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Transcript
INTRODUCTION
During the spring of 2009, a novel influenza A (H1N1) virus of swine origin emerged among
people in Mexico. This spread with travelers worldwide resulting in the first influenza pandemic since
1968. As of October 2009, 195 countries have confirmed cases of H1N1. Even though majority of
illnesses caused by this pandemic have been self-limited causing mild-to-moderate uncomplicated
disease, there were reports of severe complications including fatal outcomes in all parts of the globe.1
As of February 2010, pandemic influenza transmission remains active but geographically localized to
regional in the South and Southeast Asia. The overall intensity of the disease activity was reported to be
low to moderately severe in most areas.2
The H1N1 pandemic differs in its pathogenicity from seasonal influenza in two aspects: First, the
impact of the infection resulted in a wider range in terms of age particularly among children and young
adults. This is mainly because the majority of human population has little or no pre-existing immunity to
the virus. Secondly, the virus is known to affect even the lower respiratory tract causing rapidly
progressive pneumonia.1
Epidemiology
The H1N1 2009 pandemic had highest attack rates among children and young adults. A wide
clinical spectrum of disease ranging from non-febrile, mild upper respiratory tract illness, febrile
influenza-like illness (ILI) to severe or even fatal complications, including rapidly progressive pneumonia
has been described. Most commonly reported symptoms included cough, fever, sore throat, muscle
aches, malaise, and headache. In some patients, gastrointestinal symptoms such as nausea, vomiting
and diarrhea have been reported. The incubation period appears to be approximately 2-3 days, but
could range up to 7 days.1
In some countries, approximately 10-30% of hospitalized patients have required admission to
intensive care units. These patients include those who experienced rapidly progressive lower respiratory
tract disease, respiratory failure, and acute respiratory distress syndrome (ARDS) with refractory
hypoxemia. Other severe reported complications include secondary invasive bacterial infection, septic
shock, renal failure, multiple organ dysfunction, myocarditis, encephalitis, and worsening of underlying
chronic disease conditions such as asthma, chronic obstructive pulmonary disease (COPD), or congestive
heart failure (CHF).1
Risk Factors
According to data gathered, risk factors for developing severe disease are similar to those risk
factors identified for complications from seasonal influenza. These include infants and young children, in
particular <2 years, pregnant women, persons of any age with chronic pulmonary disease (e.g. asthma,
COPD), persons of any age with chronic cardiac disease (e.g. CHF), persons with metabolic disorders (e.g.
diabetes), persons with chronic renal disease, chronic hepatic disease, certain neurological conditions,
hemoglobinopathies, or immunosuppression, whether due to primary immunosuppressive conditions,
such as HIV infection, or secondary conditions, such as immunosuppressive medication or malignancy,
children receiving chronic aspirin therapy, persons aged 65 years and older. There is also a higher risk
among obese and among disadvantaged and indigenous populations.1,2
Diagnosis
Laboratory diagnosis of pandemic H1N1 virus has important implications for case management,
such as infection control procedures, consideration of antiviral treatment options and avoiding the
inappropriate use of antibiotics. Currently diagnostic tests can be done such as reverse transcriptase
polymerase chain reaction (RT-PCR). This will provide the most timely and sensitive detection of the
infection. Diagnostic testing, when availably, should be prioritized for patients in whom confirmation of
influenza virus infection may affect clinical management, including patients considered at-risk and/or
those with complicated, severe, or progressive respiratory illness. This may also be valuable in guiding
infection control practices and management of a patient’s close contact to avoid spread of the
infection.1
The Department of Health released a Case Report Form for initial screening of Influenza A
(H1N1) (Figure __) which was used by hospitals all over the country for screening those who presented
with the usual symptoms of H1N1.3 This served as a tool for data gathering in the country.
Figure _. DOH Case Report Form for Initial Screening of Influenza A (H1N1)
REVIEW OF RELATED LITERATURE
I.
DEFINITION
The World Health Organization (WHO) announced a pandemic outbreak of respiratory
illness associated with the novel influenza (H1N1) variant virus in June 11, 2009. The H1N1
virus is a subtype of influenza A virus. Every influenza A virus has a gene coding for 1 of 16
possible hemagglutinin (HA) surface proteins and another gene coding for 1 of 9 possible
neuraminidase (NA) surface proteins. Genetic characterization found that the hemagglutinin
(HA) gene was similar to that of swine flu viruses present in United States pigs since 1999.
The Neuraminidase (NA) and matrix (M) protein genes resembled version present in
European swine flu isolates. The virus isolated from patients in the United States was found
out to be composed of genetic elements from four different flu viruses – North American
swine influenza, North American avian influenza, human influenza and swine influenza virus
typically found in Asia. The new strain seems to be a reassortment and variation of swine
influenza and human influenza (WHO 2009).
The history of influenza A (H1N1) virus is punctuated by frequent, sporadic cross-species
transmissions from swine to humans. Although the sporadically transmitted swine viruses
are sufficiently pathogenic in humans to cause clinically apparent disease, they are rarely
transmitted among humans. Exposure and infection are necessary but not sufficient for a
new epidemic virus to emerge; the virus must also adapt and transmit (Parrish CR, Holmes
EC, Morens DM et al. 2008). The infection with H1N1 pandemic was considered mild but it is
highly transmissible (Palacios et al. 2009).
The transmission of the H1N1 virus is affected by the host range which reflects natural
hosts that are infected either as part of a principal transmission cycle or, less commonly, as
"spillover" infections into alternative hosts. Rarely, viruses gain the ability to spread
efficiently within a new host that was not previously exposed or susceptible. These transfers
involve either increased exposure or the acquisition of variations that allow them to
overcome barriers to infection of the new hosts. In these cases, devastating outbreaks can
result. Steps involved in transfers of viruses to new hosts include contact between the virus
and the host, infection of an initial individual leading to amplification and an outbreak, and
the generation within the original or new host of viral variants that have the ability to spread
efficiently between individuals in populations of the new host (Parrish CR, Holmes EC,
Morens DM et al. 2008).
Seasonal influenza A is transmitted directly by large droplets or indirectly by fomites.
With the study performed by the Chinese Center for Disease Control and Prevention in
China they found out based on their data that the disease is transmitted to people by talking
to them in close proximities which indicates droplet transmission (Han, K. et al. 2009).
Patients afflicted of Pandemic (H1N1) 2009 present symptoms that are similar to
seasonal influenza, such as fever, cough, headache, muscle and joint pain, sore throat and
runny nose, and sometimes vomiting and diarrhoea (WHO 2009).
II.
Morbidity and Mortality
The World Health Organization announced as of July 30, 2009 a total of 138,260
laboratory confirmed cases with 817 laboratory confirmed deaths in 157 affected areas
(WHO 2009). In the Philippines alone, the DOH reported 3,207 laboratory confirmed cases
with associated 6 deaths (DOH 2009). Mortality and morbidity is greater in high risk people
like those who have chronic respiratory conditions like asthma and other obstructive
pulmonary diseases, cardiac diseases, diabetes, chronic metabolic and renal diseases,
chronic neurologic conditions, haemoglobinopathies, those who are immunosuppressed,
persons with morbid obesity, pregnant women, the very young and the very old (Palacios et
al. 2009).
III.
Treatment and Prevention
People are advised to avoid exposure by avoiding crowded places, cover their mouths
when sneezing and to self quarantine if they are experiencing symptoms pertaining to H1N1
virus (WHO 2009).
The novel influenza A (H1N1) virus that is circulating is said to be susceptible to the
neuraminidase inhibitor antiviral medications, oseltamivir and zanamivir. These durgs
reduced the severity and duration of symptoms of seasonal influenza if started within 48
hours of illness onset (CDC MMWR 2009).
Neuraminidase inhibitors (e.g Oseltamivir) have become the global public health drugs
in the world. The use of Neuraminidase inhibitors have increased since April 2009 along
with the spread of AH1N1 pandemic. Neuraminidase inhibitors act by blocking the function
of viral neuraminidase protein therefore interfering the virus from reproducing by budding
in the host cell (Jefferson T. 2009)
IV.
Complications associated with H1N1 viruses
The H1N1 virus can cause viral pneumonia which leads to other possible complications.
According to one multicenter study, Severe cases of H1N1 virus infections are correlated
with the presence of Streptococcus pneumonia coinfections. Streptococcus Pneumoniae
was present in 56.4% of severe cases versus 25% of mild cases (Palacios et al. 2009)
Staphylococcal coinfection can also worsen the disease process attributing to further
complications among patient afflicted with H1N1 (Rothberg, M. and Haessler, S. 2009)
Sources:
Journal Articles:
Parrish CR, Holmes EC, Morens DM, et al. (2009) Cross-species virus transmission and the emergence of
new epidemic diseases. Microbiol Mol Biol Rev 2008;72:457-470.
Jefferson T. Jones, Del Mar C. (2009) Neuraminidase inhibitors for preventing and treating influenza in
healthy adults: systematic review and meta analysis. BMJ 2009.339:n5106 doc10/1136/bmjb5106
Palacios G. Hornig M, Cisterna D, Savji N, Bussetti AV, et al. (2009) Streptococcus pneumoniae
Coinfection is correlated with the Severity of H1N1 Pandemic Influenza PLoS ONE 4(12): eB540.
Doi:10.1371/journal.pone.0.0008540
Kumar A., Zarychanski R., Pinto R et al. (2009) Critically Ill Patients With 2009 Influenza A(H1N1)
Infection in Canada. JAMA. 2009;302(17):1872-1879 (doi:10.1001/jama.2009.1496)
References:
1. World Health Organization. Clinical management of human infection with pandemic (H1N1)
2009; revised guidance, Nov. 2009
2. World Health Organization. Pandemic (H1N1) 2009 Update 86. Feb 2010
3. Influenza A (H1N1). Department of Health, Manila, Philippines. 2009