Gastrointestinal tract infection

Level: 4
Module: GIT 204 - Gastrointestinal System Module
Topic: Traveler’s diarrhea

Prof. Dr. Ghada Boghdadi

2024
 ILOs

By the end of this lecture, the students are expected to:

➢ Acquire knowledge about clinical presentations of Travelers’ diarrhea (TD) and their microbiological
aspects.

➢ Recognize the basic characteristics and laboratory diagnostic methods of Vibrio cholerae.

➢ Recognize pathogenicity, routes of infection, and predisposing factors of Vibrio cholerae.

➢ Get an idea about treatment and prevention outlines of Vibrio cholerae.

Travelers' diarrhea (TD)

➢ Stomach and intestinal infection.

➢ The most common travel related illness.

➢ Passage of unformed stool (one or more by some definitions, three or more by others) while traveling.

➢ Accompanied by abdominal cramps, nausea, fever, headache and bloating. Occasionally bloody diarrhea may
occur.

➢ Most travelers recover within three to four days with little or no treatment. About 10% of people may have
symptoms for a week.

➢ Bacteria are responsible for more than half of cases, typically via foodborne illness and waterborne diseases. The
bacteria enterotoxigenic Escherichia coli (ETEC) are typically the most common except in Southeast Asia, where
Campylobacter is more prominent
Vibrios
➢ Comma-shaped, curved rod-shaped Gram-negative.

➢ Motile by a polar flagella in darting form.

➢ on Thiosulphate-citrate-bile-sucrose (TCBS) agar on which it

produces yellow colonies

➢ Grows at a very high pH (8.5-9.5) (alkaline) and is readily killed

by acid. Therefore, the infective dose is very high
Classifications:

➢ Halophilic vibrios
- V. parahaemolyticus
➢ Non-halophilic vibrios
- V. cholera o1: classical, El Tor biotype
- Non o1 V. cholerae
❑ O antigens distinguish strains of V. cholerae into not less than 139 known serogroups, almost
all are non-virulent.
❑ Strains designated (O1) and (O139) are known to be responsible for epidemic cholera.
❑ Non O1/non-O 139 cause sporadic cholera-like disease.
❑ O1 serogroup is also divided according to biochemical reactions into 2 biotypes: the classic V.
cholerae and El Tor.
❑ There are three distinct O1 serotypes, named Ogawa, Inaba, and Hikojima, and each type may
display the "classical" or El Tor biotype.
Virulence factors and pathogenesis

1. Colonizing factor.

2. Heat-stable endotoxin.

3. Enterotoxin [cholera toxin CT] or choleragen Toxins:

CT is a heat-labile exotoxin. It is formed of two toxic (A1, A2) and five

binding (B) subunits. The B subunits bind to receptor on cell surface of enterocytes

enabling subunit A1 to enter the cells and perform its activity. Subunit A1 activates

adenylate cyclase enzyme which in turn increases the level of cAMP. The net result is

excessive secretion of chloride, potassium, bicarbonate, sodium and water

molecules out of cell into the lumen leading to a severe form of diarrhea.

4. Mucinase: It degrades the mucous layer.

Cholera
❑ Endemic in India but it may occur in epidemics and even worldwide pandemics.
❑ Incubation period: 1-4 days.
❑ Mode of transmission:
1. By ingestion of water or food that has been fecally contaminated by patients’ or carriers’
excreta.
2. Ingestion of inadequately cooked marine shellfish which may function as reservoirs of
infection.
❑ Clinical picture of cholera:
Sudden onset of severe vomiting, rice watery diarrhea with abdominal cramps. Diarrhea
is severe; the patient may lose up to 20 liters of fluid per day.
Complications include dehydration, hypokalemia, metabolic acidosis, shock and death.

❑ Infection starts in the ileum where the organism attaches to the intestinal microvilli and starts to
produce its exotoxin. The infection remains localized with no invasion into the blood.
Diagnosis

❑ Diagnosis of the first case in a non-endemic area and carrier state:

Full lab. diagnosis must be done before reporting the case as positive for V.
cholera.

❑ Diagnosis of secondary cases during an epidemic:

Cases are diagnosed just by microscopic examination of stools for comma
shaped bacilli with darting motility which can be immobilized by specific anti-O
sera.
Treatment & prevention
❑ The most important part of the treatment of cholera is intravenous fluids to correct fluid and electrolyte imbalance.
❑ Tetracyclines can be used to shorten the period of excretion of the organism in convalescence.

Prevention:
General
❑ Increased sanitation and purification of water and isolation of patients.
❑ Proper washing of foods before eating and good observation of food handlers.
❑ Quarantine measures: Cholera is a quarantinable disease. As cholera is a highly infectious disease, during an
epidemic, any newly discovered cases of cholera should be quarantined until the disease is controlled

Specific measures
❑ Chemoprophylaxis by tetracyclines for exposed persons.
❑ Vaccines:
Parenteral: A killed whole-cell vaccine is available (Koll's vaccine) and oral: B subunit-whole cell vaccine:
(it induces the formation of antibacterial and antitoxin antibodies. Because it is given orally, it induces production of IgA in the intestinal
mucosa which plays a major role in providing immunity against infection).
Vibrio parahemolyticus

❑ Halophilic (salt-friendly) species found in warm oceans.

❑ Cause gastroenteritis epidemics.
❑ Transmitted to humans with food (seafood, raw fish). The illness is transient in most cases
and symptomatic therapy is sufficient.
Viral causes of diarrhea

➢ - Rota virus
➢ - Norwalk virus
➢ - Astrovirus
➢ - adenovirus
Rota virus

➢ The most common cause of severe diarrhea among infants and young children.
➢ It is a genus of non-enveloped, double-stranded, segmented RNA viruses.

➢ There are five species of this virus, referred to as A, B, C, D, and E. Rotavirus A, the most common, causes
more than 90% of infections in humans.

➢ Adults are rarely affected.

➢ Rotavirus is usually an easily managed disease of childhood, but worldwide more than 500,000 children
under five years of age still die from rotavirus infection each year.
➢ fecal-oral route.

➢ Rotaviruses are stable in the environment. Sanitary measures adequate for eliminating
bacteria and parasites seem to be ineffective in control of rotavirus.

➢ Once a child is infected by the virus, there is an incubation period of about two days before
symptoms appear.

➢ Symptoms often start with vomiting followed by four to eight days of profuse diarrhea.
Dehydration is more common in rotavirus infection than in most of those caused by
bacterial pathogens.
Treatment & prevention

• Treatment of acute rotavirus infection is nonspecific and involves the management of symptoms
and, most importantly, maintenance of hydration.

• Rotarix is a live attenuated monovalent vaccine. It is given in 2 doses 1ml each in the first 6 months
of life.
• Rotateq is a new vaccine. It is a live oral pentavalent human/bovine reassortant vaccine containing 5
reassortant rotaviruses. It is given to infants in the USA in 3 oral doses 2ml each at 2, 4, and 6
months.
Adenoviruses

➢ There are about 52 serotypes.

➢ Transmission occurs by respiratory droplets, feco-oral, direct contact, or via swimming pool water.
➢ Most infections are self-limited, asymptomatic, or mild and give long-life immunity.

➢ Diseases: Respiratory tract diseases:

Acute febrile pharyngitis
Pharyngoconjunctivitis (swimming-pool conjunctivitis)

Gastrointestinal diseases
Gastroenteritis in infants