Untitled Essay, Research Paper

The Worlds Fight Against Microbes Many infectious diseases that were nearly eradicated from the

industrialized world, and newly emerging diseases are now breaking out all over the world

due to the misuse of medicines, such as antibiotics and antivirals, the destruction of our

environment, and shortsighted political action and/or inaction.

Viral hemorrhagic fevers are a group of diseases caused by viruses from

four distinct families of viruses: filoviruses, arenaviruses, flaviviruses, and

bunyaviruses. The usual hosts for most of these viruses are rodents or arthropods, and in

some viruses, such as the Ebola virus, the natural host is not known. All forms of viral

hemorrhagic fever begin with fever and muscle aches, and depending on the particular

virus, the disease can progress until the patient becomes deathly ill with respiratory

problems, severe bleeding, kidney problems, and shock. The severity of these diseases can

range from a mild illness to death (CDC I).

The Ebola virus is a member of a family of RNA (ribonucleic acid)

viruses known as filoviruses. When these viruses are magnified several thousand times by

an electron microscope they have the appearance of long filaments or threads. Filoviruses

can cause hemorrhagic fever in humans and animals, and because of this they are extremely

hazardous. Laboratory studies of these viruses must be carried out in special maximum

containment facilities, such as the Centers for Disease Control (CDC) in Atlanta, Georgia

and the United States Army Medical Research Institute of Infectious Diseases (USAMRIID),

at Fort Detrick in Frederick, Maryland (CDC I,II).

The Ebola hemorrhagic fever in humans is a severe, systemic illness

caused by infection with Ebola virus. There are four subtypes of Ebola virus (Ebola-Zaire,

Ebola-Sudan, Ebola-Ivory Coast, and Ebola-Reston), which are not just variations of a

single virus, but four distinct viruses. Three of these subtypes are known to cause

disease in humans, and they are the Zaire, Sudan, and Ivory Coast subtypes. Out of all the

different viral hemorrhagic fevers known to occur in humans , those caused by filoviruses

have been associated with the highest case-fatality rates. These rates can be as high as

90 percent for epidemics of hemorrhagic fever caused by Ebola-Zaire virus. No vaccine

exists to protect from filovirus infection, and no specific treatment is available (CDC

II).

The symptoms of Ebola hemorrhagic fever begin within 4 to 16 days after

infection. The patient develops chills, fever, headaches, muscle aches, and a loss of

appetite. As the disease progresses vomiting, diarrhea, abdominal pain, sore throat, and

chest pain can occur. The blood fails to clot and patients may bleed from injection sites

as well as into the gastrointestinal tract, skin, and internal organs (CDC I).

The Ebola virus is spread through close personal contact with a person

who is very ill with the disease, such as hospital care workers and family members.

Transmisson of the virus can also occur from the reuse of hypodermic needles in the

treatment of patients. This practice is common in developing countries where the health

care system is underfinanced (CDC I).

Until recently, only three outbreaks of Ebola among people had been

reported. The first two outbreaks occurred in 1976. One was in western Sudan, and the

other in Zaire. These outbreaks were very large and resulted in more than 550 total cases

and 340 deaths. The third outbreak occurred in Sudan in 1979. It was smaller with only 34

cases and 22 deaths. Three additional outbreaks were identified and reported between 1994

and 1996: a large outbreak in Kikwit, Zaire with 316 cases and 244 deaths; and two smaller

outbreaks in the Ivory Coast and Gabon. Each one of these outbreaks occurred under the

challenging conditions of the developing world. These conditions including a lack of

adequate medical supplies and the frequent reuse of needles, played a major part in the

spread of the disease. The outbreaks were controlled quickly when appropriate medical

supplies were made available and quarantine procedures were used (CDC I).

Ebola-Reston, the fourth subtype, was discovered in 1989. The virus was

found in monkeys imported from the Philippines to a quarantine facility in Reston,

Virginia which is only about ten miles west of Washington, D.C. (Preston 109). The virus

was also later detected in monkeys imported from the Philippines into the United States in

1990 and 1996, and in Italy in 1992. Infection caused by this subtype can be fatal in

monkeys; however, the only four Ebola-Reston virus infections confirmed in humans did not

result in the disease. These four documented human infections resulted in no clinical

illness. Therefore, the Ebola-Reston subtype appears less capable of causing disease in

humans than the other three subtypes. Due to a lack of research of the Ebola-Reston

subtype there can be no definitive conclusions about its pathogenicity (CDC II).

Staphylococcus is a genus of nonmotile, spherical bacteria. Some

species are normally found on the skin and in the throat, and certain species can cause

severe life-threatening infections, such as staphylococcal pneumonia (Mosby 1477). Despite

the age of antibiotics, staph infections remain potentially lethal. By 1982 fewer than 10

percent of all clinical staph cases could be cured with penicillin, which is a dramatic

shift from the almost 100 percent penicillin susceptibility of Staphylococcus in 1952.

Most strains of staph became resistant to penicillin’s by changing their DNA

structure (Garrett 411).

The fight against staph switched from using the mostly ineffective

penicillin to using methicillin in the late 1960’s. By the early 1980’s,

clinically significant strains of Staphylococcus emerged that were not only resistant to

methicillin, but also to its antibiotic cousins, such as naficillin. In May 1982 a newborn

baby died at the University of California at San Francisco’s Moffit Hospital. This

particular strain was resistant to penicillin’s, cephalosporin’s, and

naficillin. The mutant strain infected a nurse at the hospital and three more babies over

the next three years. The only way further cases could be prevented was to aggressively

treat the staff and babies with antibiotics to which the bacteria was not resistant, close

the infected ward off to new patients, and scrub the entire facility with disinfectants.

This was not an isolated case, unfortunately. Outbreaks of resistant bacteria inside

hospitals were commonplace by the early 1980’s. The outbreaks were particularly

common on wards that housed

the most susceptible patients, such as burn victims, premature babies, and intensive care

patients. Outbreaks of methicillin resistant Staphylococcus aureus (MRSA) increased in

size and frequency worldwide throughout the 1980’s (Garrett 412).

By 1990, super-strains of staph that were resistant to a huge number of

drugs existed naturally. For example, an Australian patient was infected with a strain

that was resistant to cadmium, penicillin, karamycin, neomycin, streptomycin,

tetracycline, and trimethoprim. Since each of these drugs operated biomechanically the

same as a host of related drugs the Australian staph was resistant, to varying degrees,

some thirty-one different drugs (Garrett 413).

A team of researchers from the New York City Health Department, using

genetic fingerprinting techniques, traced back in time over 470 MRSA strains. They

discovered that all of the MRSA bacteria descended from a strain that first emerged in

Cairo, Egypt in 1961, and by the end of that decade the strain’s descendants could be

found in New York, New Jersey, Dublin, Geneva, Copenhagen, London, Kampala, Ontario,

Halifax, Winnipeg, and Saskatoon. Another decade later they could be found world wide

(Garrett 414).

New strains of bacteria were emerging everywhere in the world by the

late 1980’s, and their rates of emergence accelerated every year. In the U.S. alone,

an estimated $200 million a year was spent on medical bills because of the need to use

more exotic and expensive antibiotics, and longer hospitalization for everything from

strep throat to life-threatening bacterial pneumonia. These trend, by the 90’s, had

reached the level of universal, across-the-board threats to humans of all ages, social

classes, and geographic locations (Garrett 414).

Jim Henson, famed puppeteer and inventor of the muppets, died in 1990

of a common, and supposedly curable bacterial infection. A new mutant strain of

Streptococcus struck that was resistant to penicillin’s and possessed genes for a

deadly toxin that was very similar to a strain of S. aureus discovered in Toxic Shock

Syndrome. This new strain of strep was later dubbed strep A-produced TSLS (Toxic

Shock-Like Syndrome). Only a year after its discovery lethal human cases of TSLS had been

reported from Canada, the U.S., and several countries in Europe. Streptococcal strains of

all types were showing increasing levels of resistance to antibiotics. According to Dr.

Harold Neu, who is a Columbia University antibiotics expert, a dose of 10000 units of

penicillin a day for four days was more than adequate to cure strep respiratory infections

in 1941. By 1992 the same illness required 24 million units a day, and could still be

lethal (Garrett 415).

The emergence of highly antibiotic resistant strains Streptococcus

pneumoniae, or Pneumococcus, was even more serious. The bacteria normally inhabited human

lungs without causing harm; however, if a person were to inhale a strain that differed

enough from those to which ho or she had been previously exposed, the individuals immune

system might not be able to keep in check (Garrett 415).

By 1990, a third of all ear infections occurring in young children were

due to Pneumococcus, and nearly half of those cases involved penicillin resistant strains.

The initial resistance’s were incomplete. This means that only some of the organisms

would die off and the child’s ears would clear up, and both parents and doctor would

believe the illness gone. The organisms that did not die off would multiply , and in a few

weeks the infection would be back. Then if the parents used any leftover

penicillin’s, they would possible see another apparent recovery, but this time the

organisms were more resistant, and the ear infection returned quickly with a vengeance

(Garrett 415-16).

In poor and developing countries the prevention of pediatric

respiratory diseases had to be handled with scarce resources, available antibiotics, and

little or no laboratory support to identify the problem. Health officials then defined the

disease process not in terms of the organisms involved but according to where the

infection was taking place, and the severity of the infection. In general, upper

respiratory infections were milder and usually viral, while deep lung involvement

indicated a potentially lethal bacterial disease. In 1990 the World Health Organization

(WHO) said that the best policy for developing countries was to assume that pediatric

pneumonia’s were bacterial, and treat with penicillin in the absence of laboratory

proof of a viral infection. This process was shown to have reduced the number of child

deaths in the test areas by more than a third, and even more surprising was that there was

a 36 percent reduction in child deaths due to all other causes. This was only the good

news. The bad ne

ws was that penicillin’s and other antibiotics offered no more benefit to children

with mild and usually viral respiratory infections than not taking any drugs at all and

staying home. This was due to the fact that antibiotics have no effect on viruses. Another

key danger was that village doctors, who lacked training and laboratory support, would

overuse antibiotics, which would in turn promote the emergence of new antibiotic resistant

S. pneumoniae (Garrett 417).

Because of drug use policies in both wealthy and poor countries,

antibiotic resistant strains of pneumococcal soon turned up all over the world. Some of

these strains were able to withstand exposure to six different classes of antibiotics

simultaneously. This emergence of drug resistance usually occurred in communities of

social and economic deprivation. Poor people were more likely to self-medicate themselves

using antibiotics purchased off the black market, or borrowing leftovers from relatives

(Garrett 417-19). " Whether one looked in Spain, South Africa, the United States,

Romania, Pakistan, Brazil, or anywhere else, the basic principle held true: overuse or

misuse of antibiotics, particularly in small children and hospitalized patients, prompted

emergence of resistant mutant organisms" (Garrett 419).

Infectious diseases thought to be common, and relatively harmless are

now becoming lethal to people of all ages, race, and socioeconomic status because of the

misuse of medicines, which make the diseases ever more drug resistant, and short sighted

political policies. It now seems that the microbes now have the macrobes on the run.

Consider the difference in size between some of the very tiniest and the very largest

creatures on Earth. A small bacterium weighs as little as 0.00000000001 grams. A blue

whale weighs about 100000000 grams. Yet a bacterium can kill a whale … Such is the

adaptability and versatility of microorganisms as compared with humans and other so called

"higher" organisms, that they will doubtless continue to colonise and alter the

face of the Earth long after we and the rest of our cohabitants have left the stage

forever. Microbes, not macrobes, rule the world.- Bernard Dixon, 1994

WORKS CITED

CDC(I).Ebola Virus Hemorrhagic Fever: General Information.

http://www.cdc.gov/ncidod/diseases/virlfv/ebolainf.htm[1996, November 20].CDC(II). Filoviruses in Nonhuman Primates: Overview of the Investigation in Texas.

http://www.cdc.gov/ncidod/diseases/virlfvr/ebola528.htm[1996,

November 20].Garrett, Laurie. The Coming Plague. Farrar, Straus. and Giroux: New York, 1994.Mosby’s Medical, Mursing, and Allied Health Dictionary 4th Ed. .

Mosby-Year Book, Inc.: St.Louis,1994.Preston, Richard. The Hot Zone. Random House Inc.: New York, 1994.Roizman, Bernard. Infectious Diseases in an Age of Change. National Academy Press:

Washington,D.C., 1995.Top, Franklin H. . Communicable and Infectious Diseases. C.V. Mosby Company: St.Louis,

1964.