CHOLERA
MD, Grand PhD in Medical sciences
Professor
Manapova Elvera Ravilevna
DEFINITION
• Cholera is an acute anthroponotic intestinal
infection caused by toxigenic Vibrio cholerae O-
group 1 or O- group 139 (Bengal) characterized by
diarrheal syndrome which leads to dehydration,
demineralization, and hypovolemic shock in
severe cases .
Patient N., 17 years old, was admitted to the infectious hospital early in the morning
with acute onset of disease. At night, liquid watery stools appeared 10 times within 2-3
hours, then defecation became more frequent, the stool became countless times,
gradually acquired the appearance and consistency of "rice water". Plentiful vomiting
"fountain" has joined.
From the epidemiological history: 3 days ago she returned from India
On examination: a serious condition. Body temperature 35.7°C. The skin is pale,
acrocyanosis. Facial features are sharpened. Skin turgor is reduced, "washerwoman's
hands". Dark circles under the eyes. There is a convulsive syndrome in the form of
"obstetrician's hand" and "horse foot". Respiratory rate - 30/min., muffled heart sounds,
pulse - 126/min., filiform, blood pressure - 60/40 mm Hg. Tongue dry, coated with thick
dark coating. Abdomen sunken, painless. On palpation, there is rumbling, noisesloshing
fluid in the mesogastrium. Anuria.
returned from a tourist trip to India.
EPIDEMIOLOGY
• The main reservoirs of V. cholerae are
1 people and carrier
2 aquatic sources such as brackish water and estuaries
• Fecal-oral mechanism
• Pathway – watery, alimentary
• Factors - contaminated water and food
PATHOGENESIS
• Bacteria are ingested in contaminated water or food.
Bacteria pass through the stomach to the gut, where
they colonize the surface of the small intestine.
V. Cholerae is non-invasive (no inflammation in
intestine)
does not cause tissue damage.
• Multiplication occurs on the surface
of the gut with secretion of Cholera toxin.
(syn.: cholerogen, enterotoxin).
• Enterotoxin promotes the secretion of fluid and
electrolytes into the lumen of the small intestine.
Pathogenesis
Causes of AII
Noninvasive Invasive
([Link], [Link] - (Salmonella, Shigella –
enterotoxigenic strains) invasive strains)
Enterotoxin Endotoxin
intestinal membranes - disturbance of water and electrolytes movement
nonInvasive pathogens:
• No invasion in enterocytes and
epithelial cells
• No cellular destruction
• No inflammation in intestine
• pathogens, Ag and toxin don’t enter
the lymphatics and bloodstream
• No toxicosis
• hemodynamic disturbances due the
to Dehydration!!!!! (exicosis)
Summary
The mechanism of diarrhae is same in
different ethiological factors:
1. hypersecretion in crypt cells
2. inhibition of absorption in villi
No intoxication syndrome
Dehydration!!!!!
1. Intoxication
Hypovolemia, hypokalemia, hypocloremia,
metabolic acidosis and respiratory alkalosis
(secondary) develop.
CLINICAL PICTURE
• Incubation period: varies with the size of the
infecting dose and lasts on average 24-48
hours, but may be up to 5 days;
• Fever is absent (endotoxin is not absorpted)
• The disease always starts with sudden onset
of watery diarrhea, which may be followed by
vomiting.
Main clinical syndromes of
cholera:
1/Diarrheal
2/Dehydratation
The degrees of dehydration by Pokrovsky and
their clinical characteristics:
• I (compensated) - with 1-3% loss of normal
body weight. Thirst, and dryness in the
mouth; BP and Ps within normal range
• II (subcompensated) – 4-6% of body weight is
lost. Dryness of the tongue, dry mucus
membranes, BP is decreased (systolic 80-90
mm Hg), in hypotonic patients up to 60 mm
Hg, tachycardia, cyanosis of lips, oliguria
• III (decompensated) – 7-10% of body weight
is lost. Unusual sleepiness or tiredness , the
signs of disturbed hemodynamics, SBP is
lower than 60 mm Hg, tachycardia,
acrocyanosis, anuria (kidneys stop producing
urine when SBP is lower than 60 mm Hg),
compensatory dispnea,
wrinkled, “washerwoman” skin, glassy or
sunken eyes,
sunken “soft spots” (fontanelles) in infants
• IV (terminal) – more than 10% of body weight
is lost.
The loss of more 12% of body weight is not
compatible with life; this condition in cholera may
be achieved in 6-12h
SPECIFIC LAB
• Presumable positive result comes after 12h,
final positive after 24h, final negative after 36h.
• Agglutination with O1 antigen: if positive then
cholera, if negative then nonagglutinating
vibrions.
• PCR - high degree of sensitivity and specificity
(extraction of Tox gene from genome).
SPECIFIC LAB
• identification of V. cholerae in the stool.
• V. cholerae grows on thiosulfate-citrate-bile
salts-sucrose (TCBS) agar or Monsur‘s gelatin
taurocholate-tellurite agar (GTTA) or 1%
alkaline peptone water (enrichment media).
NONSPECIFIC LAB
• elevated hematocrit value may be noted as a
result of hemoconcentration.
• Neutrophil leukocytosis may be observed,
especially in severe cases.
• elevated blood urea nitrogen and creatinine
due to prerenal azotemia.
SPECIFIC TREATMENT
The goal of antibiotic therapy is to eradicate infection.
The drugs used for adults include tetracycline, doxycycline,
ciprofloxacin and cotrimoxazole
DURATION(3-5 days).
•Antibiotic should be started when cholera is suspected without
waiting for lab confirmation
NONSPEFIC TREATMENT
• goal of therapy is to replenish fluid losses caused by
diarrhea and vomiting.
• Rehydration is accomplished in 2 phases
1/ rehydration (primary) and
2/ maintenance (correcting).
– rehydration phase is to restore normal hydration status,
which should take no more than 1-2 hours (in other acute
intestinal infections 2-4h, but for children and elderly 6-8h).
– maintenance phase is to maintain normal hydration
status by replacing ongoing losses. The oral route is
preferred, and the use of oral rehydration solution (ORS)
at a rate of 500-1000 mL/h is recommended.
TREATMENT/4
• One standard remedy is the WHO/UNICEF glucose-based
Oral Rehydration Salts (ORS) solution. WHO/UNICEF ORS
solution contains:
Reduced osmolarity ORS grams/litre
Sodium chloride 2.6
Anhydrous Glucose 13.5
Potassium chloride 1.5
Trisodium citrate, dihydrate 2.9
There are several commercially available products but an
inexpensive home-made solution consists of 8 level
teaspoons of sugar and 1 level teaspoon of table salt mixed
in 1 liter of water. Fructose (fruit sugar) or artificial
sweeteners should not be used instead of sugar as they may
increase diarrhea and/or not provide sufficient energy. A half
cup of orange juice or half of a mashed banana can be
added to each liter both to add potassium and to improve
taste.
Share
Cholera outbreak in an informal settlement
at Shahpur huts, Panchkula District,
Haryana State, India, 2019.
Jain A, Choudhary S, Saroha E, Bhatnagar
P, Harvey P.
Indian J Public Health. 2021
Jan;65(Supplement):S51-S54. doi:
10.4103/ijph.IJPH_970_20.
PMID: 33753593 Free article.
In September 2019, after a reported death
due to acute diarrheal disease in Shahpur
village, Panchkula district, Haryana state,
India, we conducted an outbreak
investigation to identify the etiological
agent, estimate the burden of disease, and
make re …
Cholera, III degree dehydration, Cholera, III
degree dehydration, severe course.
Hypovolemic shock III [Link]
course. Hypovolemic shock III degree.
