Infectious Disease Epidemiolog

A Presentation on:

Epidemiology of Influenza
Prabesh Ghimire

This presentation will cover

What is Influenza
Influenza Virus
Antigenic shift and antigenic drift
Epidemiology of H1N1 Influenza

Epidemiological Burden (Global, Regional and National)

Epidemiological Determinants (Agent, Host & Env
Factors)
Mode of Transmission
Clinical Features
Diagnosis
Management
Prevention & Control
National Response

What is Influenza?

Highly infectious viral illness

Acute respiratory disease

Upper respiratory tract

Lower respiratory tract

Influenza Virus

Single stranded RNA virus

Orthomyxoviridae family
3 types: A,B, C
Type A- moderate to severe illness

Type B- milder disease

Primarily affects children

Humans only

Type C- rarely reported in humans

All age groups

Humans and other animals

No epidemics

Influenza A Virus

Characterized by 2 main surface glycoproteins

Hemagglutinin (HA)- 16 subtypes

Neuraminidase (NA)- 9 subtypes

Influenza A virus subtypes classified based on

combinations of HA and NA subtype
All the subtypes can affect birds (natural hosts)
Only a few subtypes capable of infecting humans
Important subtypes of public health importance

H5N1 Influenza A virus

Pandemic H1N1 Influenza A virus

Antigenic Shift and Antigenic Drift

Influenza A viruses are dynamic and can evolve by

two processes:

Antigenic drift

Occurs by point mutations in the two genes coding for HA and

NA
Causes minor changes in surface proteins
leads to a new strain which is not recognized by antibodies to
previous influenza strains.

Antigenic shift
Major change through genetic reassortment
Produces a novel influenza A subtype in humans
Occurs through mixing of human and animal influenza A
virus genes or by animal to human transmission
May cause pandemics

H1N1 Influenza (Swine Flu)

H1N1 Influenza

Novel strain due to antigenic shift

Evolved from a reassortant between triple reassortant swine influenza viruses in North American
pigs and influenza A virus circulating in Eurasian
pigs
April 2009: WHO declared the emergence of human
cases of H1N1 swine influenza virus
11 June 2009: WHO raised the pandemic alert
(phase 5 to 6)

Epidemiological Burden
Global

Till May 2010: >214 countries reported lab confirmed

influenza H1N1 2009, including over 18097 deaths

pandemic
(Source WHO)

SEAR

Till May 2010: 1808 deaths

As of 19 October 2009, in the WHO Southeast Asia region, 10 of 11
member countries have reported 41 513 cases of H1N1 virus infection
and 573 deaths.
The 3 hardest hit countries in the region were Thailand, India and
Indonesia

(Source WHO)

Nepal

Jun 2009: First detection in human specimen collected at TIA

Till May 2010: Total no. of confirmed positive cases- 172
Till May 2010: Total death cases -3. All were Female patients
(Source NPHL)

10

Epidemiological Determinants

Causative agent:
Influenza A virus

Host Factors

11

Pandemic

H1N1

(2009)

Occurs in every age-group. Population does not

have immunity to virus
Complications higher in people with underlying
diseases such as asthma, cardiac diseases, renal
diseases and in pregnancy.
Obesity has also found to predispose to severe
disease

Environment

Influenza viruses are highly resilient in the

environment.
Low temperature and low humidity favor aerosol
transmission, explaining the seasonal nature of
influenza in temperate climates.
In tropical climates influenza infections are
associated with increased rainfall
The best environment for a novel virus is a
population without pre-existing immunity to it,
enabling it to spread pandemically

12

Mode of Transmission

Through droplets from coughing or sneezing,

and
Through direct or indirect contact with the
respiratory secretions of an infected person

13

Food is not yet known to be a vehicle for the

transmission
The secondary attack rate in households:18% to
30%

Incubation Period

Between 1 and 7 days

Period of Communicability

From a day prior to onset of symptoms till after 24

hours after symptoms have subsided.

14

Clinical Features

Ranging from mild self-limiting upper respiratory

illness to lower respiratory infection including ARDS,
cardiac involvement, neurological involvement,
multiorgan failure, septicemia and death.
Common features: mild respiratory illness with
fever, cough, sore throat, dyspnea, rhinorrhea,
myalgias, chills, headache and fatigue.
Diarrhea and vomiting are more commonly seen
than with seasonal flu.
Reported complications: myocarditis, pericarditis,
encephalitis, seizures, myositis, multiorgan failure
and toxic shock syndrome
15

Diagnosis

Reverse-transcriptase polymerase chain reaction

(RT-PCR) provides the most timely and sensitive
evidence of infection.
Clinical diagnosis (based on acute onset of fever
and cough) can be increasingly predictive of
infection as the prevalence of infection increases.

16

Case Management

Hospitalization and antiviral therapy not required for

most patients
Supportive
care
includes antipyretics such
as
paracetamol or acetaminophen, for fever or pain, and
fluids, as needed.
The virus is currently susceptible to neuraminase
inhibitors (oseltamivir and zanamivir).Oseltamivir is
believed to reduce the severity and duration of the
illness, and might contribute to preventing its
progression to severe disease and death.
Antiviral therapy may be beneficial especially for
pregnant patients, patients with progressive lower
respiratory tract disease or pneumonia, and those with
underlying medical conditions
17

Prevention and Control Measures

Non-Pharmacological Interventions

Personal protective measures

Isolation and social distancing

Shielding ones mouth and nose while coughing or sneezing,

Frequently washing ones hands with soap
Home quarantine
School closure and cancellation of mass gathering

Pharmacological Interventions

Chemoprophylaxis

18

If the likelihood of complications is high, oseltamivir or

zanamivir may be used as post-exposure chemoprophylaxis
for affected individuals, especially healthcare workers

Prevention and Control Measures

contd.

Pharmacological Interventions

Vaccination

19

Vaccine against the H1N1 virus is presently available in

a few countries.
Commercial production is about to commence.
The first priority of all countries should be to immunize
their healthcare workers
The next priority should be pregnant women.
Inactivated non-adjuvant vaccines similar to most
seasonal influenza vaccines are considered the
preferred option.

National Response

National Influenza Surveillance Network (10 sentinel

sites)
Molecular
diagnostic
assay
based
influenza
surveillance started in 2009 with the introduction of
Real-Time PCR (RT-PCR) at National Public Health
Laboratory (NPHL)
Community spread of Pandemic Influenza A/H1N1 2009
was established in Kathmandu valley on 15 thOctober,
2009.
NPHL designated as National Influenza Centre (NIC) on
19thApril, 2010
Influenza Pandemic Preparedness and Response Project
(IPPRP) implemented by PAHS under grants from CDC
20

Open Discussion

21

References
Narain JP, Kumar R, Bhatia R. Pandemic (H1N1) 2009: epidemiological, clinical and
prevention aspects. The National Medical Journal of India. 2009;22(5).
Gularia R, Kumar J, Mohan A, Wig N. Influenza A: From highly pathogenic H5N1 to
pandemic 2009 H1N1. Epidemiology and clinical features. Indian Journal of
Microbiology. 2009;49:315-19.
Mpolya EA, Furuse Y, Nukiwa N, Suzuki A, Kamigaki T, Oshitani H. Pandemic (H1N1)
2009 Virus Viewed from an Epidemiological Triangle Model. Journal of Disaster
Research. 2009;4(5):1-7.

1.
2.

3.

WHO. Pandemic (H1N1) 2009 - update 101, [cited 2016 Sep 3], Available from
http://www.who.int/csr/don/2010_05_21/en/
CDC.
Influenza,
[cited
2016
Sep
3],
Available
from
http://www.cdc.gov/vaccines/pubs/pinkbook/flu.html

4.
5.

22