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.
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