OROFECAL ROUTE

AND
DISEASES
 INTRODUCTION
• Route of transmission of a disease wherein
pathogens in fecal particles pass from one
person to the mouth of another person. Main
causes of fecal–oral disease transmission
include lack of adequate sanitation (leading to
open defecation), and poor hygiene practices.
 Oro fecal route
• The common factors in the fecal-oral route
can be summarized as five Fs: fingers, flies,
fields, fluids, and food.
 DISEASES

• The list below shows the main diseases that

can be passed via the fecal–oral route
BACTERIA Viruses
•Vibrio cholerae (cholera) •Hepatitis A
•Clostridium difficile (pseudomembranous •Hepatitis E
enterocolitis) •Enteroviruses
•Shigella (shigellosis / bacillary dysentery) •Norovirus acute gastroenteritis
•Salmonella typhii (typhoid fever) •Poliovirus (poliomyelitis)
•Vibrio parahaemolyticus] •Although most human Coronaviruses are
•Escherichia coli not transmitted fecally (Feline
•Campylobacter coronavirus, in contrast, is), there have
also been reports of SARS-CoV-2 being
PROTOZOANS found in stool samples.
•Entameba histolytica(amoebiasis / •Rotavirus gastroenteritis
amoebic dysentery) •Adenovirus gastroenteritis
•Giardia (giardiasis)
•Cryptosporidium (cryptosporidiosis)
•Toxoplasma gondii (toxoplasmosis)
CHOLERA
 CHOLERA
• Cholera is an acute diarrheal illness caused by infection
of the intestine with the bacteria Vibrio cholerae.
 Introduction

 A life-threatening secretory diarrhea induced by

enterotoxin secreted by V. cholerae
 Water-borne illness caused by ingesting water/food
• contaminated by copepods infected by V. cholerae
 An enterotoxic enteropathy (a non-invasive diarrheal
disease)
 A major epidemic disease
 HISTORY
1. 1816-1826 - First cholera pandemic: the pandemic began in Bengal,
and then spread across India by 1820. 10,000 British troops and
countless Indians died during this pandemic.
2. 1829-1851 - Second cholera pandemic reached Russia , Hungary
• and Germany in 1831, London and Paris in 1832.
3. 1852-1860 - Third cholera pandemic mainly affected Russia, with over a
million deaths. In 1853-4, London's epidemic claimed 10,738 lives.
 1854 - Outbreak of cholera in Chicago took the lives of 5.5%
of the population. The Soho outbreak in London ended after
removal of the handle of the Broad Street pump by a
committee instigated to action by John Snow.
 Deaths in India between 1817 and 1860 are estimated to
have exceeded 15 million persons. Another 23 million died
betw4een 1865 and 1917.
 1863-1875 - Fourth cholera pandemic spread mostly in
Europe and Africa. At least 30,000 of the 90,000 Mecca
pilgrims fell victim to the disease.
 Cholera claimed 90,000 lives in Russia in 1866.
 The epidemic of cholera that spread with the Austro-
Prussian War (1866) is estimated to have claimed
165,000 lives in the Austrian Empire.
 Hungary and Belgium both lost 30,000 people. In 1867,
Italy lost 113,000 lives.
 1866 - Outbreak in North America. It killed some 50,000
• Americans.
 1881-1896 - Fifth cholera pandemic; According to Dr A. J. Wall,
the 1883-1887 epidemic cost 250,000 lives in Europe and at
least 50,000 in Americas.
 Cholera claimed 267,890 lives in Russia (1892); 120,000 in
Spain; 90,000 in Japan and 60,000 in Persia. In Egypt
cholera claimed more that 58,000 lives.
 1899-1923 - Sixth cholera pandemic had little effect in Europe
because of advances in public health, but major Russian cities
were particularly hard hit by cholera deaths.
 The 1902-1904 cholera epidemic claimed 200,222 lives in
the Philippines.
 The sixth pandemic killed more than 800,000 in India.

1961-1970s - Seventh cholera pandemic began in Indonesia, called

El Tor after the strain, and reached Bangladesh in 1963, India in
1964, and the USSR in 1966.
January 1991 to September 1994 - Outbreak in South America,
apparently initiated when a ship discharged ballast water. Beginning
in Peru there were 1.04 million identified cases and almost 10,000
deaths.
 RECENT CHOLERA PANDEMICS
 1-6th pandemic:
 1817- west bengal = home of cholera
 V. cholerae O1 biotype classical
 1817-1923, Asia, Africa, Europe, America and Australia
 7th pandemic:
 V. cholerae O1 biotype El Tor
 Began in Indonesia in 1961, reached India in 1964
 Spread to other continents in 1970s and 1980s
 Spread to Peru in 1991 and then to most of South & Central
• America and to U.S. & Canada
 By 1995 in the Americas, >106 cases; 104 dead
 1993: Cholera in Bengal caused by O139 may be
cause of 8th pandemic
• 1831-1832- 22,000 deaths
• 1848-1849- 52,000 deaths
• 1853-1854- John Snow’s work
Massive public concern and sanitary reform
followed.
• Final epidemic was in 1866 there were only
around 2,200 deaths
 VIBRIO CHOLERA
•The organism that causes cholera
was discovered 25 years after John
Snow’s death by Robert Koch
 EPIDEMIOLOGY
Cholera was prevalent in the 1800s, but due to
proper treatment of sewage and drinking water,
• has become rare in developed countries.

Cholera is a fecal disease, meaning that it spreads

when the feces of an infected person
• come into contact with food or water.

 Incidence: 1 in 100,000 worldwide.

DISTRIBUTION
 VIBRIO CHOLERA
• Gram negative.
• Oxidase-positive,
• Facultative anaerobic,
• curved or comma-shaped rods
• Highly motile; polar flagellum
• Sensitive to low pH and die
rapidly in solutions below pH 6
• Proliferate in summers
• Pathogenic and nonpathogenic
strains
• 206 serogroups
 Grows in salt and fresh water
 Endemic in areas of poor sanitation (India and
Bangladesh ), transmitted by fecal-oral route
 Can survive and multiply in brackish water by infecting copepods
 Only O1 and O139 are toxigenic and cause Cholera disease
 PHSIOLOGY OF VIBRIO
 Broad temperature & pH range for growth on media
 18-37C
 pH 7.0 - 9.0 (useful for enrichment)
 Grow on variety of simple media including:
 MacConkey’s agar
 TCBS (Thiosulfate Citrate Bile salts Sucrose) agar
 V . cholerae grow without salt
 Most other vibrios are halophilic
 Incubation period: few hours – few days
 Infective material: stool and vomitus of cases and
carrier
 Period of infectivity:
 Case: 8-10 days
 Convalescent carrier: 15-20 days
 Chronic carrier: months to years
Pathophysiology of Cholera
• Incubation period 2hrs-5 days
• most people do not become ill or show any
symptoms
• Only about 10-20% of infected people show
moderate or
severe symptoms.
• Moderate symptoms difficult to differentiate from
other types of acute diarrhoea
• Group O blood group highest risk
 Signs and Symptoms
• Most people remain asymptomatic. The
symptoms of
• cholera include :profuse, watery diarrhea
stomach pains,leg cramps Mild feverVomiting
Sunken eyes and cheeks ,Dry mucous
membranes ,Decreased urinary output
complications
• More severe symptoms Rapid loss of body
fluids 6 liters/hour 107 vibrios/mL Rapidly lose
more than 10% of bodyweight Dehydration
and shock Death within 12 hours or less Death
can occur within 2-3 hours
Risk factors
WHEN DOES CHOLERABECOME EPIDEMIC?

• After heavy period of rainfall

• When water temperatures rise
• When normal diarrhoeal incidence increases
• Endemic cholera with good sanitation needs
permanent source of vibrio, but with poor
sanitation higher secondary transmission can
maintain endemic status
 LABORATORY DIAGNOSIS
• Visualization by dark field or phase microscopy
– Look like “shooting stars”
• Gram Stain
– Red, curved rods of bacteria
• Isolate V. cholerae from patient’s stool
• Plate on sucrose agar
• Yellow colonies form
• Additional methods of detection include PCR
and monoclonal antibody-based stool tests.
Treatment
 PREVENTION
• Basic health education and hygiene
• Mass chemoprophylaxis
• Provision of safe water and sanitation
• Comprehensive Multidisciplinary Approach:
water, sanitation, education, and
communication
• Blocking routes of transmission – water
disinfection (source and /or household), hand
washing, sanitation, good food hygiene and
well-cooked
• Cholera vibrio doesn’t like acid environment
(block with acidic water eg. With citrus juice,
healthy stomach acid levels, acid food)
 VACCINES
• Parenteral Vaccine : killed
– 2 doses administered 4 weeks apart
– Efficacy of approximately 50% and hardly exceeds 6 months
– Not recommended
• Oral: Killed WC/rBS Vaccine :
– Killed whole-cell V.cholerae in combination with a recombinant B-subunit
of cholera toxin
– 2 doses 15 days apart
– Safe in pregnancy and breastfeeding
– Efficacy of approximately 50% after 3 years
– Only mild side-effects
• Oral: Live, attenuated CVD 103-HgR Vaccine :
– Protection as early as 1 week after vaccination, with >90%
– Unknown efficacy for children under
– No adverse side-effects
 PROGNOSIS
• The prognosis of cholera can range depending
on the severity of the dehydration and how
quickly the patient is given and responds to
treatments.
• Death (mortality) rates in untreated cholera
can be as high as 50%-60% during large
outbreaks but can be reduced to about 1% if
treatment protocols are rapidly put into action.
 CONTROLLING CHOLERA
• Treatment centers
– Set up treatment centers for prompt treatment.
• Sanitary measures.
– food safety and animal health measures
• Comprehensive surveillance data
– (adapt to each situation) for a comprehensive
multidisciplinary approach