reported here show that the lead clinical IDR, SGX94, has broad-spectrum activity against Gram-negative and Gram-positive bacterial infections caused by intracellular or extracellular bacteria and also complements the actions of standard of care antibiotics. Based on in vivo and primary cell culture studies, this activity is shown to result from the primary action of SGX94 on tissue-resident cells and subsequent secondary signaling to activate myeloid-derived cells, resulting in enhanced bacterial clearance and increased survival. Data from non-clinical and clinical studies also show that SGX94 treatment modulates pro-inflammatory and anti-inflammatory cytokine levels, thereby mitigating the deleterious inflammatory consequences of innate immune activation. Since they act through host pathways to provide both broad-spectrum anti-infective capability as well as control of inflammation, IDRs are unlikely to be impacted by resistance mechanisms and offer potential clinical advantages in the fight against emerging and antibiotic resistant bacterial infections.

Concepts: Immune system, Inflammation, Bacteria, Microbiology, Virus, Innate immune system, Infection, Antibiotic resistance

188

Emerging infectious diseases are a key threat to wildlife. Several fungal skin pathogens have recently emerged and caused widespread mortality in several vertebrate groups, including amphibians, bats, rattlesnakes and humans. White-nose syndrome, caused by the fungal skin pathogen Pseudogymnoascus destructans, threatens several hibernating bat species with extinction and there are few effective treatment strategies. The skin microbiome is increasingly understood to play a large role in determining disease outcome. We isolated bacteria from the skin of four bat species, and co-cultured these isolates with P. destructans to identify bacteria that might inhibit or kill P. destructans. We then conducted two reciprocal challenge experiments in vitro with six bacterial isolates (all in the genus Pseudomonas) to quantify the effect of these bacteria on the growth of P. destructans. All six Pseudomonas isolates significantly inhibited growth of P. destructans compared to non-inhibitory control bacteria, and two isolates performed significantly better than others in suppressing P. destructans growth for at least 35 days. In both challenge experiments, the extent of suppression of P. destructans growth was dependent on the initial concentration of P. destructans and the initial concentration of the bacterial isolate. These results show that bacteria found naturally occurring on bats can inhibit the growth of P. destructans in vitro and should be studied further as a possible probiotic to protect bats from white-nose syndrome. In addition, the presence of these bacteria may influence disease outcomes among individuals, populations, and species.

Concepts: Immune system, Infectious disease, Bacteria, Evolution, Microbiology, Infection, Pathogen, Mammal

185

We report the results of a study we conducted using a simple multiplayer online game that simulates the spread of an infectious disease through a population composed of the players. We use our virtual epidemics game to examine how people respond to epidemics. The analysis shows that people’s behavior is responsive to the cost of self-protection, the reported prevalence of disease, and their experiences earlier in the epidemic. Specifically, decreasing the cost of self-protection increases the rate of safe behavior. Higher reported prevalence also raises the likelihood that individuals would engage in self-protection, where the magnitude of this effect depends on how much time has elapsed in the epidemic. Individuals' experiences in terms of how often an infection was acquired when they did not engage in self-protection are another factor that determines whether they will invest in preventive measures later on. All else being equal, individuals who were infected at a higher rate are more likely to engage in self-protective behavior compared to those with a lower rate of infection. Lastly, fixing everything else, people’s willingness to engage in safe behavior waxes or wanes over time, depending on the severity of an epidemic: when prevalence is high, people are more likely to adopt self-protective measures as time goes by; when prevalence is low, a ‘self-protection fatigue’ effect sets in whereby individuals are less willing to engage in safe behavior over time.

Concepts: Epidemiology, Disease, Infectious disease, Infection, Behavior, Human behavior, Epidemic, Massively multiplayer online game