Cholera is a acute diarrhoeal disease caused by Vibrio cholerae.
Majority of infection are mild or asymptomatic.
IV B.PHARM, 8-SEMESTER ,SOCIAL AND PREVENTIVE PHARMACY.
CHOLERA DISESASE
DEFINITION, SYMPTOMS, CAUSES, TREATMENT, PREVENTION.
A PowerPoint describing what Cholera is and the effects it has on people. Graphs showing cases and deaths around the world are shown as well as a case study of Cholera in Zimbabwe.
Non-typhoidal Salmonellosis, is one of the most common and widely distributed foodborne diseases, with tens of millions of human cases occurring worldwide every year.
In the United States, the incidence of NTS infection has doubled in the past 2 decades.
In 2009 there were 14 million cases of NTS.
Cholera is a acute diarrhoeal disease caused by Vibrio cholerae.
Majority of infection are mild or asymptomatic.
IV B.PHARM, 8-SEMESTER ,SOCIAL AND PREVENTIVE PHARMACY.
CHOLERA DISESASE
DEFINITION, SYMPTOMS, CAUSES, TREATMENT, PREVENTION.
A PowerPoint describing what Cholera is and the effects it has on people. Graphs showing cases and deaths around the world are shown as well as a case study of Cholera in Zimbabwe.
Non-typhoidal Salmonellosis, is one of the most common and widely distributed foodborne diseases, with tens of millions of human cases occurring worldwide every year.
In the United States, the incidence of NTS infection has doubled in the past 2 decades.
In 2009 there were 14 million cases of NTS.
Vibrio cholera and Halophilic vibrio.pptDrmayuribhise
A 4-year-old boy developed severe watery diarrhea and vomiting. The stool collected has a rice water type of appearance. It was sent for bacteriological analysis.
a. What is the probable etiological diagnosis of this condition?
b. Describe in detail the pathogenesis of this condition.
c. Add a note on its laboratory diagnosis.
Which of the following media can be used as transport medium for vibrio?
a. Selenite F broth
b. Nutrient broth
c. Tetrathionate broth
d. Venkatraman–Ramakrishnan medium
All of the following tests can differentiate between classical and El Tor biotypes of V. cholerae, except:
a. β-hemolysis on sheep blood agar
b. Chick erythrocyte agglutination
c. Growth on TCBS agar
d. Polymyxin B (50 IU)
Pathogenesis of V. cholerae involves one of the following second messenger systems:
a. cGMP
b. cAMP
c. Ca2+
d. IP3
Selective media for Vibrio cholerae:
a. TCBS
b. Mannitol salt agar
c. Robertson cooked meat medium
d. Modified Thayer Martin medium
All of the following Vibrio species are halophilic, except:
a. V. cholerae
b. V. parahaemolyticus
c. V. alginolyticus
d. V. vulnificus
O139 (Bengal strain)—all are true, except:
a. Capsulated
b. Toxigenic
c. Clinically similar to El Tor
d. More common than El Tor
All are selective media for V. cholerae, except:
Alkaline peptone water
Alkaline bile salt agar
TCBS agar
Monsur’s agar (GTTTA) medium
Which of the following confirms the isolate of V. cholerae as Hikojima serotype?
a. If agglutinated with Ogawa antisera
b. If agglutinated with Inaba antisera
c. If agglutinated with Hikojima antisera
d. If agglutinated with both Ogawa and Inaba antisera
Gram negative
Rigid, curved rods
“Vibrio” – vibratory motility
Non - sporing
Non - capsulated
Present in marine environments & surface waters worldwide
1854 – observed by Pacini
1883 – first isolated by Koch
Vibrio cholerae Top
V. cholerae was first described as the cause of cholera by Pacini in 1854. Pathogenic V. cholerae
produces a heat-sensitive enterotoxin that causes the characteristic cholera symptoms, including
"rice water stool." The species comprises several somatic (O) antigen groups, including O-group1, which is associated with classical and El Tor biotypes. V. cholerae Ol may have several
serotypes, including Inaba, Ogawa, and Hikojima. V. cholerae non-O1 (referred to in older
literature as nonagglutinable or NAG vibrios) also can cause gastrointestinal disease, though
typically less severe than that caused by V. cholerae O1 (Yamamoto et al., 1983). Serotype O139
is an exception, and produces classic cholera symptoms. This serotype was first identified in
1992 (CWG, 1933) as the cause of a new epidemic of cholera in India and Bangladesh. Non-O1
V. cholerae is found more readily in estuarin! e waters and seafood in the United States than is
the Ol serogroup; however, the 0139 serogroup has not yet been found here. Because this species
can grow in media lacking sodium chloride, it is not considered a halophilic Vibr
Epidemiology and Control Measures for CholeraAB Rajar
It is an acute diarrheal disease caused by Vibrio Cholera typically characterized by sudden onset of profuse,effortless,watery diarrhea followed by vomiting, rapid dehydration, muscular cramps and suppression of urine.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
3. Introduction
• Cholera is an ancient disease
• Since 1817, seven (7) cholera pandemics have been recorded. The pandemics
originated from the Indian subcontinent,
• The seventh pandemic of cholera began in 1961; by 1991 it has affected 5
continents and it continues till today. Recognised to be caused by the El Tor
biotype of V Cholerae O1.
• It is common in areas with civil unrest, war, natural disaster (flooding),
crowded living conditions and poor sanitation.
• It is an epidemic prone disease for notification on the integrated disease
surveillance And response Platform in Nigeria (IDSR).
4. • Cholera is an intestinal infection caused
by Vibro cholerae.
• Comma shaped gram negative aerobic
or facultative anaerobic bacillus
• 1.3 um in length by 0.5-0.8um in
diameter.
• Antigenic structure: flagella H antigen
and somatic O antigen (determines
pathogenic and non-pathogenic strain).
• Epidemic cholera serogroup: V cholerae
O1 and V cholerae O139
• Current predominant pathogen the El
Tor biotype of V cholerae.
5. • Serotype Inaba: O antigens A
and C
• Serotype Ogawa: O antigens A
and B
• Serotype Hikojima: O antigens
A, B and C
• Disease caused by 0139 and
O1 strains are similar as they
both produce enterotoxin that
promote secretion of fluid and
electrolytes into the lumen of
the small intestine.
6. Epidemiology
• Cholera can be endemic, an epidemic or a pandemic disease.
• Worldwide : 1 – 4 million reported cases annually
• Mortality : 21,000 to 143,000
• US:Between January 1,1995 and 31st December 2000 61 cases were reported, 37
had travel-associated cases, 24 were acquired in the US.
• International travellers: 1 case per 500,000 population, range of 0.05-3.7 cases
per 100,000 population.
• Between 1970 and 2011, Africa reported 3,221,050 representing 46 % of all cases
reported globally.
• Sub-Saharan Africa accounted for 86 % of reported cases and 99 % of deaths
worldwide in 2011.
• CFR: 0 in many countries to 3.2% in Zambia, 5.2% in Angola and 6.8% in Cha
7. • Nigeria: cholera is endemic and seasonal (late weeks of February to October).
• first series of cholera outbreaks reported between 1970 and 1990.
• Major epidemics also occurred in 1992, 1995-1996, and 1997.
• January - October 2010: 37,289 cases mortality 1,434
• In 2011: 22,797 cases 728, case fatality rate of 3.2%
• Outbreaks were also recorded in 2018 with the NCDC reporting 42,466 suspected cases
including 830 deaths with a case fatality rate of 1.95% from 20 out of 36 States from the
beginning of 2018 to October 2018.
8. • The duodenum, and upper jejunum are
most affected, due to the volume of fluid
produced the absorptive capacity of the
large bowel is overwhelmed, with
resultant severe diarrhea,
shock(dehydration), acidosis (loss of
bicarbonate).
• The enterotoxin acts locally, it does not
invade the intestinal wall. Hence few
neutrophils are appreciated in the stool.
• 0139 Bengal strain: produces novel 0139
lipopolysaccharide (LPS) and an
immunologically related O-antigen
capsule. These enhance virulence and
resistance to human serum in vitro and
sometimes development of bacteremia.
9. • Enterotoxin : protein molecule composed
of 5 B subunits and 2 A subunits.
• B subunit binds to the Monosialosyl
ganglioside, GM1.
• A1 subunit activates adenylate cyclase,
increase cAMP.
• cAMP: blocks absorption of sodium and
chloride by the microvilli, whilst
promoting the secretion of Cl and water
by the crypt cells. Fluid, bicarbonate,
and potassium are lost with the osmotic
pull of the NaCl as it travels down the
intestine.
• Resulting in isotonic watery diarrhea.
10. Host Factors/Risk factor
• Poor sanitary conditions and water contamination
• Age: Children and elderly more susceptible
• Sex: Nil pridelection
• Raw /undercooked food :
• Immunocompromised more susceptible
• Hypochlorhydra: Low gastric acid levels
• Blood group: O greater than B greater than A greater than AB
11. Transmission
• Humans only reservoir
• Casual contact in unsanitary conditions
• Contamination of food and water
12. Communicability
• During acute stage
• Few days after recovery
• By end of week 70% non-nfectious
• By end of third week 98% non-infectious
13. Incubation
• Few hours to 5 says
• Average 1-3 days
• Shorter in people with high gastric pH and consumption of large doses of
bacteria
15. Clinical presentation
• Asymptomatic 75%
• mild 20%
• Severe 2-5%
• Painless watery diarrhea
• Vomiting
• Abdominal cramps
• Nil fever
• Death 18hrs to several days without
treatment.
16. • Cholera gravis : 5% of infected patients, severe watery diarrhea, vomiting,
and dehydration.
• Cholera sicca: ileus and abdominal distention from massive outpouring of
fluid and electrolytes into intestinal loops. High mortality from toxemia
before nausea and vomiting.
17. • Diarrhea: main symptom
• >5yrs : severe dehydration, from acute severe diarrhea (usually without
vomiting).
• >2yrs : acute watery diarrhea in an area where a cholera outbreak was
recorded.
• Volume: >240mL/kg body weight in 24hrs.
• Initially contain fecal matter and progress to opaque white liquid “rice
water” often not malodorous.
18. • Diarrhea: main symptom
• >5yrs : severe dehydration, from acute
severe diarrhea (usually without
vomiting).
• >2yrs : acute watery diarrhea in an
area where a cholera outbreak was
recorded.
• Volume: >240mL/kg body weight in
24hrs.
• Initially contain fecal matter and
progress to opaque white liquid “rice
water” often not malodorous.
19. • Dehydration: develop rapidly within
hours. Isotonic dehydration, which
can lead to Acute tubular necrosis,
and renal failure. When it is Severe,
dehydration can lead to vascular
collapse, shock and death.
• Tachypnea and hypercapnia due to
metabolic acidiosis.
20. • Metabolic/ systemic manifestations:
• Hypoglycemia: convulsion and coma
• Acidemia.
• Hypokalemia: K+ loss in stool, mean
serum K+ app 3.0mmol/L. children
can have normal serum K+ despite
severe K+ depletion.
• Hypocalcemia: rehydration with HCo3
containing fluids. Chvostek and
Trousseau sign present, and
spontaneous tetanic contractions.
22. Investigations
• Direct microscopic examination of stool (dark-field examination), gram stain,
culture and serotype and biotype identification.
• Hematologic test: hematocrit, serum specific gravity and serum protein are
elevated, leukocytosis without a left shift.
• Serum Na: 130-135 mmol/L, K+ normal initially and reduced after correction of
acidiosis, hyperglycemia (systemic release of epinephrine, glucagon, and cortisol).
• Raised BUN and Cr.
• Reduced HCO3: <15mmol/L
• Elevated anion gap (increase in serum lactate, protein and phosphate levels)
• Low arterial pH 7.2
• Mg and Ca elevated due to hemoconcentration
• PCR testing for screening food samples.
• Rapid test kits
23.
24.
25.
26.
27. Criteria for discharge
• Adequate oral intake Post hydration
• Normal urinary flow
• Maximum diarrhea flow of 400mls /hr
28. Prevention
• Multisectorial approach necessary (health, water and sanitation, fishery and
agriculture and education).
• Sanitation of water supply and making water safer (boiling and addition of
Chlorine).
• Appropriate hygiene for food preparation and personal hygiene.
• Sensitive surveillance and prompt reporting.
29. Vaccine
• 3 oral vaccines identified by the WHO
• Used mostly by travellers
• One vaccine consists of a monovalent killed whole-cell V cholerae O1 with
purified recombinant B-subunit of cholera toxoid (WC/rBS).
• Shanchol and ORCVAX are bivalent vaccines that are based on serogroups
O1 and O139
• CVD 103-HgR is a cholera vaccine developed by the Swiss Serum and
Vaccine Institute in Berne, Switzerland