The first cholera pandemic occurred in the Bengal region of India starting in 1817 through 1824. The disease dispersed from India to Southeast Asia, China, Japan, the Middle East, and southern Russia. The second pandemic lasted from 1827 to 1835 and affected the United States and Europe. The third pandemic erupted in 1839, persisted until 1856, extended to North Africa, and reached South America, for the first time specifically infringing upon Brazil. Cholera hit the sub-Saharan African region during the fourth pandemic from 1863 to 1875. The fifth and sixth pandemicsraged from 1881–1896 and 1899-1923. These epidemics were less fatal due to a greater understanding of the cholera bacteria. Egypt, the Arabian peninsula, Persia, India, and the Philippines were hit hardest during these epidemics, while other areas, like Germany in 1892 and Naples from 1910–1911, experienced severe outbreaks. The final pandemic originated in 1961 in Indonesia and is marked by the emergence of a new strain, nicknamed El Tor, which still persists today in developing countries.  From a local disease, cholera became one of the most widespread and deadly diseases of the 19th century, killing an estimated tens of millions of people.  In Russia alone, between 1847 and 1851, more than one million people perished of the disease.  It killed 150,000 Americans during the second pandemic.  Between 1900 and 1920, perhaps eight million people died of cholera in India. 
Heinrich Hermann Robert Koch was a German physician. He became famous for isolating Bacillus anthracis, the Tuberculosis bacillus and Vibrio cholerae and for his development of Koch's postulates
El Tor v agglutinate sheep & chicken erythrocytes Resistance classical PhageIV & polymixinn B -50 unit disk VP reaction & haemolytic test do not give consistent results
Notes about this slide: Of the more than 200 strains that have been identified, only O1 and the newly emerged O139 have been associated with severe disease and cholera outbreaks (Weir, 2004). In any epidemic, one strain predominates. There is a complex classification system. V. cholerae is divided into two epidemic serotypes - O1 and O139 (there are many other environmental serotypes). All of the information presented below was derived from the review by (Crowcroft, 1994). The O1 strain predominated as the primary epidemic strain until 1992. O1 is further divided into two biotypes, Classical and El Tor. The Classical biotype was responsible for the first six pandemics until it was replaced by the El Tor biotype in 1961. The Classical and El Tor biotypes are further divided into three ribotypes based on the antigens they present: Inaba (A&C antigens); Ogawa (A & B antigens); and Hikojima (A&B&C antigens). The O139 serotype replaced the O1 serotype as the predominant pandemic strain in 1992 when it emerged in Southeast Asia and became the primary strain.
Resistance to heat 56deg 30 minutes boiling few second Alive in ice 4-6 weeks
John snow Food, fluid flies fomite fruits& veg fingers
Sudden, large outbreaks are usually associated with water supply contamination. V. cholerae transmission has also been linked to drinking water drawn from shallow wells, rivers or streams, and even to bottled water and ice. Food is the other important source of V. cholerae transmission. Seafood, especially raw or undercooked shellfish harvested from sewage-contaminated beds or environments where V. cholerae naturally occurs, has repeatedly been shown to be a source of V. cholerae infection. V. cholerae grows well on moist, alkaline foods from which other competing organisms have been eliminated by cooking. Fruits and vegetables grown in sewage and eaten without cooking or other decontamination are potential vehicles for cholera transmission. Freezing foods or drinks does not prevent cholera transmission. Person-to-person contact has not been shown to occur, but may, according to the WHO, still be a possible source of infection.
Unless otherwise noted, the information presented in the notes for this slide was assimilated from the website: www.who.int/entity/water_sanitation_health/dwq/en/admicrob6.pdf After gaining entry into the host through ingestion, the organism colonizes the epithelial lining of the small intestine. The incubation period is one to five days, and patients are symptomatic for two to seven days. The production of Cholera Toxin, discussed in detail later, induces most of the symptoms associated with the disease cholera. For serious cases, death can occur as a result of hypovolemic shock (loss of vital organ function due to rapid fluid loss) within two to four hours of colonization. Two case types: Mild cases (90%) are difficult to distinguish from normal diarrheal diseases. Severe cases (10%) are associated with painless, watery diarrhea, with as much as 20 L day -1 fluid loss (Cotter, 2000) in as little as three to four hours, leading to hypovolemic shock. Severe dehyrdration results in muscle cramps, loss of skin turgor, scaphoid abdomen and weak pulse. (http://gsbs.utmb.edu/microbook.ch024.htm). 3. The onset of diarrhea in cholera allows for the rapid dissemination of copious quantities of this organism into the environment.
90 casesof el tor r mild resembles add typical
This information was assimilated from (Sack et al., 2004). Microbiological methods of detection: Culture from fecal or water samples. Start culture from fecal matter in TCBS (thiosulphate citrate bile salts supports the growth of Vibrios but suppresses most other organisms) and allow it to grow for 18 hours. Start culture of fecal matter in peptone water, a high pH enrichment broth. After incubation in peptone water for 6-12 hours, inoculate a second TCBS plate and allow it to grow for 18 hours. V. cholerae appears as smooth yellow colonies with slightly raised centers. Appearance of these colonies gives a presumptive positive and should be reported to the government health department. Samples must be sent to the appropriate regional reference laboratory for confirmational testing. Rapid tests Dark field microscopy - inoculate a wet mount of the fecal specimen and examine for the appearance of darting microbes that are halted by the addition of O1 or O139 antiserum. Rapid immunoassays PCR and DNA probes If the reader wishes to know additional information about V. cholerae typing and microbiological methods of identification, the information presented below was derived from a publication of the Government of Canada on Laboratory Procedures for the Isolation and Identification of Vibrio cholerae O1 and Non-O1 from foods. 1995. Polyscience Publications . The procedures were written by S. Stavric and B. Buchanan. Biotyping (distinguishing between the Classical and El Tor biotypes as defined on slide 13) can be performed by the following tests: Polymyxin B sensitivity - Classical biotypes show a 12 to 15 mm zone of growth inhibition when subjected to polymixin B whereas El Tor biotypes show only a 1 to 2 mm zone. Hemolysin production - most El Tor biotypes will produce hemolysin and will lyse sheep red blood cells. Classical biotypes do not produce hemolysin and so will not lyse red blood cells. Phage sensitivity - El Tor biotypes are not sensitive to phage IV and will not be lysed. Classical biotypes are sensitive to phage IV and will be lysed. Agglutination with chicken red blood cells - El Tor strains will agglutinate while the Classical biotypes will not.
Floroquinolone,tetracycline,azithro, ampicillin, TM SMXlIf d iarrgoea persist after 48 hrs of starting resistance to antibiotics is suspected
Coal – disinfectantwith arrdeal – walker coefficient 10 or more
10-12% house contacts bacteriologically positive and some develop clinical cases butTo prevent 1 clinical cases10000 person must be given .6-1% community excreat
CHOLERA (AOO)Epidemiology & Control
Cholera Cholera is a severe diarrheal disease caused by the bacterium Vibrio cholerae. The toxin released by the bacteria causes increased secretion of water in the intestine, which can produce massive diarrhea.
Sudden profuse effortless watery diarrhoea followed by vomiting muscular cramps dehydration acidosis renal failure shock and death
History Ancient disease 1817-1923- 6 pandemic VC-classical 1854 - Filippo Pacini 1855- John Snow 1883 – Robert Koch 1961- 7th - Indonesia- El Tor Vibrio 1992 – new strain 0139 emerged Public health importance-Economic losses
Four Phases of Incidence I - < 1817 India II -1817-1923 Pandemic Phase (6 pandemics) SEA, India, China, M.east,USSR , Europe, Africa III -1923-1960 India & the East IV -1961 7th Pandemic
Problem WORLD 4.6million deaths / year 15-40 % of all deaths <5 in tropics 5-10% of all diarrhea in non epidemic situation 98% -India, Pakistan, Bengladesh INDIA 1.7 episodes of diarrhea/ child / year 1/3 of total pediatric admissions Endemic in Bengal, Bihar, Orissa, Assam, TN
Keralaoutbreak in Wayanad district among tribal population 2012 Kozhikode- Medical college 23 cases, waynad (16) kkd(5) mlp(2) & 1 death (wynd)
Epidemiological features 1. Both an epidemic & endemic disease 2. Causes pandemics 3. No stable endemicity 4. Seasonal fluctuations are common 5. Seasonal fluctuations differs between regions
Cholera Epidemic Abrupt onset Create acute public health problem Affects adults as well as children High potential to spread fast & cause death Case fatality 30-40 %
Epidemic curve of cholera Self limiting Sudden rise & gradual fall Tail due to contacts & carriers Hidden among carriers-inter epidemic period
Epidemiology Gram negative non spore forming curved rods ferment glucose sucrose and mannitol
Disease Agent V.Cholera 01 El Tor - ogawa, enaba, hikojima V.Cholera 0139 (Bengal) El Tor - has greater epidemicity - In apparent & mild cases are more - More resistant to disinfectants - Chronic carriers are more - Fewer secondary cases- Survive longer in the external environment
Classification Scheme Toxigenic V. cholerae Division into 2 epidemic serotypes O1 Division into 2 biotypes O139 Classical El Tor Each O1 biotype can have 3 serotypes inaba ogawa hikojima Division into ribotypes A&B A&C A, B, C (A little C) AntigensDesigned using information presented in review by NS Crowcroft. 1994. Cholera: Current Epidemiology. TheCommunicable Disease Report. 4(13): R158-R163.
Agent factors…….. Destroyed by - Boiling , Cresol - Super chlorination Exotoxin acts on cAMP-Pathogenesis H –flagellar & O somatic antigen
Viability of Cholera Vibriooutside the body:-- In tap water (contam. with feces) = 5 days- In stool: (in summer) = 2 days- In stool: (in winter) = 8 days- In corpes = 4 wks- In clothings = 2-6 days- In dates (peelings) = 3 days- In fish = 2-10 days- In milk (raw) = 3 days- In milk (boiled) = 10 days
Epidemiology Reservoir Man - Cases & Carriers - Asymptomatic & mild cases Sub clinical cases &carriers- community spread 1 :50-100 Infective dose - 10¹¹ organisms Incubation period - Hours –5 days (1-2 days) Communicability - 7-10 days
Carries in Cholera Pre clinical / Incubatory Convalescent - 2-3 weeks Contact / healthy < 10 days Chronic >10 yrs Bacteriological examination Estimation of Antibody titre
Host Age Sex Epidemics- adult Non epidemic -children
Environmental factors Climate & season Earthquake ,flood Fairs ,festivals & Pilgrimage Poverty , illiteracy, ignorance, poor standards of living with lack of sanitation
All are susceptible Faeco oral transmission- direct contact water(fluid) Faeces fruits&veg & Fomite Food Mouth Urine Flies Fingers
Collection of samplesStool , Water or food samples Rectal swab Rubber catheterTransport media – Venkatraman – ramakrishnan(VR) or alkaline peptone water
Microbiological & MolecularMethods of Detection Microbiological culture-based methods using fecal or water samples Rapid Tests Dark-field microscopy Rapid immunoassays Molecular methods - PCR & DNA probes www.city.niigata.niigata.jp/ info/sikenjo/521s...
Control of CholeraEpidemic I. Verification of the diagnosis II. Notification Disease under international health Regulations So notifiable to the WHO within 24 hours Continued till the area is declared free of cholera (Twice the incubation period after last case)
III. Appropriate clinical management (a) Early case finding -by rapid & aggressive search (b) Establish treatment centers (c) Rehydration Therapy - No Dehydration - HAF - Some Dehydration - ORS -Severe Dehydration - IVF (d) Maintenance Therapy (e) Antibiotic Therapy
Antibiotic therapy Children TM (5mg/kg) + SM (25mg/kg) bd X 3days Adults Doxycycline ( 300mg single dose) Pregnancy Furazolidone (100mg qid X 3days)
IV. EpidemiologicalinvestigationV. SANITATION MEASURES Water control Excreta disposal Food Sanitation Disinfection – concurrent & terminal -cresol
VI. Chemo prophylaxis Given to close contacts Mass chemo prophylaxis is not indicated Tetracycline 500 mg bd X 3 days Doxycycline 300 mg (6mg/kg)
Oral Vaccines -2 types KILLED WHOLE CELL VACCINE V.cholera 01 +Recombinant β-sub unit of toxin 2 doses 10-14 days apart Protective value 50-60 % Duration of protection 3 years
LIVE ATTENUATED VACCINE Genetically attenuated classical V.cholerae CVD 103-HgR strain Single dose Protection 80 % Antibiotics & proguanil to be avoided ( 1week before &1week after vaccination) Contra indication - Hypersensitivity
Health educationa- Cooking food thoroughly & eating it while still hot;b- Preventing cooked food from being contaminated by contact with raw food (water & ice), or with contaminated surfaces or flies.c- Avoiding raw fruits or vegetables unless they are first peeled.d- Hand washing after defecation, esp. before contact with food or drinking water.
National ADD control programme ORT programme-1986-87 CSSM programme RCH programme ORT corner ORT depots