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Water borne diseases


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Water borne diseases

  2. 2. WATER BORNE DISEASES Diseases caused by ingestion of water , contaminated by , human or animal excrement , containing various pathogenic micro-organisms.
  3. 3. WATER BORNE DISEASES Diseases caused by ingestion of water , contaminated by , human or animal excrement , containing various pathogenic micro-organisms. Includes : Cholera Typhoid Dysenteries
  4. 4.  An acute diarrheal disease, caused by Vibrio Cholerae.  In the severe form , Painless watery diarrhea and copious effortless vomiting occurs, leading to hypovolemic shock and death within 24 hours.  If treated early , then the disease lasts for around 4-6 days , during which the patient loses huge amounts of liquids and electrolytes from his body.
  5. 5. CLINICAL FEATURES :  Stool is typically , a colorless watery fluid with flecks of mucus , called rice water stools.  Has a characteristic inoffensive sweetish odor, with bicarbonate-rich isotonic electrolyte solution and little protein.  It leads to diminution of ECF volume, hemoconcentration, hypokalemia, base-deficit acidosis and shock.  Muscular cramps, Renal failure, pulmonary edema, cardiac arrhythmias, and paralytic ileus.  Clinical illness begins slowly with mild diarrhea and vomiting within 1-3 days OR abruptly with sudden massive diarrhea.
  6. 6. ORGANISM :  Vibrios are Gram –ve , rigid, curved rods.  They are actively motile by means of a polar flagellum. The movement is vibratory motility , hence the name Vibrio.  They are asporogenous and noncapsulated.  Most important member of this genus is Vibrio cholerae, causative agent of cholera. MORPHOLOGY :  It is a short, curved, cylindrical rod with rounded/pointed ends.  Size : 1.5µm * 0.2-0.4 µm
  7. 7.  Koch described these organisms as ‘ fish in stream’ appearance –as seen in thin films of mucous flakes from acute cholera cases.  Strongly aerobic . In anaerobic conditions , growth is scanty.  Temperature range that supports their growth is 16 – 40ºC , with optimum temperature being 37ºC.  Ph that supports their growth is 6.4 – 9.6 ; optimum being 8.2 .  Distinguishing feature : Oxidase test : +ve
  8. 8.  Nutrient Agar : Moist, translucent, round discs, about 1-2mm in diameter, with bluish tinge in transmitted light. Has distinctive odor.  MacConkey Agar : Colorless colonies at first, but later become reddish, due to prolonged incubation- late fermentation of lactose occurs.  Blood Agar : Initially green colored zone appears, which later becomes clear due to hemodigestion. Various special media have been employed for cultivation or orgs.
  9. 9. TRANSPORT MEDIUM :  Delicate organisms do not survive the time taken for transport of the specimen to the diagnostic labs / they may be overgrown by non-pathogens, Hence a special media is devised for transporting these samples , known as Transport Media.  Examples :  Venkataraman-Ramakrishnan medium (VR) 20g crude sea salt 5g Peptone 1L Distilled water. PH is 8.6 - 8.8  Cary-Blair medium : Sodium chloride + Sodium thioglycollate + Disodium Phosphate + Calcium Chloride. At PH 8.4  Autoclaved Sea water also serves as Transport media.
  10. 10. Carbohydrate Fermentation : BIOCHEMICAL TESTS : Glucose Mannitol Maltose Sucrose Lactose Acid produces Acid produces Acid produces Acid produces Acid produces No Gas No Gas No Gas No Gas Late Fermentation
  11. 11. Carbohydrate Fermentation : BIOCHEMICAL TESTS : Glucose Mannitol Maltose Sucrose Lactose Acid produces Acid produces Acid produces Acid produces Acid produces No Gas No Gas No Gas No Gas Late Fermentation Indole formation and Reduction of nitrates to Nitrites, contributes to Cholera red reaction. Catalase Oxidase Methyl Red Urease +ve +ve -ve -ve Other Tests :
  12. 12. CLASSIFICATION : VIBRIO Group A Cholera vibrios Biochemical similarities 01 Non-01 Group B Biochemically, antigenically heterogenous
  13. 13. CLASSIFICATION OF 01 : 01 Classical Ogawa Inaba E1 Tor Hikojima
  14. 14. PATHOGENESIS : origin and development  Vibrios enter orally via contaminated food and water  In small intestine, vibrios cross mucus and reach epithelial cells by chemotaxis, motility, mucinase and with help of other proteolytic enzymes.  Hemagglutinin-protease cleaves mucus & fibronectin thereby releasing the vibrios to bowel mucosa facilitating their spread to remaining parts of intestine.  Adhesion to the epithelial surface is due to presence of ‘toxin co-regulated pilus’ , special type of fimbria.
  15. 15. Mechanism:  Throughout the course of infection , vibrios remain bound to the surface.  Vibrios multiply on the intestinal epithelium and produce a toxin, ‘cholera enterotoxin’ of 84K Daltons MW.  The toxin inhibits intestinal absorption of Na and clˉ .  Thereby causing clinical manifestations of cholera i.e., depletion of massive water and electrolytes.  Vibrios also possess lipopolysaccharide O antigen - endotoxin; It has no role in pathogenesis , but helps in providing immunity induced by killed vaccines.
  16. 16. Laboratory Diagnosis :  Stool collected at the acute stage, before administration of antibiotics, is most useful specimen in diagnosis.  Isolation is easy, as vibrios are present @106 – 109 /ml.  Samples are collected by lubricated catheters, rectal swabs – absorbing around 0.1 – 0.2 ml.  Vomits are not useful, as they have negligible amount or no amount of morgs.  Collected samples ought to be preserved at 4ºC, as vibrios die at tropical temperatures.  They are sent to labs in T.M. and then asap are transferred to Monsur’s medium.
  17. 17. Lab tests:  No direct microscopic examination is done.  Motility of vibrio is seen under dark- field/phase contrast microscope.  Non-specific fluorescence is common yet complicated technique.  Slide-agglutination tests may also be done, followed by chick red cell agglutination.  The strains are sent to NICED : National Institute of Cholera & Enteric Diseases, Kolkata ; for further tests.
  18. 18. TREATMENT:  Up to 80% of cases can be treated through oral rehydration salts  Severe cases require intravenous fluids  Parenteral Vaccine : 2 doses administered 2 weeks apart 50% efficiency provides 6 months protection  Killed Vaccine : Killed whole-cell + recom. B-subunit of CT Safe even during pregnancy & breastfeeding Efficiency is 75-80%,decreases to 50% - 3yrs
  19. 19. Prevention & Control  Hygiene education  Good nutrition  Good sanitation  Water related issues should be addressed immediately  Public health infrastructure is of utmost importance to control outbreaks  Avoid contacting soils that may be contaminated with feces  Do not defecate outdoors ~ rural areas  Wash /Sanitize our hands before eating  While travelling to places with poor sanitation , avoiding contaminated water
  20. 20. World Distribution of Cholera
  21. 21. Also Known As :  Enteric Fever  Bilious Fever  Yellow Jack
  22. 22. Typhoid fever is caused by Salmonella typhi. The term ‘Enteric fever’ consists of both typhoid and paratyphoid fever. Typhoid was once not demarcated from normal fevers, but a detailed study of the diseases was given by Bretonneau, 1826 – identified the intestinal lesions. Louis gave the name ‘Typhoid’ in 1829
  23. 23. Salmonella:  Belongs to Enterobactericieae family  Gram –ve rods causing intestinal infections  Facultative anaerobes & Aerobes  Size :1-3µm * 0.5µm  Motile with peritrichate flagella CULTURAL CHARACTERISTICS : • Grows readily on simple media • PH range : 6-8 • Temperature : 15-41ºC • Large colonies,2-3mm in diameter- circular, low convex translucent and smooth
  24. 24. Growth on media :  MacConkey & Deoxycholate Citrate media : Colorless colonies – due to absence of lactose fermentation .  Wilson and Blair bismuth sulphite medium : Jetblack colonies with metallic sheen- H2S forms  Selenite F and Tetrathionate broth are employed as Enrichment media.
  25. 25.  Salmonella possess the following 3 antigens , based on which they are classified and identified.  3 main antigenic factors are : Flagellar antigen or H antigen Somatic antigen or O antigen Surface antigen or Vi antigen  H antigen : Antigen on flagella. Heat labile protein, i.e. destroyed on heating. When mixed with antisera, agglutinate rapidly producing large, fluffy, loose clumps. Strongly Immunogenic.  O antigen : Phospholipid-protein-polysaccharide complex. It is an integral part of cell wall. Identical to endotoxin. Heat resistant. On mixing with antisera, a compact, chalky, granular clumps are formed.  Vi antigen : known as surface antigen or encapsulation antigen, as it encapsules or serve as a outer cover for O antigen. Heat labile, HELPS cause clinical diseases more consistently .
  26. 26. MODES OF TRANSMISSION :  Ingestion of contaminated food or water  Rarely , from person to person – fecal-oral route.  Food handlers/ Carriers. . . ‘Typhoid Mary’, is a classic example of carrier transmission of the diseases. Mary Mallon, a cook in New York City in early 1900s was affected by Typhoid fever; She was responsible for infecting at least 78 people and killing 5 people . She was later put in prison, to avoid passing of the infection further.
  27. 27. CLINICAL FEATURES :  ENTERIC FEVER  SEPTICEMIA- with(out) local suppurative lesions  GASTROENTERITIS / FOOD POISONING Typhoid fever is a septicemia characterized by fever, bradycardia, splenomagaly, abdominal symptoms, and ‘rose spots’- which are clusters of pink mauls on the skin. Complications viz., intestinal haemorrhage or perforations develop in untreated patients or when there is a delayed treatment.
  28. 28. PATHOGENECITY:  The organisms penetrate ileal mucosa reach mesenteric lymph nodes via lymphatics, multiply, invade blood stream via thoracic duct.  In 7-10 days , they infect Liver, Gall-Bladder, Spleen, Kidney, Bone-Marrow.  After multiplication, bacilli pass into blood causing secondary and heavy Bacteremia. Mechanism:  From gall bladder, invasion occurs in intestines.  Involvement of peyer’s patches, gut lymphoid tissues leads to inflammatory reaction.  Finally leading to necrosis and formation of characteristic typhoid ulcers.
  29. 29. SYMPTOMS:  Diarrhea  Severe headache  Abdominal pain  Anorexia  Fever  Ulcers on intestinal wall  Shock  Rose spots  intestinal hemorrhage + perforations
  30. 30. Blood cultures:  In adults, 5-10ml blood is collected by venepuncture inoculated into 50-100ml bile broth (0.5%)  Bacteremia occurs early in blood : Week 1 90% Week 2 75% Week 3 60% Week 4 =< 25%
  31. 31. Biochemical tests IMViC Test : Name of the test Result Indole test -ve Methyl Red +ve Voges-Proskauer -ve Citrate utilization +ve Urease -ve Sugar Fermentation :Sugars Glucos e Maltose Mannito l Sorbitol Sucros e Lactose Acid +ve +ve +ve +ve -ve -ve Gas +ve +ve +ve +ve +ve -ve Further confirmatory tests done by Slide agglutination tests
  32. 32. Widal Test :  The Widal test is used to make a presumptive diagnosis of enteric fever. Although the test is no longer performed in the U.S. or other developed countries, it is still in use in many developing countries where enteric fever is endemic and limited resources require the use of rapid, affordable testing alternatives.  the method relies on a reaction in a test tube or on a slide between antibodies of the infected person's blood sample and specific antigens of S. typhi, which produces clumping that is visible to the naked eye.
  33. 33. Control & Prevention :  Simple hand hygiene and washing can reduce several cases of typhoid.  Choose processed foods for safety  All milk and dairy products should be pasteurized.  Control fly populations  Any bleeding from rectum, bloody stools, sudden acute abdominal pains should be reported at once to the physician.