Population-level analyses often use average quantities to describe heterogeneous systems, particularly when variation does not arise from identifiable groups. A prominent example, central to our current understanding of epidemic spread, is the basic reproductive number, R(0), which is defined as the mean number of infections caused by an infected individual in a susceptible population. Population estimates of R(0) can obscure considerable individual variation in infectiousness, as highlighted during the global emergence of severe acute respiratory syndrome (SARS) by numerous 'superspreading events' in which certain individuals infected unusually large numbers of secondary cases. For diseases transmitted by non-sexual direct contacts, such as SARS or smallpox, individual variation is difficult to measure empirically, and thus its importance for outbreak dynamics has been unclear. Here we present an integrated theoretical and statistical analysis of the influence of individual variation in infectiousness on disease emergence. Using contact tracing data from eight directly transmitted diseases, we show that the distribution of individual infectiousness around R(0) is often highly skewed. Model predictions accounting for this variation differ sharply from average-based approaches, with disease extinction more likely and outbreaks rarer but more explosive. Using these models, we explore implications for outbreak control, showing that individual-specific control measures outperform population-wide measures. Moreover, the dramatic improvements achieved through targeted control policies emphasize the need to identify predictive correlates of higher infectiousness. Our findings indicate that superspreading is a normal feature of disease spread, and to frame ongoing discussion we propose a rigorous definition for superspreading events and a method to predict their frequency.

/pdf/superspreading-and-the-effect-of-individual-variation-on-1hf80n09pb.pdf

Superspreading and the effect of individual variation on disease emergence

Emerging infectious diseases , Emerging infectious diseases , کتابخانه دیجیتالی دانشگاه علوم پزشکی و خدمات درمانی شهید بهشتی

/pdf/emerging-infectious-diseases-t66fc9g8n5.pdf

Emerging Infectious Diseases

Crimean-Congo haemorrhagic fever (CCHF) is an often fatal viral infection described in about 30 countries, and it has the most extensive geographic distribution of the medically important tickborne viral diseases, closely approximating the known global distribution of Hyalomma spp ticks. Human beings become infected through tick bites, by crushing infected ticks, after contact with a patient with CCHF during the acute phase of infection, or by contact with blood or tissues from viraemic livestock. Clinical features commonly show a dramatic progression characterised by haemorrhage, myalgia, and fever. The levels of liver enzymes, creatinine phosphokinase, and lactate dehydrogenase are raised, and bleeding markers are prolonged. Infection of the endothelium has a major pathogenic role. Besides direct infection of the endothelium, indirect damage by viral factors or virus-mediated host-derived soluble factors that cause endothelial activations and dysfunction are thought to occur. In diagnosis, enzyme-linked immunoassay and real-time reverse transcriptase PCR are used. Early diagnosis is critical for patient therapy and prevention of potential nosocomial infections. Supportive therapy is the most essential part of case management. Recent studies suggest that ribavirin is effective against CCHF, although definitive studies are not available. Health-care workers have a serious risk of infection, particularly during care of patients with haemorrhages from the nose, mouth, gums, vagina, and injection sites. Simple barrier precautions have been reported to be effective.

/pdf/crimean-congo-haemorrhagic-fever-1mjnt47obh.pdf

Crimean-Congo haemorrhagic fever

Background: Zika virus (ZIKV) is a mosquito-borne flavivirus distributed throughout much of Africa and Asia. Infection with the virus may cause acute febrile illness that clinically resembles dengue fever. A recent study indicated the existence of three geographically distinct viral lineages; however this analysis utilized only a single viral gene. Although ZIKV has been known to circulate in both Africa and Asia since at least the 1950s, little is known about the genetic relationships between geographically distinct virus strains. Moreover, the geographic origin of the strains responsible for the epidemic that occurred on Yap Island, Federated States of Micronesia in 2007, and a 2010 pediatric case in Cambodia, has not been determined. Methodology/Principal Findings: To elucidate the genetic relationships of geographically distinct ZIKV strains and the origin of the strains responsible for the 2007 outbreak on Yap Island and a 2010 Cambodian pediatric case of ZIKV infection, the nucleotide sequences of the open reading frame of five isolates from Cambodia, Malaysia, Nigeria, Uganda, and Senegal collected between 1947 and 2010 were determined. Phylogenetic analyses of these and previously published ZIKV sequences revealed the existence of two main virus lineages (African and Asian) and that the strain responsible for the Yap epidemic and the Cambodian case most likely originated in Southeast Asia. Examination of the nucleotide and amino acid sequence alignments revealed the loss of a potential glycosylation site in some of the virus strains, which may correlate with the passage history of the virus. Conclusions/Significance: The basal position of the ZIKV strain isolated in Malaysia in 1966 suggests that the recent outbreak in Micronesia was initiated by a strain from Southeast Asia. Because ZIKV infection in humans produces an illness clinically similar to dengue fever and many other tropical infectious diseases, it is likely greatly misdiagnosed and underreported.

/pdf/genetic-characterization-of-zika-virus-strains-geographic-3l36pxg54p.pdf

Genetic Characterization of Zika Virus Strains: Geographic Expansion of the Asian Lineage

ObjectiveTo develop consensus-based recommendations for measures to be taken
by medical and public health professionals if hemorrhagic fever viruses (HFVs)
are used as biological weapons against a civilian populationParticipantsThe Working Group on Civilian Biodefense included 26 representatives
from academic medical centers, public health, military services, governmental
agencies, and other emergency management institutionsEvidenceMEDLINE was searched from January 1966 to January 2002 Retrieved references,
relevant material published prior to 1966, and additional sources identified
by participants were reviewedConsensus ProcessThree formal drafts of the statement that synthesized information obtained
in the evidence-gathering process were reviewed by the working group Each
draft incorporated comments and judgments of the members All members approved
the final draftConclusionsWeapons disseminating a number of HFVs could cause an outbreak of an
undifferentiated febrile illness 2 to 21 days later, associated with clinical
manifestations that could include rash, hemorrhagic diathesis, and shock
The mode of transmission and clinical course would vary depending on the specific
pathogen Diagnosis may be delayed given clinicians' unfamiliarity with these
diseases, heterogeneous clinical presentation within an infected cohort, and
lack of widely available diagnostic tests Initiation of ribavirin therapy
in the early phases of illness may be useful in treatment of some of these
viruses, although extensive experience is lacking There are no licensed vaccines
to treat the diseases caused by HFVs

https://jamanetwork.com/journals/jama/articlepdf/194908/JST20006.pdf

Hemorrhagic Fever Viruses as Biological Weapons: Medical and Public Health Management

A restricted, hospital-centred outbreak of Lassa fever involving 28 persons occurred early in 1970 in Jos, Nigeria 24 patients were in hospital Every patient, save the index, could be traced to some prior known human source of infection Complement-fixing antibody to Lassa virus was detected in the sera of only 4 of 172 family and hospital contacts bled These 4 persons had all been ill Animal studies have so far failed to reveal a non-human host

Lassa fever. Epidemiological aspects of the 1970 epidemic, Jos, Nigeria.

The Virus Research Laboratory of the University of Ibadan, Nigeria, was notified on 23 October 1969 that cases of suspected yellow fever had occurred in the Jos area. The diagnosis was confirmed by virus isolation and the existence of a widespread outbreak on the Jos Plateau and adjacent areas was established. This was the first recognized epidemic of yellow fever in Nigeria since 1953. Between September and the end of December 1969, an estimated total of 252 patients with yellow fever were hospitalized. The case—fatality ratio for hospitalized patients was approximately 40%. The diagnosis of yellow fever was confirmed by virus isolation, serology, or pathology in 55 patients. It is estimated that up to 100 000 cases of yellow fever may have occurred during the epidemic.

Epidemiological aspects of the 1969 yellow fever epidemic in Nigeria.

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Lassa fever. Epidemiological aspects of the 1970 epidemic, Jos, Nigeria.

Epidemiological aspects of the 1969 yellow fever epidemic in Nigeria.