November 2010|Vol 7|Issue 11

November 2010 | Volume 7 | Issue 11


Pathogenesis of Swine Flu


Dr. A. Alphonse Immanuel, B.H.M.S,
Lecturer, Dept of Pathology,
Venkateswara Homoeopathic Medical College, Porur,
Mobile : 9841880991
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         The Influenza viruses are classified into 3 major genera (A, B, and C),of which influenza A is of greatest clinical significance.

    Each genus is further classified into serotypes based on the viral proteins hemagglutinin (HA) and neuraminidase (N). Among the various possible subtypes (denoted by combinations of H and N) of seasonal influenza A virus, only 3 (H1N1, H1N2, and H3N2) are currently circulating among humans.Novel influenza A (H1N1) virus (also known as new influenza virus, swine-like influenza virus, swine-origin influenza virus, and colloquially as “swine flu”) is a novel form of influenza A virus resulting from a combination of genes derived from 2 types of swine influenza, one of which is, in turn, a “triple reassortant” of human, avian, and swine influenza A strains.This new virus is not only antigenically and genetically distinct from seasonal influenza A (H1N1) virus, but is also usually sensitive to oseltamivir, a neuraminidase inhibitor to which 10.9% of recent seasonal influenza A viruses were resistant.

    The pathologic features of (seasonal) influenza pneumonia are well documented. Most existing pathologic data on influenza pneumonia are derived from autopsy series, with only a few reports of biopsy findings.

    The histologic findings of influenza pneumonia can be divided into those caused by the virus and those attributable to superimposed bacterial infection. The two often coexist in the same case. Findings attributed to viral infection include parenchymal and airway abnormalities. The major parenchymal abnormalities are DAD and intra-alveolar hemorrhage. DAD may be seen as early as the second day of illness and as late as day 21.It is more prominent in patients requiring mechanical ventilation and supplemental oxygen. Abnormalities in the trachea, bronchi, and bronchioles occur in most cases, the most important being acute necrotizing tracheobronchitis, bronchitis, or bronchiolitis. These changes appear between days 3 and 13 of the illness. Mild chronic inflammation of the airways and degenerative changes of the lining epithelium are also common. Immunohistochemical techniques have demonstrated viral antigens within airway epithelium.

    Another major finding in the airway mucosa in influenza is squamous metaplasia,which sometimes is so striking as to suggest a neoplastic squamous proliferation.Unlike many other viral infections, viral inclusions and viral cytopathic effects are not seen in influenza infection. The major finding attributable to superimposed bacterial infection is acute bronchopneumonia, characterized by a neutrophilic infiltrate within alveolar spaces, accompanied by varying amounts of fibrin and edema. The superimposed bacterium is mostly Staphylococcus aureus, S pneumoniae, or Haemophilus influenzae.

    With regard to pathology, the autopsy findings were consistent with a viral pneumonia and fit well with descriptions of “uncomplicated influenza pneumonia” in the literature. The major histologic findings were DAD and intra-alveolar hemorrhage, and there was no evidence of superimposed bacterial bronchopneumonia. Necrotizing bronchitis/bronchiolitis and squamous metaplasia, findings frequently seen in seasonal influenza A, were absent or inconspicuous. A specific diagnosis of influenza A (H1N1) viral pneumonia was made only retrospectively, after results of postmortem studies were available.}

    Novel influenza A (H1N1) virus infection may be encountered in widely disparate clinical settings and may result in strikingly dissimilar pathologic findings. The diagnosis should be suspected clinically in patients with an unexplained flu-like illness or acute pneumonia. Pathologists should add novel influenza A (H1N1) virus infection to the list of causes of DAD. Classic findings of influenza pneumonia, such as necrotizing bronchitis/bronchiolitis and squamous metaplasia, may not be prominent. A superimposed acute bacterial bronchopneumonia may mask underlying virus-related histologic changes. The diagnosis can be confirmed by rRT-PCR on specimens obtained at autopsy.
    Characteristics of H1N1 “Mutant genes”

    The biggest concern is that H1N1 could mutate into something much nastier. Influenza viruses not only mutate quickly and unpredictably, but they can swap genes, especially if a person or animal becomes infected with two strain.

    A leading virologist has described the new H1N1 influenza virus as “very unstable”, meaning it could mix and swap genetic material when exposed to other viruses’s at once.

    “Both H1N1 and H5N1 are unstable so the chances of them exchanging genetic material are higher, whereas a stable (seasonal flu) virus is less likely to take on genetic material.”

    While H1N1 appears to be mild so far with many infected people recovering even without treatment, the H5N1 has a mortality rate of between 60 to 70 percent.

    “Guan: an expert on both the H5N1 and SARS, has analysed the genetic sequences of the new virus, which is a triple reassortant containing genetic material from swine, human and bird.He said there was a huge information gap due to a lack of regular surveillance on animal disease.

    Each one of the eight gene segments in the new virus has been seen in pigs in the past 10 years, but experts have no clue when this new H1N1 virus strain first appeared and in which animal species it had been incubating.

    “We know when each gene segment appeared, but we don’t know when this strain first appeared, there is an information gap of about five to 10 years, from 1999 to 2009.”We don’t know if this reassortment happened in pigs or human. It’s likely to have come from pigs because all the segments have been found in pig.