excerpt:infectious history

[Guest guest]

i post this for the ironic statement in paragraph 6: " Smaller but lethal

outbreaks of dramatic, hypervirulent viruses have been raising public fear.

Among

these are the Ebola virus outbreak in Africa in 1976 and again in 1995 and the

hantavirus outbreak in the U.S. Southwest in 1993. In hindsight, these posed

less of a public health risk than the publicity they received might have

suggested. "

http://www.univie.ac.at/hygiene-aktuell/lederberg.htm

Wake-Up Calls

The overoptimism and complacency of the 1960s and 1970s was shattered in 1981

with the recognition of AIDS. Since then, the spreading pandemic has

overtaken one continent after another with terrible costs. Its spread has been

coincident with another wake-up call--the looming problem of

antibiotic-resistant

microbes. This was a predictable consequence of the evolutionary process

operating on microbes challenged by the new selection pressure of antibiotics,

arising

in part from medical prescriptions and in part from unregulated sales and use

in feed for crop animals.

AIDS's causative agent, the human immunodeficiency virus (HIV), is a member

of the retrovirus family. These viruses had been laboratory curiosities since

1911, when Francis Peyton Rous discovered the Rous sarcoma virus (RSV) in

chickens. Early basic research on retroviruses later helped speed advances in

HIV

research. By the time AIDS began to spread, RSV had been studied for years as a

model for cancer biology, because it could serve as a vector for transferring

oncogenes into cells. That work accelerated the characterization of HIV as a

retrovirus, and it also helped guide our first steps toward medications that

slow HIV infection.

AIDS and HIV have spurred the most concentrated program of biomedical

research in history, yet they still defy our counterattacks. And our focus on

extirpating the virus may have deflected less ambitious, though more pragmatic,

aims,

including learning to live with the virus by nurturing in equal measure the

immune system that HIV erodes. After all, natural history points to analogous

infections in simians that have long since achieved a mutually tolerable state

of equilibrium.

Costly experiences with AIDS and other infectious agents have led to

widespread reexamination of our cohabitation with microbes. Increased monitoring

and

surveillance by organizations such as the U.S. Centers for Disease Control and

Prevention (CDC) and the World Health Organization (WHO) have revealed a

stream of outbreaks of exotic diseases. Some have been due to the new

importation

of microbes (such as cholera in the Southern Hemisphere); some to older

parasites (such as Legionella) that have been newly recognized as pathogenic;

and

some to newly evolved antibiotic-resistant pneumonia strains.

Even maladies that had never before been associated with infectious agents

recently have been revealed as having microbial bases. Prominent among these are

gastric ulcers, which previously had been attributed almost entirely to

stress and other psychosomatic causes. Closer study, however, has shown a

Helicobacter to be the major culprit. Researchers are now directing their

speculations

away from stress and toward Chlamydia infection as a cause of atherosclerosis

and coronary disease.

The litany of wake-up calls goes on. Four million Americans are estimated to

be infected with hepatitis C, mainly by transfusion of contaminated blood

products. This population now is at significant risk for developing liver

cancer.

Those harboring hepatitis C must be warned to avoid alcohol and other

hepatotoxins, and they must not donate blood.

Smaller but lethal outbreaks of dramatic, hypervirulent viruses have been

raising public fear. Among these are the Ebola virus outbreak in Africa in 1976

and again in 1995 and the hantavirus outbreak in the U.S. Southwest in 1993. In

hindsight, these posed less of a public health risk than the publicity they

received might have suggested. Still, studying them and uncovering ecological

factors that favor or thwart their proliferation is imperative because of their

potential to mutate into more diffusible forms.

Our vigilance is mandated also by the facts of life: The processes of gene

reassortment in flu viruses, which are poorly confined to their canonical hosts

(birds, swine, and people), goes on relentlessly and is sure to regenerate

human-lethal variants. Those thoughts were central in 1997 when the avian flu

H5N1 transferred into a score of Hong Kong citizens, a third of whom died. It is

likely that the resolute actions of the Hong Kong health authorities, which

destroyed 2 million chickens, stemmed that outbreak and averted the possibility

of a worldwide spread of H5N1.

Complacency is not an option in these cases, as other vectors, including

wildfowl, could become carriers. In Malaysia, a new infectious entity, the Nipah

virus, killed up to 100 people last year; authorities there killed a million

livestock to help contain the outbreak. New York had a smaller scale scare last

summer with the unprecedented appearance of bird- and mosquito-borne West Nile

encephalitis, although the mortality rate was only a few percent of those

infected. We need not wonder whether we will see outbreaks like these again. The

only questions are when and where?

These multiple wake-up calls to the infectious disease problem have left

marks in vital statistics. From midcentury to 1982, the U.S. mortality index

(annual deaths per 100,000) attributable to infection had been steady at about

30.

But from 1982 to 1994, the rate doubled to 60. (Keep in mind that the index

was 500 in 1900 and up to 850 in 1918-19 due to the Spanish flu epidemic.) About

half of the recent rise in deaths is attributable to AIDS; much of the rest

is due to respiratory disease, antibiotic resistance, and hospital-acquired

infection.