The threat of swine flu has put all health care providers on high alert, and dentists and dental practices are no exception. Recent months have seen a rise and spread of the type A influenza virus .On June 11 2009 the swine flu outbreak was upgraded to a Phase 6 Pandemic. Now when the deaths are being reported because of awine flu , one should become aware of the signs and symptoms of the swine flu and should know about the preventive measures being taken to prevent the swine flu. Swine flu basically is the respiratory disease which effects the pigs and is caused by Type A influenza virus. Thus most of the human cases of swine flu happen in people who are around pigs. This article is to make to people aware about the swine flu, its symptoms and the actions needed to take to stop its spread and provide an efficient clinical practice guideline for dental professionals.
The human influenza was caused by influenza (H1N1 )virus or Swine flu which is the sub type of influenza Avirus. On April17, 2009 for the very first toime 2 cases of influenza ( H1N1) virus or Swine flu infection were diagnosed in Calfornoia and it had spread so fast that by 11 June ,2009 WHO raised the pendimis leel to phase 6. It means that the global pandemic has begun. This influenza flu was given the name of swine flu by the public media. This influenza virus has spread world wide and caused around 17,000 deaths by the start of 2010..
Influenza A viruses (Family Orthomyxoviridae, Genus Influenzavirus A) are single-stranded, negative-sense RNA viruses, comprising eight genome segments that are enveloped by a lipid bilayer containing haemagglutinin (HA) and neuraminidase (NA) glycoproteins. Both surface
proteins are the key antigen targeted by human humoural immunity and are used to subtype the virus: H (H1-H16) and 9 N (N1-N9) subtypes. Thus, theoretically there are 16×9 serologic subtypes. All subtypes are found in aquatic wildfowl; only some in other animals: H1 and H3 in pigs, H3 and H7 in horses, and recently equine H3 subtype in dogs in North America. Six serotypes infect humans: H1, H2, H3, H5, H7 and H9.8,17 In 1918, there was the highly contagious influenza outbreak caused by H1N1 influenza virus or Swine flu, and it spread to nearly every world region, commonly known as ‘Spanish flu’. This virus remains endemic in pigs to date. Infected and asymptomatic carrier pigs can transmit three swine influenza A viruses: H1N1 or Swine flu, H3N2 and H1N2, to other hosts. Their tracheal epithelial cell surface also contains α2,3-galactose- and α2,6-galactose-linked sialic acid receptors for avian (any H, N) and human (H1N1 or Swine flu and H3N2) influenza viruses, respectively. As an intermediate host, porcine natural susceptibility contributes to a host-species jump of viruses and allows a random evolution of new genetic lineages: ‘avian-like’ and ‘human-like’ swine lineages in the same cell of the same host. The ‘avian/ human reassortant’ viruses seemed to be involved in the 1957 to 1963 (A/H2N2; ‘Asian flu’) and 1968 to 1970 (A/ H3N2; ‘Hong Kong flu’) pandemics. At times, zoonotic transmission of ‘classical’ H1N1 virus or Swine flu occurs, leading to flu-like illness with a mortality rate of 17%. Human-to-human transmission is rare. However, the vaccine campaign in the USA was terminated because the vaccine caused Guillain-Barré syndrome (risk, 1/100,000) and subsequent deaths. It remains unknown how and where the new virus emerged exactly. The first two infected cases in the USA had no history of swine contact.An evolutionary analysis shows that multiple reassortment of the viral lineages may have occurred between 9.2 and 17.2 years before the current outbreak.. Genetically, S-OIV differs greatly from the predecessor swine and human influenza isolates.It is a ‘quadruple’ reassortant (derived from four lineages). Of the eight genome segments, its NA (N1) and M segments are derived from Eurasian avian-like swine H1N1 lineages. The other RNA segments are from the North American ‘triple-reassortant’ lineages: HA (H1), NP and NS from ‘classical’ porcine H1N1 lineage; PB2 and PA from avian lineage; PB1 from seasonal human H3N2 lineage. Movement of live pigs between Eurasia and North America may be the main cause of the multiple reassortment events and subsequent genetic ‘mixing-vessel’. Roles of each genome segments in viral pathogenicity were fully detailed by other authors.More data need to be collected on multigenic interplay between viral and host factors.
Influenza A's pandemic potential Influenza A's pandemic potential results from the absence of life-long immunity in humans. In case of S-OIV, it may be due to its ‘antigenic drift’: considerable changes in both HA and NA surface antigens, 27.2% and 18.2% of the amino acid sequence, from prior H1N1 isolates in 2008. The antigenic drift enables the virus to escape the pre-existing antibodies and the ‘herd immunity’. Gallaher suggested that penetration of the novel virus into humans seems unsuccessful because its estimated prevalence is far lower than that of an ‘ordinary’ strain of influenza. Either incrementally adaptive mutations in HA and NA proteins of circulating viruses (‘antigenic drift’) or further genetic reassortment in animal reservoirs may render the virus better adaptable to human replication and spread. However, in some countries such as Chile the S-IOV has indeed been replacing the seasonal influenza viruses. It was found to be the dominant strain in March
and June 2009 (autumn and winter of the southern hemisphere). Further investigations on transmissibility and virulence of the S-OIV during the winter, the typical transmission season for influenza, are desirable.
Age-stratified epidemiology data suggest that most of the confirmed S-OIV-infected cases in Mexico and the USA are ≤60 years of age. It is probable that intense immune selection pressure from the ‘herd immunity’ against the viruses occurs in ‘some’ persons aged > 60 years. This finding suggests that H1N1 viruses circulating in humans before 1950 have the closer homology to classical swine H1N1 viruses and S-OIV than seasonal H1N1 viruses. A
possible explanation of this might be that immune response is greatly stimulated after the first exposure to antigens during childhood (the ‘original antigenic sin’ concept), whereas antigenic cross-reactivity between S-OIV and seasonal H1N1 influenza viruses is uncommon.
The incubation period ranges from 2 to 7 days. The median age of 642 patients in the USA was reportedly 20 years (range, 3 months to 81 years). Diagnosis of S-OIV influenza is challenging. Similarly to seasonal influenza (with the exception of vomiting and diarrhoea), there is no specific signs. It shows normal symptoms like fever, sore throat , cough . Headache, fatigue, rhinorrhoea, chill, myalgia, nausea, abdominal pain, diarrhoea, vomiting, shortness of breath and joint pain may be found. Most symptoms are self-limiting. During the initial phase of the pandemic in Mexico and the USA, young age was found to be a risk factor of morbidity and mortality.
Some evidence suggests that in most cases, the illness is mild, self-resolving and short lived. The virus itself is less virulent than contemporary seasonal influenza viruses. However, a substantial group of patients are at high risk of developing significant complications. This ‘mild’ pandemic has led to over 10,03,536 confirmed cases and at least 17,000 deaths in more than 206 countries and overseas territories/communities.
Case-fatality rates, albeit probably underestimated, in Mexico are approximately 0.4%, ranging from 0.3% to 1.5%, and seem to be low outside that country (<0.2%). Many deaths result due to the pneumonia which is severe in form, multifocal infiltrate and rapid progression to severe sepsis with multi-organ system failure with findings such as acute respiratory distress syndrome, fever, leukocytosis or leukopenia, liver impairment, renal failure, rhabdomyolysis, and hypotension. Direct injury of respiratory epithelium with a secondary cytokine storm is a possible mechanism of tissue damage. However, severe illness and death occurs even in previously healthy persons that are usually young to middle-aged. Possible causes of death are delayed hospitalisation and delayed initiation of antiviral therapy. Further work is required to investigate the pathogenicity of this virus and the mechanisms by which it causes complications.
Antigen detection testing, either rapid/point-of-care or immunofluorescence, can differentiate between influenza A and B, but not between seasonal (H3 or H1) and the novel H1N1 influenza or Swine flu. The definite diagnosis of S-IOV is based on viral nucleic acid detection in specimens from a nose or throat swab or a combination of both.The WHO recommends using three laboratory confirmation methods:
specific reverse-transcriptase-polymerase-chain-reaction testing to distinguish S-OIV from seasonal influenza viruses;
The isolation and identification of S-OIV;
The detection of a 4-fold rise of neutralisation or haemagglutination inhibition test for antibodies to S-OIV.
In areas without established transmission, the Australian Society for Infectious Diseases and the Swine Influenza Task Force of the Thoracic Society of Australia and New Zealand suggest that anyone with acute febrile respiratory illness: a fever, ≥38 C or a good history, with cough and/or sore throat, be tested for the S-OIV. In endemic regions, testing is advisable only for severely unwell patients or those at risk of complications, or in individuals working with vulnerable populations. Early treatment is recommended whenever feasible.
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