Vibrio cholerae is a Gram-negative, comma-shaped bacterium that is the cause of cholera. It produces a cholera toxin that increases cyclic AMP in intestinal cells, causing an efflux of chloride ions and water into the intestines and resulting in profuse watery diarrhea. Transmission occurs through ingestion of food or water contaminated with the feces or vomit of infected individuals. Treatment focuses on oral rehydration with fluids and electrolytes as well as antibiotics like doxycycline.

1. Cholera
Dr. Aswartha Harinatha Reddy
Assistant Professor
Department of Biotechnology
Bangalore

2.  Vibrio cholerae is a Gram-negative, comma-shaped bacterium.

 The bacterium's natural habitat is water.
 V. cholerae is a facultative anaerobe and has a flagellum at one
cell pole.
 V. cholerae cause diarrhea and vomiting in a host within
several hours to 2–3 days of ingestion.
 V. cholerae was first isolated by Robert Koch.
Vibrio cholerae:

3. Pathogenesis:
 Cholera toxin (also known as choleragen and sometimes
abbreviated to CTX, Ctx or CT) is protein complex secreted by the
bacterium Vibrio cholerae.
 The heat-labile enterotoxin is inactivated at high temperatures.
 The cholera toxin is an oligomeric complex made up of six protein
subunits:
 A single copy of the Alpha subunit (part A, enzymatic), and five
copies of the Beta subunit (part B, receptor binding), denoted as
AB5.
 Subunit B binds while subunit A activates the G protein which
activates adenylate cyclase.

4.  Vibrio Cholerae enterotoxin
activates the stimulatory Gs
protein via ADP-
ribosylation. This stimulates
secretion of chloride ions
and water from enterocytes
into the small intestines, and
causing watery diarrhea.
Pathogenesis

5.  CT’s bind to the GM1 gangliosides .
 Once the Beta subunits bind GM1 molecules (located in the
plasma membrane of the mucosal cells).
 The toxin complex gets endocytosed and transported to the
endoplasmic reticulum.
 Once in the ER, the disulfide bond in the A subunit then gets
reduced, causing the A subunit to dissociate from the complex
and enter the cytoplasm.


6.  Where it binds an ADP ribosylation factor.
 This process causes the activation of adenylate cyclase,
which produces cyclic adenosine monophosphate (cAMP)
from ATP.
 The increase in cAMP changes the transmural ion flow,
causing the secretion of Cl-, K+, Na+ H2O2 in to
intestine.

8. Symptoms of Cholera:
 Watery diarrhea with mucus, which is called rice-water
stool and is the hallmark of cholera.
 In very severe cases, a person can lose 1 L of fluid an hour!
This intense diarrhea leads to other complications, including
 Dehydration
 Muscle cramps due to the loss of potassium ions
 Low blood pH (acidosis)
 Sunken eyes and skin
 Loss of blood volume, leading to very low blood pressure
(hypotension)
 Coma in young children
 Very fast heart rate.

9. Transmission:
 The bacteria causing cholera is present in faeces or other
effluent that may seep into and contaminate waterways, soil or
sources of drinking water.
 Drinking infected water or even just using it to wash foods,
kitchen utensils or culinary items can lead to transmission of
the infection.

10. Treatment of Cholera:
Fluids:
 In most cases, cholera can be successfully treated with
oral rehydration therapy, which is highly effective, safe,
and simple to administer.
 Rice-based solutions are preferred to glucose-based ones
due to greater efficiency.


11. Electrolytes:
 The potassium levels may decrease rapidly in cholera, and
thus need to be replaced.
 This may be done by eating foods high in potassium like
bananas or green coconut water.

12. Antibiotics:
 Doxycycline is typically used first line, although some strains
of V. cholerae have shown resistance.
 Other antibiotics proven to be effective include erythromycin,
tetracycline and chloramphenicol.

13. Streptococcus pneumoniae

14. Pathogenesis:
 Pneumonia caused by Streptococcus pneumoniae, Gram positive,
facultative anaerobic member of the genus Streptococcus.
 S. pneumoniae was recognized as a major cause of pneumonia.
 S. pneumoniae typically colonizing the respiratory tract and
nasal cavity.
 However, in individuals with weaker immune systems and
young children, the bacterium may become pathogenic and
spread to other locations to cause disease.

15.  The capsulated, a polysaccharide capsule that acts as a
virulence factor.
 Usually they are found in pairs of cocci, or diplococci or in
short chains or singly.
 When cultured on blood agar they demonstrate alpha
hemolysis.
 They are non motile organisms.

16. Pathogenesis:
 S. pneumoniae colonization of the nasopharynx is
facilitated by mucus degradation by the enzymes NanA,
BgaA, StrH, and NanB. Ply decreases epithelial cell
ciliary beating, enhancing bacterial adherence.
 Pneumococcal cell wall peptidoglycans may be destroyed
by lysozyme.
 PdgA and Adr deacetylate pneumococcal cell surface
petidoglycan molecules, rendering them resistant to
lysozyme.

17. Symptoms:
Pneumonia may begin suddenly.
 High fever
 Cough
 Shortness of breath
 Rapid breathing
 Chest pains

18. Treatment:
Antibiotics:
 The most commonly used antibiotics, including penicillins,,
cephalosporins, rifampin and vancomycin.
Vaccine:
 There are two types of pneumococcal vaccines: conjugate
vaccines and polysaccharide vaccines.
 They are given by injection either into a muscle or just under
the skin.

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