The Worlds Fight Against Microbes Essay Research

The Worlds Fight Against Microbes Essay, Research Paper The Worlds Fight Against Microbes Many infectious diseases that were nearly eradicated from the

The Worlds Fight Against Microbes 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


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


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


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 news 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


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,



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