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torsdag 27 april 2017

Liberia Sinoe joen varrella . uusi?tappava virustauti tai jokin entisistä pahempana 24.4. 2017 lähtien

https://www.liberianobserver.com/news/7-die-mysteriously-in-greenville/
 Residents of the port city of Greenville, Sinoe County woke up yesterday to discover that half a dozen of their kinsmen had died under mysterious circumstances.

In his reaction to the news, Derry S. Dokie, the Ministry of Health’s representative in River Cess with oversight responsibility for Sinoe County, said in a text response to the Daily Observer that there were “unexplained causes of the deaths which started at about 5 a.m.”
“Since 5 a.m. today (yesterday morning) six persons have died from suspected fever of unknown cause,” which health personnel in the county are investigating.
The Ministry of Health in Monrovia has been urgently called upon to put into place interventions before the situation gets out of hand.
The Liberian National Police (LNP) spokesperson, Sam Collins, confirmed to the Daily Observer that the LNP is investigating the deaths, and have dispatched homicide and forensic investigators to the county.
Collins spoke on a radio phone-in program yesterday after many versions of the deaths started filtering in to Monrovia from Greenville.
Collins called on the public to remain calm as the LNP is carefully reviewing the situation.
An ELBC correspondent in the county told the station that some of the dead were students and that their bodies are at the Francis Grant Hospital.
He reported that because of the intensity of the crisis, health authorities in the county were in a meeting for most of yesterday.
Meanwhile, the Ministry of Health has confirmed the news and told ELBC that investigation is ongoing to ascertain the circumstances leading to the deaths.
The Ministry of Health’s communication director, Sorbor George, said a rapid response team has already taken specimen of the dead for testing.
He said the tests will be conducted at a laboratory in Marshall, Lower Margibi County.
According to Mr. George, the victims had earlier complained of headaches and abdominal pains, and doctors struggled to resuscitate them “to no avail until they died at various intervals.”

Huomaan uutisen hesarissa keskiyöllä 27.4. 2017.  Tappava kuumetauti alkoi 24.4. 2017. 8 jo kuollut ja 6 vakavasti sairasta. 

fredag 31 mars 2017

Ruotsissa on meneillään ROTA-virusta käsittävä laaja tutkimus.

Kun tulokset on saatu kokoon, saadaan tietään myös ROTA-virustaudin merkityksestä yli 70-vuotiaiden  virusperäisissä  mahataudeissa: Siteeraan tutkimuksen netistä. Se on jopa juuri  tämän läänin projekti! http://www.researchweb.org/is/vgr/project/222941

 Hain  tietoja yli 70 vuotiaiden Rotaviruksen luonteesta, muta tietoja  puuttuu vielä
" IÄKKÄIDEN ROTAVIRUS" --"Tutkimustuloksia puuttuu."


Rotavirus genotyper i Västsverige under 2015-2017
Projektnummer : 222941
Skapat av: Maria Andersson, 2016-12-08
Senast ändrad av: Maria Andersson, 2017-02-13
Projekt inkommet till: FoU i Västra Götalandsregionen

Publicerad

1.Översiktlig projektbeskrivning

Engelsk titel

Rotavirus genotypes i western Sweden, 2015-2017.

Populärvetenskaplig sammanfattning av projektet

Gastroenterit som ger symtom i form av diarré, ofta i kombination med kräkning eller feber, orsakad av rotavirus i Sverige är relativt vanlig, särskilt hos små barn. Rotavirus indelas i undergrupper, genotyper, baserat på genetiska skillnader mellan olika virusstammar. Genom att studera förekomsten av olika virusgenotyper hos olika grupper av individer och genotypernas förändring över tid kan man få en bättre uppfattning om dessa infektioners epidemiologi. Syftet med studien är att undersöka cirkulerande rotavirus genotyper i Västsverige under åren 2015-juni 2017, både bland barn och äldre. Studien är viktigt för att bättre förstå spridningen av rotavirus i samhället och på sjukhus där infektionen också drabbar äldre, samt övervakning av genotyper inför och efter introduktionen av vaccin mot rotavirus. Rotavirus vaccin erbjuds kostnadsfritt i Västra götaland för alla barn sedan april 2016 .

Inkommande prover med misstanke om gastroenterit, för diagnostik hos Klinisk mikrobiologi, SU, analyseras med PCR avseende gastroenteritorsakande virus (rotavirus, norovirus, sapovirus, astrovirus, adenovirus). Prover med ett positivt utfall för rotavirus kommer att väljas ut för vidare analys av genotyp. Den metod som kommer att användas för genotypning i projektet är utvecklad vid vårt laboratorium, en multiplex realtids- PCR som riktar sig mot genotypspecifika gener. Humant rotavirus grupp A indelas i serotyper utefter skillnader i två ytproteinerna, glykoprotein VP7 och det proteas känsliga proteinet VP4. VP7 representerar så kallade G-typer och VP4 P-typer. Kombinationen av dessa G och P typer bestämmer genotypen. Analysen kommer att innehålla PCR-reaktioner mot 6 olika G-typer (G1, G2, G3, G4, G9 och G12) och 3 olika P-typer (P4, P6 och P8). Valet av genotyper som ingår i analysen är gjort för att kunna detektera de dokumenterat vanligaste genotyperna, G1P[8], G2P[4], G3P[8], G4P[8] och G9P[8], vilka tillsammans står för 80% av rotavirus infektionerna i världen.

Vetenskaplig sammanfattning av projektet

Infektiös gastroenterit är en relativt vanlig infektion som ger symtom i form av diarré, ofta i kombination med kräkning eller feber. Orsaken kan vara virus, bakterier eller protozoer. Virusorsakad gastroenterit orsakad av rotavirus i Sverige är relativt vanlig, särskilt hos små barn där morbiditeten är hög men mortaliteten låg. Studier av rotavirus hos äldre saknas både i Sverige och internationellt men misstänks även vara ett problem även för den populationen.
Rotavirus indelas i undergrupper baserat på genetiska skillnader mellan olika virusstammar. Genom att studera förekomsten av olika virusgenotyper hos olika grupper av individer och genotypernas förändring över tid kan man få en bättre uppfattning om dessa infektioners epidemiologi, vilket är viktigt bl.a. för beslut om förebyggande åtgärder såsom vaccination. Senaste decenniet har rotavirusvaccination införts i det generella barnvaccinationsprogrammet i många länder efter rekommendation från WHO 2009 (1), dock ännu inte i Sverige. Vaccin mot rotavirus har erbjudits kostnadsfritt lokalt i vissa regioner och från och med april 2016 gäller detta även Västra götalands regionen. Tidigare studier av rotavirus har fokuserat på barn och den senaste studien redovisar genotyper som cirkulerade för snart 10 år sedan (2). För att kunna studera effekten av vaccinet är det viktigt att dokumentera den uppskattade sjukdomsbördan av rotavirus men även vilka genotyper av viruset som cirkulerar före, under och efter introduktion av vaccin (3).
För att dokumentera vilka genotyper som cirkulerade före eventuellt införande av rotavirus vaccin analyserades alla rotavirus prover med avseende på genotyp, som utföll positiva vid rutin diagnostik på Klinisk Mikrobiologi, SU, under 2010-2014. Resultatet av denna studie visade stora förändringar över tid av cirkulerande genotyp samt en skillnad av genotypsdistributionen hos barn och äldre.
Syfet med aktuell studie är att undersöka cirkulerande genotyper i Västsverige under åren 2015-juni 2017, vilket medför en uppdatering av kunskapsläget precis före och under införande av vaccination samt ny kunskap om samband mellan infektioner hos barn och äldre.Följande frågeställningar föranleder arbetet av att studera cirkulerande rotavirus genotyper, i anslutning till och under införandet av vaccin:
  • Vilka rotavirusgenotyper förekommer i olika åldersgrupper under 2015-2017 i Västsverige
  • Har det skett en förändring i cirkulerande genotyper under 2015-2017 jämfört med 2010-2014?
  • Finns det skillnader i cirkulerande rotavirus genotyper som kan härledas till införande av vaccin?
  • Ändras eller kvarstår skillnaden i rotavirus frekvens mellan barn och äldre samt finns det ett mönster i vilken genotyp som i större utsträckning drabbar en viss åldersgrupp under 2015-2017 i relation till 2010-2014?
Påvisning av rotavirus i rutindiagnostik utförs med realtids-PCR som riktar sig mot en generell gen för humant rotavirus grupp A, NSP3. Den metod som kommer att användas för genotypning i projektet är utvecklad vid vårt laboratorium, en multiplex realtids- PCR som riktar sig mot genotypspecifika gener. Humant rotavirus grupp A indelas i serotyper utefter skillnader i två ytproteinerna, glykoprotein VP7 och det proteas känsliga proteinet VP4. VP7 representerar så kallade G-typer och VP4 P-typer. Kombinationen av dessa G och P typer bestämmer genotypen (4,5). Analysen kommer därför att innehålla PCR-reaktioner mot 6 olika G-typer (G1, G2, G3, G4, G9 och G12) och 3 olika P-typer (P4, P6 och P8). Valet av genotyper som ingår i analysen är gjort för att kunna detektera de dokumenterat vanligaste genotyperna, G1P[8], G2P[4], G3P[8], G4P[8] och G9P[8], vilka står för 80% av rotavirus infektionerna i världen (6, 7). Om ett prov utfaller negativt för ovanstående genotyper kommer det att genomgå efterföljande analys med publicerad metod (8) för sekvensering.
Den främsta betydelsen av detta arbete är att öka den epidemiologiska kunskapen och skapa ett utgångsläge som ger möjlighet att studera effekten av införande av rotavirus vaccin på molekylär nivå. Trots att upptagningsområdet för studien är begränsat till Väst Sverige kan den ha ett nationellt intresse då antalet studier i Sverige är mycket få och dessutom utförda för många år sedan. Vikten av den här typen av studier har visats i många länder, där utarbetade rutiner föra att studera rotavirus vaccinet redan finns tillgängliga. Studien inkluderar alla åldersgrupper, till skillnad från majoriteten av rotavirus studier i världen som framför allt riktar sig mot barn, vilket även det kan ge oss ökad kunskap om hur rotavirus infektioner beter sig i olika åldersgrupper, med tyngdvikt på de över 70 år. Att studera rotavirus lokalt kan även ge Smittskyddsläkare stöd i att utarbeta en uppföljningsplan för rotavirusvaccination efter ett regionalt införande.
Referenser
1. Weekly epidemiological record. 2009 Dec 17;:1–8.
2. Rinder M, Tran AN, Bennet R, Brytting M, Cassel T, Eriksson M, et al. Burden of severe rotavirus disease leading to hospitalization assessed in a prospective cohort study in Sweden. Scand J Infect Dis. 2014 Apr;46(4):294–302.
3. Rotavirusinfektion i Sverige; Sjukdomsbörda, genotypsdistribution, förväntad effekt av rotavirusvaccin och förslag på en nationell övervakningsplan; Folkhälsomyndigheten Sverige. 2015
4. Estes MK, Kapikian AZ. Rotaviruses, p 1917–1974. Fields virology; 2007.
5. MATTHIJNSSENS J, Ciarlet M, McDonald SM, Attoui H. Uniformity of rotavirus strain nomenclature proposed by the Rotavirus Classification Working Group (RCWG) - Springer. Archives of …. 2011.
6. Gentsch JR, Laird AR, Bielfelt B, Griffin DD, Bányai K, Ramachandran M, et al. Serotype diversity and reassortment between human and animal rotavirus strains: implications for rotavirus vaccine programs. J Infect Dis. 2005 Sep 1;192 Suppl 1:S146–59.
7. Banyai K, LÁSZLÓ B, Duque J, Steele AD, Nelson E. Systematic review of regional and temporal trends in global rotavirus strain diversity in the pre rotavirus vaccine era: Insights for understanding the impact of rotavirus vaccination programs. Vaccine. 2012.
8. van Doorn LJ, Kleter B, Hoefnagel E, Stainier I, Poliszczak A, Colau B, et al. Detection and Genotyping of Human Rotavirus VP4 and VP7 Genes by Reverse Transcriptase PCR and Reverse Hybridization. J Clin Microbiol. 2009 Aug 31;47(9):2704–12.

Typ av projekt

Forskningsprojekt

MeSH-termer för att beskriva typ av studier

Hälso- och sjukvårdsundersökningar (Health Care Surveys)
Retrospektiva studier (Retrospective Studies)

(Endast valda alternativ visas. Klicka här om du vill se alla alternativ)

MeSH-termer för att beskriva ämnesområdet


NOROVIRUKSISTA- ( vinterkräkssjuka)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3185648/
Vahingoittaa suolinukkaa ,  vaurion paranemiseen menee 2 3 viikkoa 
 Pylorustienoo . focus.

Virusripuleista: ROTAVIRUS

(Muistiin 31.3. 2017, käännettävä myöhemmin)
 http://abdominalkey.com/viral-diarrhea/
Rotavirus tuhoaa  enterosyyttejä. Vähentää suolen toimivaa pintaa.Nukkakärki tuhoutuu ja kryptaalue kompensatorisesti proliferoituu. Monimuotoinen imeyttämisvaje sekä joniripuli, koleramaineen nesteen menetys.

Viral Diarrhea

Established
Probable
Possible in selected children
Rotavirus
Torovirus
HIV
Norovirus
Aichi virus enterovirus 22
Cytomegalovirus
Adenovirus
 
Epstein–Barr virus picobirnavirus
Astrovirus
  
The viruses most frequently responsible for acute gastroenteritis in children belong to four distinct families: rotaviruses, caliciviruses, astroviruses, and enteric adenoviruses. Rotavirus and norovirus are the two leading agents of acute diarrhea. Other viruses, such as toroviruses, picornaviruses (the Aichi virus), and enterovirus 22, play a minor epidemiological role. Finally, selected viruses induce diarrhea only in children at risk. These include cytomegalovirus, Epstein–Barr virus, picobirnaviruses, and HIV.

Pathophysiology of Viral Diarrhea

In the classic and simple view, the pathogenesis of diarrhea may be divided into osmotic and secretory. Viral diarrhea was originally believed to be the consequence of endoluminal fluid accumulation osmotically driven by non-absorbed nutrients due to cell invasion and epithelial destruction by enteropathogenic agents. It is now known that several mechanisms are responsible for diarrhea, depending on the specific agents and the host features. In addition, selected viruses have multiple virulence pathways that act synergistically to induce diarrhea.

The mechanisms of diarrhea induced by group A rotaviruses have been extensively investigated and provide a paradigm of the pathophysiology of viral diarrhea [2022]. Rotavirus has both a tissue- and a cell-specific tropisms, and it infects the mature enterocyte of the small intestine. The first step is virus binding to specific receptors located on the cell surface, the GM1 ganglioside. However, different rotavirus strains bind in either a sialic-acid-dependent or sialic-acid-independent fashion. Most rotaviruses, including all human strains, infect polarized enterocytes through both the apical and the basolateral side, in a sialic-acid-independent manner, suggesting the presence of different receptors. The early stages of rotavirus binding involve the viral protein (VP4) spike attachment and cleavage. After binding, rotavirus enters into the cell by a multistep process that requires both VP7 and VP4 proteins. Infection of the villous enterocytes leads to cell lysis, compromising nutrient absorption and driving fluid into the intestinal lumen through an osmotic mechanism. However, the destruction of villus-tip cells induces a compensatory proliferation of crypt cells. These immature enterocytes physiologically maintain a secretive tone, thus contributing to diarrhea with ion secretion, as the result of the imbalance between absorptive villous and secretory crypt cells. Thus, the cytopathic effect of rotavirus results in both osmotic and secretory diarrhea . Histological changes induced by rotavirus infection occur within 24 h of infection in animal models .

The enteric nervous system may also play a direct role in inducing fluid secretion, similar to that induced by cholera toxin and other intestinal secretagogues. The molecular mechanisms of fluid secretion have also been investigated. Rotavirus induces an increase in intracellular calcium levels, which is responsible for the disassembly of microvillar F-actin, the perturbation of cellular protein trafficking, the damage of tight junction, with a disruption of cell–cell interaction and cytolysis .

In children with rotavirus infection, the onset of diarrhea is abrupt and occurs in the absence of histological changes, suggesting that in the initial phase of the infection a secretory pathway is responsible for diarrhea. The identification of the nonstructural protein (NSP4), an enterotoxin produced by rotavirus, responsible for fluid secretion but not for epithelial damage may explain this phenomenon. NSP4 is a multifunctional virulence factor (VF), as it possesses the following features (Fig. 14.1): It is released from infected cells and enters the cells through a specific receptor causing calcium-dependent chloride secretion. NSP4 also alters plasma membrane permeability and is cytotoxic. NSP4 is the only rotavirus gene product capable of eliciting intracellular calcium mobilization. NSP4 further contributes to diarrheal pathogenesis by directly altering enterocyte actin distribution and paracellular permeability. Finally, NSP4 plays a role in the inhibition of the Na+-dependent glucose transporter (SGLT-1). Glucose absorption as well as disaccharidase activities are impaired in rotavirus enteritis, whereas the Na/amino acid co-transporters are not involved .
Fig. 14.1
Combined effects by NSP4 in the pathophysiology of rotavirus diarrhea. Rotavirus infects epithelial cells of the small intestine, replicates, and induces cell lysis. NSP4 is released by infected cells and functions as a Ca2+-dependent enterotoxin triggering Cl secretion. It decreases fluid and electrolyte transport by inhibiting Na–glucose symport SGLT1 and, possibly Na–K adenosine triphosphatase (ATPase). It also impairs disaccharidase expression. Furthermore, rotavirus and/or NSP4 may diffuse underneath the intestinal epithelium activating secretory reflexes in the enteric nervous system. Late during the infection, an inflammatory response in the lamina propria may be detected, and the production of inflammatory substances and cytokines may further contribute to the increase of intestinal permeability and diarrhea. NSP4 nonstructural protein, SGLT-1 Na+-dependent glucose transporter, NO nitrous oxide. (Reprinted with permission from Ref. [19], 2004, Fig. 9.3, p. 131)
Rotavirus diarrhea may also have an inflammatory component. The induction of cytokines is important in developing an inflammatory and immune response, especially in intestinal infection caused by bacteria. In rotavirus infection, limited inflammation is detected by histological studies, suggesting that cytokines are effective in inducing a host immune response to rotavirus diarrhea. However, it has been shown that rotavirus-infected enterocytes activate nuclear factor kappa B (NF-κB) and the production of chemokines interleukin (IL)-8, Rantes, and growth related oncogene (GRO)-a, of interferon (IFN)-α, and of granulocyte/macrophage–colony-stimulating factor (GM-CSF). Recent evidence suggests that rotavirus-induced diarrhea may be also associated with an increase of intestinal motility through the stimulation of myenteric nerve plexus [23].
In conclusion, the primary target of rotavirus is the enterocyte, which is induced to secrete fluids and electrolytes and is subsequently destroyed. On the other hand, the enterocyte acts as a sensor to the mucosa with the production of viral and endogenous factors and the activation of other cell types including neurons. Thus, rotavirus-induced diarrhea is a multistep and multifactorial event, in which fluid secretion and cell damage are observed in a precise sequence, as shown in an intestinal cell line-based experimental model [24] (Fig. 14.2). A summary of the multiple mechanisms involved in the rotavirus–intestine interaction is provided in Table 14.2 .
Fig. 14.2
Biphasic effect of rotavirus in Caco-2 cells. Rotavirus induces a biphasic response, in an in vitro model of infection in Caco-2 enterocytes mounted in Ussing chambers. An early secretion is evident in the first few hours of infection, with a peak at 2-h postinfection, as shown by the increase in short circuit current (Isc, µA). Subsequently, rotavirus exerts a cytotoxic effect with a loss of tissue integrity, as demonstrated by the fall of transepithelial resistance (TER) (Ohm/cm2) which is evident at 24-h postinfection. The results suggest that rotavirus diarrhea is initially the result of an early secretory mechanism and of a subsequent osmotic pathway, due to cell damage and loss of functional absorptive surface, leading to nutrient malabsorption. (Reprinted with permission from Ref. [19]. Reprinted from Ref. [24], by Permission of Oxford University Press)
Table 14.2
Mechanisms involved in rotavirus-induced diarrhea
Mechanism
Effect
Enterocyte damage
Nutrient malabsorption/osmotic diarrhea
Crypt cell proliferation
Ion and water secretion/secretory diarrhea
NSP4 production
Increase in intracellular calcium, chloride secretion/secretory diarrhea
NSP4 inhibition of SGLT-1
Glucose malabsorption/osmotic diarrhea
Neuromediated vascular ischemia
Secretory diarrhea induced by neurotransmitter release
Inflammation
NF-kB, IL-8, Rantes release/osmotic, and secretory diarrhea
Stimulation of myenteric nerve plexus
Increase in intestinal motility
NSP4 nonstructural protein, NF-κB nuclear factor kappa B, IL interleukin, SGLT-1 Na+ -dependent glucose transporter



onsdag 1 mars 2017

Lancetissa 11.2. 2017 ZIKA-viruksesta

A year ago, on Feb 1, 2016, WHO declared the Zika virus epidemic a public health emergency. In a brave show of leadership no doubt spurred by the embarrassment of failing to act sooner on the Ebola outbreak threats, Director-General Margaret Chan sounded the alarm about the potential links between Zika virus and rising neurological disorders despite a lack of conclusive data. By doing so she stimulated an international collective effort, scientific research, and funding that helped stabilise the crisis.

 A year on she has reflected on the rightness of that decision, writing in a commentary on WHO's website that it strengthened integrated surveillance for mosquito-borne viruses, and accelerated understanding of the modes of transmission and the abnormalities associated with congenital Zika virus syndrome. The coordination that occurred between international and national authorities and health professionals, especially in Latin American countries, to detect, diagnose, and characterise cases of microcephaly is commendable.
But the warm glow of that reflection must be tempered by the challenges ahead. It would be tempting to laud the Zika response as a success and redirect attention to other emergent issues. To do so would ignore the continued spread of Zika virus and its under-appreciated long-term effects. As WHO shifts direction under a new Director-General, we need even bolder Zika leadership that keeps victims and their families firmly on our public health agenda.

As of Feb 1, 2017, the number of countries reporting a Zika virus outbreak since 2015 has grown to 59, 48 of them in North and South America. Seven countries have reported active local transmission of the virus in 2016 or 2017. 13 countries report person-to-person transmission. New affected areas have emerged including Angola, already struggling under yellow fever and cholera epidemics, which reported its first two cases in January.

Continued geographical spread of Zika virus would be a challenge enough were it not for the anticipated long-term effects. Chan's commentary says WHO “must be ready for the long-haul” but misses the opportunity to urge and specify international attention, research, and resources for the individuals left devastated by Zika virus. It leaves invisible the needs of thousands of children, their families, and future families; and overlooks the responsibility of the world's community to support them.

Indeed, Zika can only be considered a long-term epidemic. 6 months ago Bruce Aylward, then head of WHO's outbreaks and health emergencies cluster, told The Lancet that “we don't know what the full spectrum of the Zika-caused congenital defects will be. Will apparently unaffected children whose mothers had Zika virus infection in pregnancy develop normally? Will they be able to walk and talk normally? Will they be mentally impaired or have other problems that only become evident years later?” We still don't know. Fully supported research to understand, track, and address the long-term sequelae of congenital, perinatal, and paediatric Zika virus infection on children's development must be prioritised.

Currently, almost 3000 cases of Zika-related microcephaly or other CNS defects have been recorded in 29 countries. Brazil has been hardest hit: 2366 babies have been born to Zika-infected women and their families, many already vulnerable and lacking the resources to shoulder the burdens of care. Whereas some of these affected children will lead normal lives, many others with congenital Zika virus syndrome will experience severe disability and need long-term medical attention. Medical interventions could involve intensive physical therapy, treatments for neurological impairments, feeding tubes, and others. 

The US Centers for Disease Control has estimated the costs of treating such children to be tens of millions of dollars. And microcephaly is likely to represent only a portion of those affected. Others will be born blind or deaf, or suffering from seizures, irritability, or swallowing disorders. Even in the absence of microcephaly, congenital brain abnormalities might be present. That Zika virus infection can trigger the autoimmune disorder Guillain-Barré syndrome in adults worsens the long-term effects. A portion of those affected will die without access to respiratory and intensive care; many more will live with disability. 

Adding to Zika's economic drain on societies because of lost productivity due to neurological deficits, these medical consequences amount to another kind of Zika public health emergency.
As the world waits for a vaccine, public health efforts will necessarily focus on prevention in the form of mosquito control and travel advisories. But health agencies like WHO, public health researchers, and policy makers must also not forget the individuals affected. They require our unrelenting attention.
For The Lancet's Zika virus resource centre see http://www.thelancet.com/campaigns/zika

Lancetissa rabieksesta uutta

http://www.who.int/bulletin/volumes/95/3/16-173039.pdf

  • Introduction
    Rabies is a preventable yet fatal disease that is responsible for
    approximately 59000 deaths each year.
    However, widespread underreporting of rabies cases means that the actual number
    of deaths is likely to be higher. Poor and rural populationsare disproportionately affected, with the majority of deathsoccurring in children younger than 15years in Asia and Af-rica.
    2
    Ninety-nine per cent of human rabies cases result from dog bites and, once symptoms begin, the disease is almostinvariably fatal.
    3
    Human rabies is preventable through canine vaccination to eliminate rabies at its source or by administering rabies vaccines and immunoglobulin following bites,scratches or saliva exposure from suspected rabid mammals (i.e. postexposure prophylaxis).
    4
    Another preventive strategy is pre-exposure prophylaxis, which involves giving a series of intramuscular or intradermal injections of rabies vaccine to prime the immune system. This enables fast recall of memory immune responses once a person is re-exposed to the virus.
    4
    Moreover, people who have received pre-exposure prophylaxis require fewer doses of postexposure rabies vaccine and can be treated without rabies immunoglobulin, which is costly and difficult to procure.
    4
    Although preventing rabies in dogs is the most cost-effective way of preventing human rabies deaths, pre-exposure prophylaxisis valuable for people at a high disease risk,
    • 5
      particularly inareas where controlling disease in the animal reservoir is difficult or has
       not been implemented and in areas where access to postexposure prophylaxis and rabies immunoglobulin is unreliable or nonexistent. National pre-exposure prophylaxis
       programmes for high-risk populations have been implemented in Peru and the Philippines.
      6
      ,
      7
      In 2010, a World Health Organization (WHO) position paper on rabies vaccines called
       for studies on the feasibility, cost–effectiveness and long-term impact of incorporating
      vaccines derived from cell culture or embryonated eggs into immunization programmes
       for children where canine rabies is a public health problem.
      5
      The paper also made recommendations on pre-exposure prophylaxis regimens and on the
      frequency of booster vaccinations and serological surveillance for at-risk individuals, 
      such as veterinarians. The aim of this study was to review the scientific literature published between 2007 and 2016, as well as field data, to assess the current use and cost–
      effectiveness of pre-exposure rabies prophylaxis(excluding travel vaccines), particularly in children and in high-risk settings, in the context of recommendations made in
      the 2010 WHO rabies vaccine position paper on pre-exposure prophylaxis and booster vaccine administration