Mrs. Smith also tells you about her sister, Nancy Hogan, age 40, another patient of yours. Mrs. Hogan never gets a flu shot because she has heard that they give you the flu and besides, she is allergic to eggs. She and Mrs. Smith "do everything together" and she came down with flu-like symptoms yesterday. Mrs. Smith reminds you that her sister is 8 months pregnant and also has a heart problem. You look at her medical record and find that she has an interventricular septal defect (IVSD). Her sister is home in bed and very sick. Mrs. Smith is worried about her and wants your advice.
For each question, one or more answers may be correct.
What should you tell her?
B) Make an appointment to see you in a few days, if she is not feeling better.
What are Mrs. Hogan's risk factors that make her case different from that of her sister?
A) Presumed infection with influenza virus.
You see Mrs. Hogan in your office later that day. She looks acutely ill, amd has a temperature of 39 degrees C, respiration rate = 36/min, and bilateral rales on exam. What should be done for Mrs. Hogan?
B) Watch her closely at home and be ready to admit her for supportive therapy.
C) Watch her at home but begin antiviral therapy with amantadine or rimantidine.
D) Admit her and give her supportive therapy.
E) Admit her for both supportive and anti-viral therapy with rimantadine or amantadine.
What about Mrs. Hogan's ideas about flu shots?
A) Flu shots almost never cause flu.
B) If she is allergic to eggs she shouldn't get flu shots.
While we're discussing flu shots, who should get them?
A) Anybody with chronic heart, lung or kidney disease or diabetes.
C) Normal healthy adults of all ages.
D) Children on long term aspirin therapy (e.g. patients with juvenile rheumatoid arthritis).
For more information on the role of IgG antibody, IgA antibody or cell-mediated immunity, click on Host Defense.
To better understand why the same views can cause lethal viral pneumonia in some people and only mild URI in others, click on Lethal in Some and Mild in Others.
For more information on vaccines, including a brief description of the authors new experimental approach, click on Vaccines.
To find out why the vaccine needs to be changed each year, click here.
To find out why the virus causes pandemics every ten to forty years, click here.
Click here for Case Study #3.
The virus undergoes changes in amino acids in the genes for the surface
glycoproteins, hemagglutinin and neuraminidase, which modify the antigenic
sites of these molecules. This is called antigenic drift, and is caused by
point mutations in the RNA genes. These changes necessitate changing the
vaccine each year to maximize the match between the vaccine-induced antibodies
and the anticipated virus. This process is facilitated by a worldwide network
that monitors the flu viruses circulating in both the northern and southern
hemispheres. The U.S. uses the viruses circulating in the southern hemisphere
to make the vaccine, thus having the most current (six month) best guess for
the coming flu season.
Most viruses have their genes linked in one molecule of nucleic acid made of
DNA or RNA. Influenza is one of the few with a segmented genome, meaning its
genes are in eight separate molecules of RNA. This makes viral replication
much more difficult because a viable virus must be at least one copy of each
of these eight. On the other hand, the segmented genome enables the virus to
totally change its surface glycoproteins, the hemagglutinin (H) and
neuraminidase (N). The best current explanation is that the change occurs
when a pig living in close contact with people is dually infected by the
existing human flu virus and an animal virus, probably transmitted by birds.
The progeny virus from this double infection theoretically have all 256
possible combinations of the eight genes, but the immunity to the existing flu
strain in the human population selects against viruses capable of replicating
in human cells which have the current surface glycoproteins and selects those
viruses with animal hemagglutinin and neuraminidase genes that are new to the
human population. Thus, the existing antibody mediated immunity is not
protective. Historically, H1N1 persisted until 1957 when H2N2 emerged and
caused a pandemic. In 1967, H3N2 replaced H2N2 and caused another pandemic.
In 1977, H1N1 reemerged and has coexisted with H2N2 since that time (then).
We are due for another antigenic shift, but (nevertheless) nobody can
accurately predict when nor what new glycoproteins may surface. For those of
you who find this explanation implausible, you should know that the H3
hemagglutinin was found in the feces of a duck in the Ukraine, years
before it emerged in the 1967 pandemic.