Really? You went with an article that chose measles as the counter-vaccination argument?

A (not so)little light reading might be illuminating. In particular pay attention to the first (pre-vaccine)numbers listed compared to the (post-vaccine)numbers towards the end.

TL:DR version: The numbers pre-vaccination are all sorts of nasty, so you’ll excuse me if I’m not buying the ‘vaccines are just a plot/don’t work’ arguments. Society has seen what happens without vaccinations and it’s not pretty, yet that’s what the anti-vaccination people seem to be pushing for, hence why they can get a rather hostile/dismissive reception at times.

Secular Trends in the United States

Before 1963, approximately 500,000 cases and 500 deaths were reported annually, with epidemic cycles every 2–3 years. However, the actual number of cases was estimated at 3–4 million annually. More than 50% of persons had measles by age 6, and more than 90% had measles by age 15. The highest incidence was among 5–9-year-olds, who generally accounted for more than 50% of reported cases.

In the years following licensure of vaccine in 1963, the incidence of measles decreased by more than 95%, and 2–3-year epidemic cycles no longer occurred. Because of this success, a 1978 Measles Elimination Program set a goal to eliminate indigenous measles by October 1, 1982 (26,871 cases were reported in 1978). The 1982 elimination goal was not met, but in 1983, only 1,497 cases were reported (0.6 cases per 100,000 population), the lowest annual total ever reported up to that time.

Measles Resurgence in 1989–1991

From 1989 through 1991, a dramatic increase in reported measles cases occurred. During these 3 years a total of 55,622 cases were reported (18,193 in 1989; 27,786 in 1990; 9,643 in 1991). In addition to the increased number of cases, a change occurred in their age distribution. Prior to the resurgence, school-aged children had accounted for the largest proportion of reported cases. During the resurgence, 45% of all reported cases were in children younger than 5 years of age. In 1990, 48% of patients were in this age group, the first time that the proportion of cases in children younger than 5 years of age exceeded the proportion of cases in 5–19-year-olds (35%).

Overall incidence rates were highest for Hispanics and blacks and lowest for non-Hispanic whites. Among children younger than 5 years of age, the incidence of measles among blacks and Hispanics was four to seven times higher than among non-Hispanic whites.

A total of 123 measles-associated deaths were reported during this period (death-to-case ratio of 2.2 per 1,000 cases). Forty-nine percent of deaths were among children younger than 5 years of age. Ninety percent of fatal cases occurred among persons with no history of vaccination. Sixty-four deaths were reported in 1990, the largest annual number of deaths from measles since 1971.

The most important cause of the measles resurgence of 1989–1991 was low vaccination coverage. Measles vaccine coverage was low in many cities, including some that experienced large outbreaks among preschool-aged children throughout the early to mid-1980s. Surveys in areas experiencing outbreaks among preschool-aged children indicated that as few as 50% of children had been vaccinated against measles by their second birthday, and that black and Hispanic children were less likely to be age-appropriately vaccinated than were white children.

In addition, measles susceptibility of infants younger than 1 year of age may have increased. During the 1989–1991 measles resurgence, incidence rates for infants were more than twice as high as those in any other age group. The mothers of many infants who developed measles were young, and their measles immunity was most often due to vaccination rather than infection with wild virus. As a result, a smaller amount of antibody was transferred across the placenta to the fetus, compared with antibody transfer from mothers who had higher antibody titers resulting from wild-virus infection. The lower quantity of antibody resulted in immunity that waned more rapidly, making infants susceptible at a younger age than in the past.

Measles Since 1993

Reported cases of measles declined rapidly after the 1989–1991 resurgence. This decline was due primarily to intensive efforts to vaccinate preschool-aged children. Measles vaccination levels among 2-year-old children increased from 70% in 1990 to 91% in 1997.

Since 1993, fewer than 500 cases have been reported annually, and fewer than 200 cases per year have been reported since 1997. A record low annual total of 37 cases was reported in 2004. Available epidemiologic and virologic data indicate that measles transmission in the United States has been interrupted. The majority of cases are now imported from other countries or linked to imported cases. Most imported cases originate in Asia and Europe and occur both among U.S. citizens traveling abroad and persons visiting the United States from other countries. An aggressive measles vaccination program by the Pan American Health Organization (PAHO) has resulted in record low measles incidence in Latin America and the Caribbean, and the interruption of indigenous measles transmission in the Americas. Measles elimination from the Americas was achieved in 2002 and has been sustained since then, with only imported and importation-related measles cases occuring in the region.

Source

On to the flu.

How the Flu Virus Can Change: “Drift” and “Shift”

Influenza viruses are constantly changing. They can change in two different ways.

One way they change is called “antigenic drift.” These are small changes in the genes of influenza viruses that happen continually over time as the virus replicates. These small genetic changes usually produce viruses that are pretty closely related to one another, which can be illustrated by their location close together on a phylogenetic tree. Viruses that are closely related to each other usually share the same antigenic properties and an immune system exposed to an similar virus will usually recognize it and respond. (This is sometimes called cross-protection.)

But these small genetic changes can accumulate over time and result in viruses that are antigenically different (further away on the phylogenetic tree). When this happens, the body’s immune system may not recognize those viruses.

This process works as follows: a person infected with a particular flu virus develops antibody against that virus. As antigenic changes accumulate, the antibodies created against the older viruses no longer recognize the “newer” virus, and the person can get sick again. Genetic changes that result in a virus with different antigenic properties is the main reason why people can get the flu more than one time. This is also why the flu vaccine composition must be reviewed each year, and updated as needed to keep up with evolving viruses.

The other type of change is called “antigenic shift.” Antigenic shift is an abrupt, major change in the influenza A viruses, resulting in new hemagglutinin and/or new hemagglutinin and neuraminidase proteins in influenza viruses that infect humans. Shift results in a new influenza A subtype or a virus with a hemagglutinin or a hemagglutinin and neuraminidase combination that has emerged from an animal population that is so different from the same subtype in humans that most people do not have immunity to the new (e.g. novel) virus. Such a “shift” occurred in the spring of 2009, when an H1N1 virus with a new combination of genes emerged to infect people and quickly spread, causing a pandemic. When shift happens, most people have little or no protection against the new virus.

While influenza viruses are changing by antigenic drift all the time, antigenic shift happens only occasionally. Type A viruses undergo both kinds of changes; influenza type B viruses change only by the more gradual process of antigenic drift.

Source

‘Since the late 19th century, five occurrences of antigenic shifts have led to pandemics (1889–1891, 1918–1920, 1957–1958, 1968–1969, and 2009-2010). A pandemic may start from a single focus and spread along routes of travel. Typically, there are high attack rates involving all age groups, and mortality is usually markedly increased. Severity is generally not greater in the individual patient (except for the 1918–1919 strain), but because large numbers of persons are infected, the number, if not the proportion, of severe and fatal cases will be large. Onset may occur in any season of the year. Secondary and tertiary waves may occur up to 2 years later, usually in the winter.

In April 2009, a novel influenza A(H1N1) virus appeared and quickly spread across North America. By May 2009 the virus had spread to many areas of the world. Influenza morbidity caused by 2009 pandemic H1N1 virus remained above seasonal baselines throughout spring and summer 2009 and was the cause of the first influenza pandemic since 1968.

In the United States, the 2009 pandemic was characterized by a substantial increase in influenza activity in Spring 2009 that was well beyond seasonal norms. Influenza activity peaked in late October 2009, and returned to the seasonal baseline by January 2010. During this time, more than 99 percent of viruses characterized were the 2009 pandemic influenza A(H1N1) virus.

In January 2011, CDC estimated that pandemic H1N1 influenza virus caused more than 60 million Americans to become ill, and led to more than 270,000 hospitalizations and 12,500 deaths. Ninety percent of hospitalizations and deaths occurred in persons younger than 65 years of age. With typical seasonal influenza approximately 90% of deaths occur in persons older than 65 years.

(Pretty nasty right? Yeah, comparatively that was a walk in the park.)

‘The pandemic of “Spanish” influenza in 1918–1919 caused an estimated 21 million deaths worldwide. The first pandemic of the 21st century occurred in 2009–2010.’

**

For practical purposes, the duration of immunity following inactivated influenza vaccination is less than 1 year because of waning of vaccine-induced antibody and antigenic drift of circulating influenza viruses. Influenza vaccine efficacy varies by the similarity of the vaccine strain(s) to the circulating strain and the age and health status of the recipient. Vaccines are effective in protecting about 60% of healthy vaccinees younger than 65 years of age from illness when the vaccine strain is similar to the circulating strain. However, the vaccine is less effective in preventing illness among persons 65 years of age and older.

Although the vaccine is not highly effective in preventing clinical illness among the elderly, it is effective in preventing complications and death. Some studies show that, among elderly persons, the vaccine is 50%–60% effective in preventing hospitalization and 80% effective in preventing death. During a 1982–1983 influenza outbreak in Genesee County, Michigan, unvaccinated nursing home residents were four times more likely to die than were vaccinated residents.

Source

What is the evidence that influenza vaccines work?

(Ran out of comment space, use this link and click on the topic link to the right to see the numbers.)