of Swine Flu
Dr. A. Alphonse Immanuel, B.H.M.S,
Lecturer, Dept of Pathology,
Venkateswara Homoeopathic Medical College, Porur,
Mobile : 9841880991
Email : email@example.com
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
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.