2. Learning objectives
• By the end of this session, the learner
should be able to:
– Define cholera and state its causative agent
– Discuss the epidemiology of cholera
– Describe the pathophysiology and clinical
manifestations of cholera
– Describe the management of cholera
– Describe the complications of cholera
– Describe the prevention of cholera
3. Cholera
• Definition
– Cholera is an acute diarrheal infection caused by
ingestion of food or water contaminated with the
bacterium vibrio cholerae.
– Vibrio cholerae is a comma shaped gram
negative aerobic or facultatatively anaerobic
bacillus.
– Its antigenic structure consists of a flagella H
antigen and somatic O antigen .
– Differentiation of pathogenic strains is dependent
on the O antigen.
4. Strands
• be classified into different serogroups
based on the structure of their O antigens
– Vibrio cholerae O1.
• This serogroup is further divided into two biotypes:
classical and El Tor. Each biotype can be further
classified into two serotypes based on the
structure of the O antigen: Inaba and Ogawa. The
classical biotype was responsible for earlier
pandemics, while the El Tor biotype is associated
with more recent outbreaks.
5. – Vibrio cholerae O139:
• This serogroup, also known as Bengal cholera,
emerged in the Indian subcontinent in the 1990s
as a result of genetic recombination between V.
cholerae O1 strains and other Vibrio species.
• It is characterized by its ability to cause cholera-
like illness despite lacking the classical O1
serogroup antigens.
7. Epidemiology
• A global estimate of 1.3 to 4 million people
get cholera each year and 21,000 to
143,000 people die from it. (WHO, 2023)
• People who get infected my may range
from no symptoms to severe states
8.
9.
10. Pathophysiology
• Transmitted by fecal oral route
• V. cholerae bacteria reach the small
intestine, where they colonize and adhere
to the mucosal surface, initiating infection
• V. cholerae produces several virulence
factors, with cholera toxin being the most
notable.
11. • Cholera toxin is an AB toxin consisting of
two subunits:
– The A subunit (active enzymatic component)
and the B subunit (binding component).
– The B subunit facilitates the entry of the toxin
into intestinal epithelial cells by binding to
specific receptors, such as GM1 ganglioside
receptors.
12. • Once inside the intestinal epithelial cells,
the A subunit of cholera toxin modifies a
regulatory G protein (Gs) by ADP-
ribosylation.
• This modification locks the Gs protein in its
active state, leading to continuous
activation of adenylyl cyclase.
• Adenylyl cyclase catalyzes the conversion
of ATP to cyclic AMP (cAMP), resulting in
elevated intracellular cAMP levels.
13. • Increased cAMP levels activate protein
kinase A (PKA), which phosphorylates and
activates the cystic fibrosis
transmembrane conductance regulator
(CFTR) channel.
• Activated CFTR channels facilitate the
secretion of chloride ions (Cl-) into the
intestinal lumen.
• Additionally, PKA inhibits sodium absorption
channels, reducing sodium reabsorption.
14. • The net effect is an efflux of chloride ions
and water into the intestinal lumen, leading
to watery diarrhea characteristic of
cholera.
15.
16. Clinical manifestations
• The hallmark symptom of cholera is profuse,
watery diarrhea often described as "rice-
water stool."
• Signs of dehydration and electrolyte
imbalances, including hyponatremia,
hypokalemia, and metabolic acidosis.
• Dehydration manifests with symptoms such
as thirst, dry mucous membranes, sunken
eyes, decreased urine output, tachycardia,
and hypotension.
• In severe cases, dehydration can progress to
hypovolemic shock and death if untreated
17. Diagnosis
• History taking
• Physical examination
• Isolation and identification of v. cholerae in
stool cultures.
18. Management
• This can be categorized into two:
– Medical management
– Nursing management
• The goal of management is to replace the
lost fluids and get rid of the
microorganism.
21. Nursing diagnoses
• Imbalanced nutrition less than body
requirement related to loss of food
components in diarrhea evidenced by loss
of weight.
• Deficient fluid volume related to fluid loss
in watery diarrhea evidenced by sunken
eyes.
22. Nursing interventions
• Assessment of frequency and volume of
diarrhea
• Rehydration therapy
• Electrolyte replacement
• Infection control by isolation
• Nutritional support- small frequent meals
• Patient education
• Psychological support
23. Complications of cholera
• Hypovolemic shock
• Renal failure
• Cardiac arrhythmias
• Respiratory failure- due to metabolic
acidosis
• Secondary infections
• Neurologic complications as seizures
24. Prevention
• Improved water and sanitation
infrastructure
• Promotion of hygiene- hand washing
• Surveillance and early detection
• Vaccination- oral cholera vaccines
• Health education of communities
• Response and preparedness
25. References
• Herrington, DA , Hall, RH , Losonsky, G , Mekalanos,
JJ , Taylor, RK , and Levine, MM . Toxin, toxin-
coregulated pili, and the toxR regulon are essential for
Vibrio cholerae pathogenesis in humans. J Exp Med.
(1988) 168:1487–92. doi: 10.1084/jem.168.4.1487
• Kirn, TJ , Lafferty, MJ , Sandoe, CMP , and Taylor, RK
. Delineation of pilin domains required for bacterial
association into microcolonies and intestinal
colonization by Vibrio cholerae. Mol Microbiol. (2000)
35:896–910. doi: 10.1046/j.1365-2958.2000.01764.x
ADP-ribosylation involves the transfer of ADP ribose group from the NAD+ (nicotinamide adenine dinucleotide) onto a specific amino acid residue cysteine 351of the Gs protein.
