ILLNESS/INFLAMMATION/

IMMUNITY/
COMMUNICABLE DISEASE
Case Presentation

CHOLERA

MUAMIR ALI ALINGAN

BSN4A
INTRODUCTION
• Cholera is an acute, bacterial, diarrheal disease with
profuse watery stools, occasional vomiting, and rapid
dehydration.
• If untreated, circulatory collapse, renal failure and
death may occur.
• More than 50% of untreated people with severe
cholera die.
• It occurs worldwide, with periodic epidemics and
pandemics.
• A recent Western Hemisphere cholera pandemic started in
Peru in 1991. By 1994, more than 950,000 cases had been
reported in 21 countries in the Western Hemisphere.
• Only 5 new U.S. cases were reported to the CDC in 2004.
Most U.S. cases involve the ingestion of raw or undercooked
seafood (e.g., oysters) from the coastal waters of Louisiana
and Texas.
• The Philippines were infected in 1858.
• The 1902-1904 cholera epidemic claimed 200,000 lives in
the Philippines.
• In the Philippines, there is an incidence rate of
approximately one person in 86,241,697.
Etiologic agent.
Certain biotypes of Vibrio cholerae serogroup 01 which
are curved, Gram-negative bacilli that secrete an enterotoxin
(a toxin that adversely affects cells in the intestinal tract)
called choleragen. Other Vibrio spp. (Vibrio parahaemolyticus,
Vibrio vulnificus) also cause diarrheal diseases. Vibrios are
halophilic and are thus found in marine environments.
Vibrio cholerae
Cholera Toxin.
The delivery region
(blue) binds membrane
carbohydrates to get into
cells. The toxic part (red)
is activated inside the
cell .
Reservoirs and Mode of Transmission.
• Infected humans and aquatic reservoirs.
• Transmission is via the fecal-oral route, contact with
feces or vomitus of infected people, ingestion of fecally
contaminated water and foods especially raw or
undercooked shellfish and other seafood and flies.
Diagnosis.
Rectal swabs or stool specimens should be
inoculated onto thio-sulfate-citrate-bile-sucrose (TCBS)
agar; different Vibrio spp. produce different reactions
on this medium. Biochemical tests are used to identify
the various species. Biotyping is accomplished using
commercially available antisera.
ANATOMY AND PHYSIOLOGY OF THE
SYSTEM INVOLVED
 The organs of the digestive system can be
separated into two main groups: those forming the
alimentary canal and the accessory digestive organs.
The alimentary canal performs the whole menu of
digestive functions (ingests, digests, absorbs, and
defecates). The accessory organs (teeth, tongue, and
several large digestive glands) assist the process of
digestive breakdown in various ways.
 Organs of the Alimentary Canal

The alimentary canal, also called the gastrointestinal

(GI) tract, is a continuous, coiled, hollow, muscular tube
that winds through the ventral body cavity and is open at
both ends. Its organs are the mouth, pharynx, esophagus,
stomach, small intestine, and large intestine. The large
intestine leads to the terminal opening, or anus.
MOUTH
Food enters the digestive tract through the mouth, or oral
cavity, a mucous membrane-lined cavity. The lips (labia) protect
its anterior opening, the cheeks form its lateral walls, the hard
palate forms its anterior roof, and the soft palate forms its
posterior roof. The uvula is a fleshy fingerlike projection of the
soft palate, which extends downward from its posterior edge.
The space between the lips and cheek externally and the teeth
and gums internally is the vestibule.
` The area contained by the teeth is the oral cavity
proper. The muscular tongue occupies the floor of the
mouth. The tongue has several bony attachments-two of
these are to the hyoid bone and the styloid processes of
the skull. The lingual frenulum, a fold of mucous
membrane, secures the tongue to the floor of the mouth
and limits its posterior movements.
 At the posterior end of the oral cavity are paired
masses of lymphatic tissue, the palatine tonsils. The
lingual tonsil covers the base of the tongue just beyond.
The tonsils, along with other lymphatic tissues, are part
of the body’s defense system. When the tonsils become
inflamed and enlarged, they partially block the entrance
into the throat (pharynx), making swallowing difficult
and painful.
PHARYNX
The pharynx or throat is a tubular structure that extends
from the base of the skull to the esophagus and is situated
immediately in front of the cervical vertebrae. The oropharynx
and laryngopharynx are food passageways connecting the oral
cavity to the esophagus. No digestion takes place in the
pharynx. Its only related function is swallowing, the mechanical
movement of food. When the bolus of food is pushed backward
by the tongue, the constrictor muscles of the pharynx contract
as part of the swallowing reflex.
ESOPHAGUS
The esophagus , or gullet, is a muscular tube of
approximately 25cm in length and 2cm in diameter. It extends
from the pharynx to the stomach after passing through an
opening in the diaphragm. The esophagus functions primarily
as a transport medium between compartments.
The walls of the alimentary canal organs from the
esophagus to the large intestine are made up of the
same four basic tissue layers, or tunics:
1. The mucosa is the innermost layer, a moist membrane
that lines the cavity, or lumen, of the organ. It consists
primarily of a surface epithelium, plus a small amount of
connective tissue (lamina propria) and a scanty smooth
muscle layer.
2. The submucosa is found just beneath the mucosa. It is a
soft connective tissue layer containing blood vessels,
nerve endings, lymph nodules and lymphatic vessels.
3. The muscularis externa is a muscle layer typically made
up of an inner circular layer and an outer longitudinal
layer of smooth muscle cells.
4. The serosa is the outermost layer of the wall. It consists
of a single layer of flat serous fluid-producing cells, the
visceral peritoneum. The visceral peritoneum is
continuous with the slick, slippery parietal peritoneum,
which lines the abdominopelvic cavity by way of a
membrane extension, the mesentery.
STOMACH
The stomach is a C shaped expanded bag, located just left
of the midline between the esophagus and small intestine. It has
two borders called the greater and lesser curvatures. The first
section is the cardia which surrounds the cardial orifice where
the esophagus enters the stomach. The fundus is the superior,
dilated portion of the stomach. The body is the largest section
between the fundus and the curved portion of the C.
 The pylorus is the curved base of the stomach. Gastric
contents are expelled into the proximal duodenum via
the pyloric sphincter. The inner surface of the stomach is
contracted into numerous longitudinal folds called rugae.
These allow the stomach to stretch and expand when
food enters.
The functions of the stomach include:
• The short-term storage of ingested food.
• Mechanical breakdown of food by churning and
mixing motions.
• Chemical digestion of proteins by acids and
enzymes.
• Stomach acid kills bugs and germs.
• Some absorption of substances such as alcohol.
SMALL INTESTINE
The small intestine is about 1 inch (2.5 cm) in
diameter and approximately 20 feet (6m) long and
extends from the stomach to the cecum of the large
intestine.
The duodenum is the first 10 inches (25 cm) of the
small intestine. The jejunum is about 8 feet long, and the
ileum is about 11 feet in length.
 Digestion is completed in the small intestine, and the
end products of digestion are absorbed in the blood and
lymph. The mucosa has simple columnar epithelium that
includes cells with microvilli and goblets cells that
secretes mucos. Enteroendocrine cells secrete the
hormones of the small intestine. Lymph nodules called
peyer’s patches are especially abundant in the ileum to
destroy absorbed pathogens.
LARGE INTESTINE
The large intestine is horse-shoe shaped and extends
around the small intestine like a frame. It consists of the
appendix, cecum, ascending, transverse, descending and
sigmoid colon, and the rectum. It has a length of approximately
1.5m and a width of 7.5cm. The cecum is the expanded pouch
that receives material from the ileum and starts to compress
food products into fecal material. Food then travels along the
colon. The wall of the colon is made up of several pouches
(haustra) that are held under tension by three thick bands of
muscle (taenia coli).
 The rectum is the final 15cm of the large intestine. It expands to
hold fecal matter before it passes through the anorectal canal to the
anus. Thick bands of muscle, known as sphincters, control the
passage of feces.
The functions of the large intestine can be summarized as:
• The accumulation of unabsorbed material to form feces.
• Some digestion by bacteria. The bacteria are responsible for the
formation of intestinal gas.
• Reabsorption of water, salts, sugar and vitamins
 Accessory Digestive Organs

SALIVARY GLANDS
Three pairs of salivary glands which are the parotid,
submandibular and sublingual glands communicate with the
oral cavity. Each is a complex gland with numerous acini lined
by secretory epithelium. The acini secrete their contents into
specialized ducts. Each gland is divided into smaller segments
called lobes.
TEETH
The function of the teeth is chewing. This is the process
that mechanically breaks food into smaller pieces and mixes
with saliva.

TONGUE
It is the principal organ of the sense of taste that also
assist in the mastication and deglutition of food.
PANCREAS
The pancreas is a lobular, pinkish-grey organ that lies
behind the stomach. Its head communicates with the
duodenum and its tail extends to the spleen. The organ is
approximately 15cm in length with a long, slender body
connecting the head and tail segments. It is made up of
numerous acini (small glands) that secrete contents into
ducts which eventually lead to the duodenum.
LIVER
The liver is a large, reddish-brown organ situated in the right
upper quadrant of the abdomen. It is divided into four lobes
namely the right, left, caudate and quadrate lobes. The liver has
important functions. It acts as a mechanical filter by filtering
blood that travels from the intestinal system. It detoxifies several
metabolites including the breakdown of bilirubin and estrogen. In
addition, the liver has synthetic functions, producing albumin and
blood clotting factors. However, its main roles in digestion are in
the production of bile and metabolism of nutrients.
GALL BLADDER
The gallbladder is a hollow, pear shaped organ that sits
in a depression on the posterior surface of the liver's right
lobe. The main functions of the gall bladder are storage and
concentration of bile.
 RISK FACTORS
Precipitating factors:
•Contaminated food and water
(contact with flies, feces )
•Raw or undercooked seafood
(e.g., shellfish)
•Poor hygiene and sanitation
•Overcrowding(e.g., refugee
camps, impoverished countries,
and areas devastated by famine,
war or natural disasters)
•Poverty
•Malnutrition
•Compromised Immunity
•Reduced or nonexistent stomach
acid (hypochlorhydria or
achlorhydria)
Predisposing factors:
•Age: children and older adults
• People who have had gastric
surgery, who have untreated
Helicobacter pylori infection, or
who are taking antacids, H-2
blockers or proton pump inhibitors
for ulcers
•Type O blood
•Household exposure
•International travel (Latin
America, Africa, Asia, Gulf of
Mexico, Middle East)
PATHOPHYSIOLOGY
 Entry of Vibrio cholerae through oral route
(entry)
leads to

Survival of virulent organisms that pass through

the stomach and into the small intestine
causes
Adherence of Vibrio cholerae to the small intestinal
epithelium

results to
Multiplication of the organisms on the
epithelial cells (colonization)
leads to

Production of cholera enterotoxin by the

bacteria
 results in
Binding of toxin to the plasma membrane of
intestinal epithelial cells
leads to
Release of an enzymatically active
subunit called adenylate cyclase
causes
A rise in cyclic adenosine monophosphate (cAMP) production
results in
Massive secretion of electrolytes and water
into the intestinal lumen
causes

Manifestations of cholera (disease)

leads to

Normal shedding of intestinal cells eventually gets rid of

the toxin (exit)
CLINICAL MANIFESTATIONS
Stage 1: Diarrheal Stage
• Abrupt onset of painless, severe, watery diarrhea that is
often voluminous, flecked with mucus and dead cells, and
has a pale, milky appearance that resembles water in which
rice has been rinsed (rice-water stool)
• Vomiting without nausea that may persist for hours at a time
• Muscle cramps
Stage 2: Dehydration Stage
• Dehydration
• Irritability
• Lethargy
• Sunken eyes
• Dry mouth
• Extreme thirst
• Dry, shriveled skin that's slow to bounce back when pinched into a fold
• Little or no urine output
• Low blood pressure
• Irregular heartbeat (arrhythmia)
• Shock
NURSING CARE MANAGEMENT
• Assess severity, quality, region and time of muscle cramps.
• Assess for signs of dehydration. Observe for excessively dry skin and
mucous membranes, decreased skin turgor, slowed papillary refill.
• Note number, color, amount, consistency and characteristic of stool and
vomitus.
• Note generalized muscle weakness or cardiac dysrhythmias.
• Observe for overt bleeding and test stool daily for occult blood.
• Monitor input and output strictly.
• Monitor vital signs. Blood pressure, pulse, respiration and temperature.
• Weigh daily.
• Increase fluid intake.
• Estimate fluid volume losses like diaphoresis.
• Measure urine specific gravity and observe for oliguria.
• Maintain oral restrictions, bed rest and avoid exertion.
• Provide bed pan or bedside commode.
• Provide a bland diet.
• Assist patient in ambulating to the bathroom.
• Medical septic protective care must be provided.
• Contact precautions must be observed.
• A thorough and careful personal hygiene must be provided.
• Stool, urine and other infected secretions must be properly disposed of.
• Concurrent disinfection must be applied.
• Food must be properly prepared.
• Environmental sanitation must be observed.
Treatment:
Cholera requires immediate treatment because the disease can cause death
within hours.
• Rehydration. The goal is to replace fluids and electrolytes lost through
diarrhea using a simple rehydration solution, Oral Rehydration Salts
(ORS), that contains specific proportions of water, salts and sugar. The
ORS solution is available as a powder that can be reconstituted in boiled
or bottled water. Without rehydration, approximately half the people
with cholera die. With treatment, the number of fatalities drops to less
than 1 percent.
• Intravenous fluids. During a cholera epidemic, most people can be helped by
oral rehydration alone, but severely dehydrated people may also need
intravenous fluids.
• Antibiotics. Recent studies show that a single dose of azithromycin
(Zithromax, Zmax) in adults or children with severe cholera helps shorten
diarrhea duration and decreases vomiting.
• Zinc supplements. Research has shown that zinc may decrease and shorten
the duration of diarrhea in children with cholera.
Prevention:
• Wash your hands. Frequent hand washing is the best way to control
cholera infection. Wash your hands thoroughly with hot, soapy water,
especially before eating or preparing food, after using the toilet, and
when you return from public places. Carry an alcohol-based hand
sanitizer for times when water isn't available.
• Avoid untreated water. Contaminated drinking water is the most
common source of cholera infection. For that reason, drink only bottled
water or water you've boiled or disinfected yourself. Coffee, tea and
other hot beverages, as well as bottled or canned soft drinks, wine and
beer, are generally safe. Carefully wipe the outside of all bottles and cans
before you open them and ask for drinks without ice..
• Eat food that's completely cooked and hot. Cholera bacteria can survive
on room temperature food for up to five days and aren't destroyed by
freezing. It's best to avoid street vendor food, but if you do buy it, make
sure your meal is cooked in your presence and served hot.
• Avoid sushi. Don't eat raw or improperly cooked fish and seafood of any
kind.
• Be careful with fruits and vegetables. When you're traveling, make sure
that all fruits and vegetables that you eat are cooked or have thick skins
that you peel yourself. Avoid lettuce in particular because it may have
been rinsed in contaminated water.
• Be wary of dairy foods. Avoid ice cream, which is often
contaminated, and unpasteurized milk.
• Cholera vaccine. Because travelers have a low risk of contracting
cholera and because the traditional injected vaccine offers minimal
protection, no cholera vaccine is currently available in the United
States. A few countries offer two oral vaccines that may provide
longer and better immunity than the older versions did. If you'd like
more information about these vaccines, contact your doctor or local
office of public health. Keep in mind that no country requires
immunization against cholera as a condition for entry.
JOURNALS
 Sari Cloth a Simple Sustainable Protector from Cholera

ScienceDaily (May 20, 2010) — A five-year follow up study in Bangladesh finds that
women are literally wearing the answer to better health for themselves, their families and
even their neighbors. Using the simple sari to filter household water protects not only the
household from cholera, but reduces the incidence of disease in neighboring households that
do not filter. The results of this study appear in the inaugural issue of mBio™, the first online,
open-access journal published by the American Society for Microbiology (ASM).
"A simple method for filtering pond and river water to reduce the incidence of cholera,
field tested in Matlab, Bangladesh, proved effective in reducing the incidence of cholera by 48
percent. This follow-up study conducted 5 years later showed that 31 percent of the village
women continued to filter water for their households, with both an expected and an
unexpected benefit," says Rita Colwell of the University of Maryland, College Park, a
researcher on the study.
In 2003, Colwell and her colleagues reported the results of a field study that
demonstrated by simply teaching village women responsible for collecting water to filter the
water through folded cotton sari cloth, they could reduce the incidence of cholera in that
group by nearly half. Though the results were promising at the time of the research, there was
concern that the practice of sari water filtration would not be sustained in later years.
 Five years later they conducted the follow-up study to determine whether sari water filtration
continued to be practiced by the same population of participants and, if it were, whether there would
continue to be a beneficial effect of reduced incidence of cholera.
Over 7,000 village women collecting water daily for their households in Bangladesh were selected
from the same population used in the previous study. Survey data showed that 31 percent continued to
filter their water, of which 60 percent used a sari. Additionally, they found that of the control group (the
one that did not receive any education or training in the first study) 26 percent of households now filter
their water.
"This is a clear indication of both compliance with instructions and the sustainability of the method,
but it also shows the need for continuing education in the appropriate use and benefits of simple filtration,"
says Colwell.
The researchers also looked at the incidence of cholera in households during the 5-year follow-up
period. While not statistically significant, they found the incidence of hospitalizations for cholera during
that period reduced by 25 percent.
"With the lower rate of filtration in this follow-up study, it is not surprising that the observed
reduction in disease rate was not as high as the 48 percent observed in the original trial, suggesting that
active reinforcement would have been effective in ensuring higher protection," says Colwell.
They also found an indirect benefit. Households that did not filter their water but were located in
neighborhoods where water filtration was regularly practiced by others also had a lower incidence of
cholera.
"Results of the study showed that the practice of filtration not only was accepted and sustained by
the villagers but also benefited those who filtered their water, as well as neighbors not filtering water for
household use, in reducing the incidence of cholera," says Colwell.
 New Insight Into Predicting Cholera Epidemics in the Bengal Delta
ScienceDaily (Nov. 16, 2009) — Cholera, an acute diarrheal disease caused by the
bacterium Vibrio cholerae, has reemerged as a global killer. Outbreaks typically occur
once a year in Africa and Latin America. But in Bangladesh the epidemics occur twice a
year -- in the spring and again in the fall.
Scientists have tried, without much success, to determine the cause of these
unique dual outbreaks -- and advance early detection and prevention efforts -- by
analyzing such variables as precipitation, water temperature, fecal contamination and
coastal salinity. Now, researchers from Tufts University, led by Professor of Civil and
Environmental Engineering Shafiqul Islam, have proposed a link between cholera and
fluct uating water levels in the region's three principal rivers -- the Ganges,
Brahmaputra and Meghna.
"What we are establishing is a way to predict cholera outbreaks two to three
months in advance," says Islam, who also holds an appointment as professor of water
and diplomacy at The Fletcher School at Tufts. "It's not a microbiological explanation.
The key is the river discharge and regional climate."
The Tufts researchers' findings were reported in the latest issue of Geophysical
Research Letters, published October 10, 2009.
 Understanding cholera's environmental catalysts

Vibrio cholerae lives and thrives among phytoplankton and zooplankton in brackish
estuaries where rivers come into contact with the sea. The Bengal Delta, which scientists
have considered the native land of cholera, is fed by three rivers.
Almost all of the rainfall in the region occurs during the four-month monsoon
season between June and September. Water levels in the river system rise, causing
floods that cover 20 percent of the land in an average year. Water levels then fall rapidly,
though low-lying, depressed areas remain submerged for weeks.
The Tufts team tracked the month-by-month incidence of cholera using data from
the International Center for Diarrhoeal Disease Research, a treatment center that
recorded incidences of cholera for the biggest population center of Bangladesh from
1980 to 2000.
The Tufts team correlated these cholera incidence statistics with an analysis of
water discharges from the three rivers. Their findings suggested two distinctive epidemic
patterns that are associated with the seasonal cycles of low river flows and floods.
A spring outbreak occurs in March, during the period of low river flow in
Bangladesh. The low river flow allows seawater from the Bay of Bengal to move inland,
transporting bacteria-carrying plankton.
 A second epidemic occurs in September and October, after monsoon rains have
raised water levels. Here, a different dynamic takes place. Floodwaters have mixed water
from sewers, reservoirs and rivers. As the floods recede, contamination is left behind..

Predicting cholera before it happens

Islam and his team linked the incidence of cholera cases to the level of water flow
in the rivers. In order to confirm their findings, the researchers looked for a consistent
pattern. They analyzed the incidence of cholera in five years of severely low river flow
from 1980 to 2000 and compared it with five years of average and below average river
flow. The same analysis was done for extreme, average and below average floods to
study the fall epidemic.
The researchers found a relationship between the magnitude of cholera outbreaks
and the severity of the region's seasonal low river flow and floods. "The more severe the
low river flow, the larger the spring epidemic," says Islam. "The same thing is true with
flooding during the fall." Islam says that the findings will contribute to the development
of systems to anticipate and predict cholera outbreaks based on the hydroclimate of the
region.
This research was funded in part by the National Science Foundation and a National
Institutes of Health Fellowship. Researchers included engineering doctoral students Ali S.
Akanda and Antarpreet S. Jutla.
 ‘

How Cholera Bacteria Becomes Infectious

ScienceDaily (Feb. 12, 2010) — In a new study, Dartmouth researchers
describe the structure of a protein called ToxT that controls the virulent nature
ofVibrio cholerae, the bacteria that causes cholera. Buried within ToxT, the
researchers were surprised to find a fatty acid that appears to inhibit ToxT,
which prevents the bacteria from causing cholera. Cholera, which causes acute
diarrhea, can be life threatening, and, according to the World Health
Organization, cholera remains a serious threat to global health.
Doctors have known that bile, found in the intestine, inhibits the
expression of the virulence genes in V. cholerae, but until now, the mechanism
behind this was not completely understood. This study provides a direct link
between the environment of the gut and the regulation of virulence genes, and
it also identifies the regulatory molecule.
 "Finding a fatty acid in the structure was quite a surprise," says F.
Jon Kull, associate professor of chemistry at Dartmouth and senior
author on the paper. Kull is also a 1988 graduate of Dartmouth. "The
exciting thing about this finding is that we might be able to use a small,
natural molecule to treat and/or prevent cholera. We will also use the
structure of the fatty acid as a framework to try and design a small
molecule inhibitor of ToxT."
Kull's co-authors on the paper are Michael Lowden and Maria
Pellegrini with the Department of Chemistry at Dartmouth; Michael
Chiorazzo, a summer undergraduate research fellow; and Karen
Skorupski and Ronald Taylor with the Department of Microbiology and
Immunology at Dartmouth Medical School.
 The researchers used X-ray crystallography to determine the structure of
ToxT. The process involves taking DNA from V. cholerae and using non-
pathogenic E. coli bacteria to produce large amounts of the target protein, in
this case, ToxT. Once protein has been purified, it is concentrated and
crystallized. Then the crystal, which is an ordered array of protein molecules, is
subjected to a powerful X-ray beam. The pattern of diffracted X-rays is
collected on a detector and then analyzed using mathematical algorithms,
eventually revealing the atomic structure of the protein.
Co-author Taylor also notes that "The results of the study are exciting
from the points of view of both the mechanistic aspect of the complex
regulation of V. cholerae virulence gene expression and the potential medical
impact as we now move forward to apply this new knowledge to influence
this mechanism to control infection in humans."
This study was funded by the National Institutes of Health, Institute of
Allergy and Infectious Diseases.
 Designing Probiotics That Ambush Gut Pathogens
ScienceDaily (Sep. 8, 2009) — Researchers in Australia are developing diversionary
tactics to fool disease-causing bacteria in the gut. Many bacteria, including those
responsible for major gut infections, such as cholera, produce toxins that damage human
tissues when they bind to complex sugar receptors displayed on the surface of cells in
the host's intestine.
At the Society for General Microbiology's meeting at Heriot-Watt University,
Edinburgh, Professor James Paton and colleagues from the University of Adelaide
explained how they had added molecular mimics of these host cell receptors onto the
surface of harmless bacteria capable of surviving in the human gut. If given during an
infection caused by a toxin-producing bacterium, these "receptor-mimic probiotics" will
bind the toxins in the gut very strongly, thereby preventing the toxins from interacting
with receptors on host intestinal cells and causing disease.
Effective vaccines are not yet available for many diarrhoeal diseases; and trying to
control or treat these diseases with antibiotics can lead to the development of drug-
resistance. One advantage of this approach to treatment is that the pathogenic bacteria
are unlikely to develop a resistance to it, as that would destroy the basic mechanism by
which they cause disease.
 A further advantage is that the receptor-mimic bacteria bind toxins
more strongly than previous technologies in which synthetic receptors were
displayed on inert silica particles. They are also more cost effective, as the
bacteria can be grown cheaply in large-scale fermenters.
"We initially developed this technology to prevent disease caused by
strains of E. coli bacteria that produce Shiga toxin. These include the
infamous E. coli O157 strain, which causes outbreaks of severe bloody
diarrhoea and the potentially fatal haemolytic uraemic syndrome. Our
prototype receptor mimic probiotic provided 100% protection against
otherwise fatal E. coli disease in an animal model." said Professor Paton, "We
have also developed similar receptor mimic probiotics that are capable of
preventing cholera and travellers' diarrhoea. As well as being able to treat
disease, these probiotics could be given to vulnerable populations following
natural disasters to help prevent outbreaks of diseases like cholera".
 New Vaccine Could Be Lethal Weapon Against Malaria, Cholera
ScienceDaily (Jan. 27, 2010) — Mankind may finally have a weapon to fight two of
the world's deadliest diseases.
A University of Central Florida biomedical researcher has developed what promises
to be the first low-cost dual vaccine against malaria and cholera.
There is no FDA approved vaccine to prevent malaria, a mosquito-borne illness that
kills more than 1 million people annually. Only one vaccine exists to fight cholera, a
diarrheal illness that is common in developing countries and can be fatal. The lone
vaccine is too expensive to prevent outbreaks in developing countries after floods, and
children lose immunity within three years of getting the current vaccine.
"I'm very encouraged because our technique works well and provides an affordable
way to get vaccines to people who need them most and can least afford them," said lead
scientist Henry Daniell.
Daniell's team genetically engineered tobacco and lettuce plants to produce the
vaccine. Researchers gave mice freeze-dried plant cells (orally or by injection) containing
the vaccine. aThey then challenged the mice with either the cholera toxin or malarial
parasite. The malaria parasite studies were completed in fellow UCF professor Debopam
Chakrabarti's lab.
 Untreated rodents contracted diseases quickly, but the mice who received the
plant-grown vaccines showed long-lasting immunity for more than 300 days (equivalent
to 50 human years).
Results from the National Institutes of Health-funded research are published in this
month's Plant Biotechnology, the top-ranked journal in the field.
Clinical trials are needed, and Daniell is hopeful that the results with mice will
translate to humans. It could be yet another example of plants delivering life-saving
medicines.
The dual vaccine follows a string of other "green" vaccines developed in Daniell's
lab. He's created vaccines against anthrax and black plague that generated a
congratulatory call from the top U.S. homeland security official and was featured on the
Discovery Channel. He's also successfully grown insulin in plants to find what could be a
long-lasting cure for diabetes. Daniell's team continues to research these vaccines and is
looking for investors to help fund clinical trials.
Producing vaccines in plants is less expensive than traditional methods because it
requires less labor and technology, Daniell said.
 "We're talking about producing mass quantities for pennies on the dollar,"
he said. "And distribution to mass populations would be easy because it could
be made into a simple pill, like a vitamin, which many people routinely take now.
There is no need for expensive purification, cold storage, transportation or
sterile delivery via injections."
For Daniell, his research is more than his day job. His passion to find
vaccines for the world's top 10 diseases as defined by the World Health
Organization comes from growing up in India. He watched many of his
childhood friends contract malaria, cholera and other diseases.
Daniell, a father of two, joined UCF's Burnett School of Biomedical Sciences
in the College of Medicine in 1998. His research led to the formation of the
university's first biotechnology company. Daniell also became only the 14th
American in the last 222 years to be elected the Italian National Academy of
Sciences. In 2007 he was named a Fellow of the American Association for the
Advancement of Sciences.
"I'm not done yet," he said. "I still have more diseases to attack."