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