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Food born

Fecal oral infection:
Food-borne infection (ingestion infection). Contaminated food: vehicles are milk & any food that may be contaminated by handling, flies, water, or dust, & sewage-polluted water.
Hand-to-mouth infection.

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Food born

  1. 1. Dr. Dalia El-Shafei Assist.Prof., Community Medicine Department, Zagazig University
  2. 2. Viral • Poliomyelitis • Hepatitis A&E • MCD Bacterial • Enteric fever • Brucellosis • Diarrheal diseases: • Food poisoning • Dysentery • Diarrhea diseases in children • Cholera Parasitic • Ascariasis • Entrobiasis • Amoebiasis • Heterophiasis • Fascioliasis • Hydatid cyst • Giardiasis • Toxoplasmosis
  3. 3. Fecal oral infection:  Food-borne infection (ingestion infection). Contaminated food: vehicles are milk & any food that may be contaminated by handling, flies, water, or dust, & sewage-polluted water.  Hand-to-mouth infection Mode of transmission
  4. 4. 1ry •Environment sanitation • Health promotion • International measures 2ry • Case: • Case finding & notification • Isolation & disinfection • ttt & release • Contacts: • Surveillance • Supervision • Segregation • Isolation • Immunization 3ry • Prevent complications & care of handicapped Prevention
  5. 5. A) General Sanitation of Environment: Safe water supply, Sanitary wastes disposal (refuse & sewage),  Insect control (flies & cockroaches). Food sanitation includes control of food handlers B)Health education : proper clean habits (including clean hands)
  6. 6. I. Control of Cases “FNIDTRR”:  Case-finding: needs efficient medical care (clinical & lab services)  Notification to the LHO.  Isolation: allowed at home when sanitary requirements are fulfilled, otherwise must be at fever hospital.  Disinfection: - concurrent: excreta (1% crude phenol), articles & fomites. - terminal for objects & cleaning of the room.  Treatment: general & specific chemotherapy.  Rehabilitation
  7. 7. Polio Hepatitis A Hepatitis E IP 7- 14 d 15- 50 d 21- 42 d Mode of transmission -Faeco-oral -Food-borne -Oral-oral (droplet) faeco-oral Parenteraly (viraemia) Contaminated water or food supplies Reservoir -Cases -Carriers (contact, incubatory, convalescent) -cases -Incubatory Carriers Infectivity From IP to convalescence Last week of IP till Jaundice Agent -Polio virus Picorna virus
  8. 8. Polio HAV HEV C/P -Inapparent 90% -Minor (Abortive) 9% -Major (CNS) 1% -Inapparent (influenza-like) -Classical: pre-icteric, icteric, post- icteric - Fulminate: fatal Diagnosis -Lab: throat wash & stools exam -Serological: rising Ab - Lab: stools exam - Serological: IGM, liver enz. Specific prevention -Vaccine -Seroprophylaxis Vaccine
  9. 9. An Egyptian stele shows a priest with a deformity of his leg characteristic of the flaccid paralysis typical of poliomyelitis
  10. 10.  Acute viral infectious disease may lead to flaccid paralysis.  Poliomyelitis may be near worldwide eradication. Localized outbreaks may occur at any time.
  11. 11. Most frequent Epidemic I Wild Endemic II Oct 1999 Sporadic III Causative Organism: Poliovirus has 3 antigenically distinct types.
  12. 12. • Polioviruses have affinity to the nervous system. • Relatively resistant & survive for long time under suitable environmental conditions. Destroyed by Heat Pasteurization Boiling of milk Chlorination of water UVR
  13. 13.  Cases: all clinical forms  Carriers: all types (incubatory. Convalescent, healthy & contact who are temporary carrier .  In endemic area health carrier are most frequent due to polluted environment.
  14. 14. Contact & healthy carriers Incubatory carriers Convalescent carriers Cases • About 2weeks. • Last days of IP. • Temporary, for some weeks. • Infectious for about 6-8 weeks (clinical period).
  15. 15. Age: incidence usually from 6 Ms-5 Ys. By compulsory vaccination programs there is age shift to adolescents & young adults Sex: Paralytic polio is more in males than females. Immunity: a- Naturally acquired Immunity Maternally acquired persists for 6 Ms. Exposure to infection by any form of clinical disease gives lasting, type-specific immunity. 2nd attack rarely occurs, from type-different poliovirus infection. b- Artificially induced immunity: by immunization.
  16. 16. Polio In apparent (90%) No clinical manifestations Acquired immunity & carrier state Manifest (10%) Abortive (minor illness) 9% CNS (major illness) 1% Non-paralytic (FHMA + Meningism) Paralytic (spinal, bulbar, bulbo-spinal)
  17. 17. Case-fatality: 2-10%
  18. 18. • Throat washing or stools • Serological (neutralizing Ab): rising titer In the abortive stage, is practically impossible. Diagnosis is suspected only when non-paralytic or paralytic picture appears. Differential diagnosis: Other causes of acute flaccid paralysis as Gillian-Barrie syndrome & transverse myelitis.
  19. 19. • Passive immunization (Sero-prophylaxis): “non-practical” Normal human Ig (0.3 ml/kg BW) Exposed susceptible (pre exposure – rapidly post exposure) • Active immunization: Sabin & Salk
  20. 20. • Oral, live attenuated trivalent vaccine made of the 3 types, of polioviruses. • 2, 4 and 6 Ms of age • 3 drops orally on the tongue. • Recently a zero dose is giving after birth as additional dose. • Booster Immunization: a booster dose is given at 9 Ms, 18-24 Ms, and school age.
  21. 21. Live attenuated viruses of the vaccine invade & multiply in the intestinal cells, stimulating humoral & local cellular immunity:  Humoral immunity: by neutralizing antibodies in serum. It protects the CNS Against invasion by the poliovirus.  Cellular immunity: local tissue immunity in the intestinal mucosa so prevents establishment of infection in the intestine, and so prevent a carrier.
  22. 22. Gives humoral & tissue immunity Excreted in stools, disseminate infection in community Easily administrated Used in mass immunization. Inexpensive. Protective value up to 95%, Life long immunity.
  23. 23. Cold chain: regenerated below 4 C Contraindications: Complications: Paralysis: very rarely (1/5 million) Pregnanc y Cortico- steroids Immune- deficienc y
  24. 24.  Trivalent vaccine, inactivated (formalin).  Used in non-endemic areas & with Sabin vaccine in endemic area.  4 doses, 1.0 ml each, IM, starting at 4 months of age.  1st 3 doses 6-8 weeks apart, 4th dose 7 months later.  Booster dose : at school age, and whenever an epidemic or outbreak threatens.
  25. 25.  Action: Salk vaccine gives humoral immunity. No cellular immunity  Protective Value: prevents <90% of paralytic cases & lowers severity of paralytic effect.  Salk is given in Egypt as quadruple Salk DPT, IM, 2 doses at 4 &6 Ms
  26. 26. Due to the preventive value of polio vaccines & reluctance of some parents to take their children for immunization, or missing 1-2 doses of 1ry immunization, periodic polio vaccination campaigns are arranged, for better coverage & complete immunization of infants & young children <5 ys.
  27. 27. Control Cases FNIDTRR Contacts Enlistment Case-finding (2wks) Booster v. or sero- prophylaxis Epidemics Mass oral v. Epid. study Avoid predisposing factors
  28. 28. • Sabin (1968):1ry & booster • Salk Immunization • Motivation • Periodic campaigns • Surveillance (1990) Satisfactory coverage rate
  29. 29. • Definition: communicable food borne acute viral disease involving the liver endemic in developing countries, and gives sporadic cases, usually in outbreaks in confined groups (camps, military units, boarding school& daycare centers). • Causative agent: viral hepatitis A virus: RNA virus, relatively resistant outside the body • Reservoir: man as incubatory carriers and cases (mild or in-apparent)
  30. 30. • Mode of transmission: 1-faeco-oral 2-parenteral rarely during viraemia • IP: average 4 weeks (15-50 days) • Clinical Picture: 1- In apparent cases: mild an-icteric cases “influenza-like picture (non-specific syndrome) & pass unnoticed”. 2- Classical disease. 3- Severe fulminate rapidly fatal disease.
  31. 31. Post-icteric Convalescence Icteric Jaundice (sclera) Enlarged tender liver Pre-icteric FHMA, myalgia, arthralgia GE, tender liver, dark urine
  32. 32. Clinically • Dark urine • Jaundice Laboratory • detecting virus in stools Serological tests • IgM in acute cases • ↑ liver enz. (not specific)
  33. 33. 1ry General •Environment sanitation •Health promotion Specific • Active immunization • Sero-prophylaxis 2ry Cases • Case Finding. • Notification: LHA. • Isolation: at home • Disinfection: feces, urine & blood. • Specific ttt: No • Release Contacts • Enlistment & Immunization: within 2 weeks of exposure. • Surveillance: for 6 weeks Epidemic measures: • Food sanitation • Seroprophylaxis. • Epidemiologic study. Prevention
  34. 34. Active immunization • Inactivated vaccine 1 ml IM(deltoid) “2 doses, 4 weeks apart” • 1- At risk: Ch. Liver Dis., travelers, lab workers. 2- Children Sero-prophylaxis • Human Ig Before or few days after exp • 1- Contacts (within 2 wks) 2- At risk: travelers (before or within 2 wks)
  35. 35. Bovine Spongiform Encephalopathy (BSE) Mad Cow Disease (MCD) Cretuzefeld Jacob Disease (CJD)
  36. 36. • Occurrence: It is a newly identified zoonotic disease. It 1st appeared in England 1989 among cows that were fed by animal meat of carcasses of died animals after their crushing. The change in the food of the cow (herbivorous animal) into feeding by animal tissues induced a pathological condition in the cow. • Causative agent: Proteinaceous non-living infectious particle that is devoid of nucleic acid (not virus or viroid) • Modes of transmission: Ingestion of infected meat of diseased cattle.
  37. 37. • Management: No specific ttt is known. • Control measures: 1. Prevent feeding of living animals (as cattle) by died animal tissues or bony meals. 2. At the international level: a) All countries must ensure condemning & safe disposal of all BSE affected animals & prevent their entry into free countries. b) Surveillance & compulsory notification for BSE disease. 3. Research for finding rapid diagnostic methods & management in both animals & man.
  38. 38. Viral • Poliomyelitis • Hepatitis A&E • MCD Bacterial • Enteric fever • Brucellosis • Diarrheal diseases: • Food poisoning • Dysentery • Diarrhea diseases in children • Cholera Parasitic • Ascariasis • Entrobiasis • Amoebiasis • Heterophiasis • Fascioliasis • Hydatid cyst • Giardiasis • Toxoplasmosis
  39. 39. Salmonellae have more than 2000 serotypes, of which pathogens of Human disease is: *Typhoidal salmonellae: S. typhi, & S. paratyphi A, B, C. *Nontyphoidal salmonellae: Food poisoning & Salmonellosis.
  40. 40. • Typhoid: Salmonella typhi (typhoid bacillus), with a big number of serotypes • Paratyphoid: 3 serotypes “A, B, C” B is the most common C is rare. • It can remain viable in the environment (water, ice, milk, milk products, ice-cream and other foods) for weeks. • But it is readily destroyed by heat & disinfectants.
  41. 41. Reservoirs Carriers cholecystitis & urinary lesions Incubatory Last days of IP (faeces) Convalescent Temporary 10% Chronic 2-5% Contact 2 wks Healthy Sub-clinical infection 2 wks Cases
  42. 42. Fecal carriers:more common than urinary Urinary: more frequent in endemic Schistosomiasis Foci&exitofinfection Small intestine (Peyers patches) & gall-bladder Feces Fecal carrier Kidney Urine Urinary carrier
  43. 43. • 10-30 ys • Markedly ↓ with ageAGE • Male > Female • Females: fecal carriers 5 times > males “cholecystitis” SEX • Significant ↑ during summer.SEASON • Repeated subclinical infection (mainly), clinical attack, or active immunizationIMMUNITY
  44. 44. Period of Infectivity: 1-Cases: Infectious from the last days of IP (incubatory carriers), throughout disease, and for varied period (months, years or lifetime) in a percent of convalescents (convalescent carriers). 2-Contact & healthy carriers: Infectious about 2 weeks. Incubation Period: 8-14 days
  45. 45. • Onset is usually gradual. • Picture of disease varies whether chemotherapy is given or not. • Treated Cases: Chemotherapy: ↓ Disease duration & incidence of complications.
  46. 46. Prodroma • FHMA (stepladder, evening, low pulse) • Rash (macular rosy spots , abdomen,7th day , 25%) Advance • High fever, worse physical & mental condition, • Abdominal distension & tenderness Decline • Gradual improvement • Drop of temperature Convalescence • Relapse(s) after 1-2 weeks: 10-20%, usually mild.
  47. 47. Atypical presentation: Infection by antimicrobial resistance strains & in children (respiratory symptoms & diarrhea) Case fatality: 15-30% in untreated cases & ↓ with ttt to 1-2%. Intestinal hge & perforation Cholecystiti s Thrombophlebitis of femoral vein Myocarditi s Pneumonia Osteomyeliti s Bone abscesses Complications
  48. 48. Bl. culture 1st wk • Bacteremia Widal test 2nd wk • Agglutination test (rising titer) • High titer O & low titer H → Recent infections • High titer H & low titer O → Past Infections Stool & Urine culture 2nd & 3rd wk • Should be repeated for 3 times • Practically valuable to detect carriers, rather than diagnosis Lab diagnosis
  49. 49. TAB (TABC) vaccine •Parenteral heat-killed •Adults: 2 doses of 0.5 & 1.0 ml SC, 4 weeks apart. •Booster Dose: adult “1.0 ml” every 3 ys. •Children >2 years can be given smaller dosage. •Protective Value: 50-75% & may not be protective on exposure to heavy infection Typhoid Oral Vaccine • Protective value: 65% • 4 oral doses on alternate days Polysaccharide vaccine • Parental vaccine containing Vi Ag in single dose
  50. 50. Vaccination in endemic areas is given to (indications): Occupational groups at-risk: Food handlers, Lab workers, HCW, waste disposal. Camps & other closed communities. Slum areas. At-risk communities during epidemics & outbreaks. Travelers to endemic areas & pilgrims.
  51. 51. Cases • Case-finding - Notification: LHO. - Isolation • Disinfection - TTT - Release Carrier s • Food handlers “pre-employment” • Chronic gall-bladder carrier Contac ts • Family & Household contacts • Nursing personnel Epidemi c Measure s • Sanitary measures - Heath education • Epidemiologic study
  52. 52. Release:  3 -ve cultures of stools & urine, 24 or more hours apart.  1st sample: 2 weeks after drop of temperature to normal (to exclude possibility of relapse).
  53. 53. • Diagnosis especially among food handlers & during pre- employment examination: Widal test for Vi antigen, if +ve: stool & urine culture can be done (repeated cultures are indicated). • For chronic gall-bladder carrier: Ampicillin for 1-3 Ms until 3-ve successive samples. cholecystectomy is indicated. • For chronic urinary carrier: Foci surgical removal.
  54. 54. Family & Household contacts Enlistment & Active immunization: Mainly during seasonal spread or outbreak Surveillance for 2 weeks, from date of last exposure to the case. Food handlers: excluded from work & bacteriologically examined until prove not to be carriers. Nursing personnel Active immunization Personal cleanliness Precautions on nursing & not to handle or serve food to the others.
  55. 55. Causative Organism: Brucella organisms are relatively resistant in the environment. Destroyed by Heat Pasteurization Boiling of milk Chlorination of water
  56. 56. Endemic in Egypt even with increasing incidence because of animals' importation from different countries.
  57. 57. No man-to-man
  58. 58. IP: varies, usually 6-60 days. Case fatality of untreated cases is 2% or less & usually results from endocarditis
  59. 59. Diagnosis Laboratory Blood culture Serologic testing Brucellin test Clinical Not characteristic Fever of unknown origin (FUO)
  60. 60. Brucellin test: ID hypersensitivity test (survey studies).
  61. 61. Prevention Man Ingestion infection Milk & Meat sanitation Health education Occupational control PPE Personal cleanliness Airborne infection Clean animal environment Sanitary disposal of infected material Dust control Masks Animals Veterinary care Sanitary wastes disposal Vaccination Agglutination survey
  62. 62. Increased bowel motions than usual own pattern of individual. OR Passage of ≥3 abnormal loose stools that may be associated with fever, vomiting & change in color & presence of blood, pus
  63. 63. Etiology: infective & no infective. Infective include: 1- Cholera 2-Infectious food poisoning 3-Infective diarrheal disease of children (GE) 4-Dysenteries.
  64. 64. 2315 case (2007)
  65. 65. Bio-type Sero-group Sero-type Vibrio cholera O1 Classical 3 El-Tor 3 O139
  66. 66. The organisms liberate potent exotoxins (enterotoxins). That remain in intestine causing destruction of mucosa. Current 7th pandemic: O1 sero-groups El-Tor biotype.
  67. 67. • V. cholera O1 & O139 can persist in water for long periods & multiply in moist leftover food. • Killed within 30 min. by heating at 56 C & within few seconds by boiling. Classical vibrio • Less resistant • More virulent • More severe clinical cases El-Tor biotype • More resistant • Less virulent • Mild cases, subclinical cases • High carrier rate &Infectivity
  68. 68. Reservoir: Man is the only source of infection either case or carriers. 1-Cases: inapparent, subclinical or clinical. 2-Carriers: incubatory, contact & convalescent. Usually temporary but in El-Tor biotype tend to be more chronic. Exit: Stool & vomitus of cases. Stool of carriers.
  69. 69. 1. Ingestion of contaminated water or food. 2. Beverages prepared with contaminated water, ice & even commercial bottled water have been incriminated
  70. 70. • All ages are affected • Attack rate is highest among childrenAGE • Both sexes are affected.SEX • Significant ↑ during summer & autumnSEASON • Infection either clinical or sub clinical gives type specific immunity.IMMUNITY
  71. 71. • Most cases: Asymptomatic or mild diarrhea, especially with El-Tor. • Profuse painless watery stool (rice water stool). • Nausea & profuse vomiting early in the course of illness.
  72. 72. Dehydration Acidosis HypoglycemiaRF Circulatory collapse Case-Fatality is high (>50%) among severe dehydrated cases. But greatly ↓ (<1%) due to better diagnostic facilities, better management through dehydration & effective chemotherapy.
  73. 73. Killed “Koll's” vaccine • Heat killed phenol preserved • 2 Doses (0.5&1 ml) 4 wks apart- booster every 6 ms. • Partial protection (50% efficacy) • Short duration (3-6 months) • Only antibacterial & not antitoxic immunity • Not prevent asymptomatic infection & carrier state. • Associated with adverse effect . • Not recommended by WHO Oral vaccines • Safe. • Significant protection for several months. • One is a single dose live vaccine. • Other is a killed vaccine consisting of in-activated vibrios + B-subunit of the cholera toxic, given on a 2- dose regimen.
  74. 74. Tetracycline • 500 mg/6 hours for 3 days • Single dose of 1gm • ½ dose for children • Contacts • Travelers • Pilgrims Doxycycline • Single daily dose of 300 mg for 3 days
  75. 75. 1- Notification to WHO. 2-Chemoprophylaxis: Tetracycline or Doxycycline for travelers coming from endemic or infected areas. Vaccination certificate is not required internationally since the vaccine is not potent
  76. 76. Early case finding and confirm diagnosis. Report to LHO & WHO. Isolation in fever hospital, quarantine or cordon. Disinfection: Concurrent disinfection of all soiled articles & fomites, stool and vomitus using heat & carbolic acid. Terminal cleaning is sufficient. Treatment: Adequate dehydration therapy using OR in mild cases, IV rehydration in severe cases. Treatment of hypoglycemia. Release after 3-ve successive stool sample.
  77. 77. • Enlistment by age, sex, occupation and residence. • Isolation for 5 days calculated from the day of exposure. • Release after 3 -ve successive stool sample. • Chemoprophylaxis. • Education, Case finding & repeated stool culture to prevent carrier state.
  78. 78. Of the public & population at risk about mode of transmission and preventive measures: • Ensure safe water supply and chlorination • Provide appropriate safe sewage disposal • Control of house flies. • Ensure sanitary preparation & supervision of food & drinks. • Investigate the situation to find the epidemic variables (TPP).
  79. 79. Infection • Presence of bacteria or other microbes which infect body after consumption. • Salmonella. • Shigella spp. • Camplobacter jejuni. • Listeria. • E.Coli. • Yarsinia enterocolitis. Intoxication • Ingestion of toxins contained within food, including bacterially produced exotoxins. • Staphylococcus aureus. • Clostridium botulinum. • Clostridium perfringens. • Bacillus cereus.
  80. 80. SalmonellaBotulismSTAPH - Outbreaks - Egypt - Rare - Sporadic cases - Commonest - Outbreaks Patter n Non typhoidal Salmonella Exotoxin of Cl . Botulineum neurotoxin Performed thremostable Enterotoxin (Exotoxin) Agent -Animals: Rodents &cattle - Man: Cases &carriers -Soil: grown vegetables, fruits contaminated with spores -Animals: excreta of cattle, pigs& Others - Man :Case or carrier(skin or resp. infec) >5% of population having foci of skin or nose infection -Cattle: staph.mastitis contaminate milk Reservoir
  81. 81. Staph food poisoning
  82. 82. Botulism
  83. 83. SalmonellaBotulismSTAPH - Ingestion of food from infected cattle or swine. -Ingestion of food contaminated with excreta of animals or rodents - Water polluted with excreta of man or animal - Hand to mouth infection “auto- infection” Ingestion of food contaminated with Performed exotoxin(preserved vegetables without proper sterilization packed or canned meats or sausages or fish) *packing of salted raw fish (fessikh) Ingestion of enterotoxin contaminated food or milk by resp. discharge of food handlers Favored by: much handling& sufficient time between contamination & consumption without Refrigeration “koshary, belela” Modeoftransmission 38 hs12-36 hs2-6 hsI P
  84. 84. SalmonellaBotulismSTAPH -Outbreaks: GE -Sporadic: salmonellosis -Enteric like-picture: self-limited disease Paralysis of occulo-motor & other cranial ns causing visual disturbances as diplopia, loss of accommodation, dysphagia, dysphonia & resp. paralysis case-fatality is high (70%) in few days due to resp. failure Abrupt onset of GE (for hours then recovery - Slight or no fever - Case-fatality is almost nil C/p - Mainly Clinically - Culture: Stool, Vomitus& Food remains (-ve results not exclude staph. as organism may be destroyed while the enterotoxin is not). Diagnosis
  85. 85. SalmonellaBotulismSTAPH General preventive measures of food borne diseases Prevention In case of botulism: 1.Proper processing, packing, canning of food after sterilization 2. Food preservation at home 3. Suspected canned food to be spoiled (bulged from gas formation) rejected 4. Specific prevention: Trivalent Botulism antitoxin As food borne infection & investigation of outbreak 1. Sero-therapy by Trivalent Botulism antitoxin :limited value (irreversible effect of exotoxin on CNS) 2.Seroprophylaxis for person sharing food with diagnosed cases but no manifestations 3. Food remnants: destroyed after sampling for bacteriological testing Control
  86. 86. Clostridium Welchii (Cl.Perfrinqens type A) Bacillus cereus Anerobic spore forming powerful enterotoxin Aerobic spore forming 2 enterotoxins “heat labile (diarrhea) & heat stable (vomiting)”. Agent Animals (cattle, poultry &fish) Man (cases &carriers). Spores found in the soil “rice”.Reservoi r Ingestion of spore-contaminated meat Ingestion of spore-contaminated rice. Mode of Infection 6-24 hours.1-6 hours in emetic 6-24 hours in diarrheal cases. IP - Intensive diarrhea, no vomiting “self-limited” - Necrotizing enteritis “highly fatal in the elderly” GIT manifestations either Emetic or Diarrhea “self-limited” C/P
  87. 87. Bacillus cereus Incubation period < 6 hours Severe vomiting Lasts 1-6 hours Incubation period > 6 hours Diarrhea Lasts 6-24 hours EMETIC FORM DIARRHEAL FORM
  88. 88. Bacillus cereus
  89. 89. Clostridium Welchii
  90. 90. Reservoir s Food Cases Outbreak
  91. 91. Many cases. Share common food. Very short IP (hours). Similar C/P
  92. 92. Measures for cases: Enlistment & distribution of cases by TPP. Proper history taking & examination. Culture of faeces & vomitus of cases. Look for other cases.
  93. 93. Attack rate for food items eaten = no. of cases among those ate certain food x100 all who ate the same food Food items: Greatest difference in attack rates between those ate this food and did not eat Measures for food items: Listening of food & remnants. Origin, preparation & storage. Culture of suspected food remnants Compare the attack rate
  94. 94. 1. Food handlers examination e.g. staph. infection: nose & throat swabbing for carriers & skin & nails for lesions 2. Other sources of contamination e.g. rodents & their excreta
  95. 95. Diarrheal Disease Of Children (Gastro-enteritis)
  96. 96. Gastro-enteritis is diarrheal disease of children below 5 years (infants & young children).
  97. 97. Bacterial Escherich ia Enterotoxigenic (ETEC) Travelers’ diarrhea Enterohaemorrh agic(EHEC) Hemorrhagic colitis Enteropathogenic (EPEC) Neonataldiarrhea Enteroinvasive (EIEC) Dysentery Staphylococcus aureus Non-typhoidal salmonellae Shigellae Campylobacter jejuni Viral RotavirusHospitalized Enteroviruses Cocksackie viruses,ECHO viruses, polioviruses,HAV Enteric Adenovirus epidemicviralGE Measles Protozoal GiardialambliaGE Entamoeba histolytica BalantidiumcoliDysentery
  98. 98. Reservoirs of Infection: 1- Man (cases or carrier) 2- Animals: non-typhoidal Salmonellae, Campylobacter jejuni, E.Histolitica, B. coli. Community Underdevelopment Insanitary environment. Illiteracy Lack of effective health services Hostfactors Malnutrition (PEM). Persisting systemic infection “chronic otitis media & bronchitis”. Season Sporadic cases all the year round. Monthly distribution of cases in developing countries shows 2 peaks: A high peak in summer & fall. A small peak, during winter months “increased incidence of acute respiratory infections”.
  99. 99. GEforms Epidemic diarrhea of the newborn “E-coli” Summer diarrhea Flies. Rapid multiplication of organisms in milk & food Diminished acid secretion of stomach Weaning diarrhea. Staphylococcal enteritis- Secondary enteritis Persistent systemic infection, specially the respiratory & urinary Recurrent diarrhea
  100. 100. IP: Vary according to the causative agents usually hours to 2-4 days. Clinical Picture Moderate & Severe cases Abrupt onset, fever (usually high), frequent liquid or rice-water stools (≥20/day), vomiting & dehydration. Mild cases Mild diarrhea (>5 times/day), No or mild fever, No vomiting, No or insignificant dehydration, and No or mild systemic manifestations (self-limited & clears up within days)
  101. 101. Early case-finding • Efficient health services • Health education for mothers. Management of case • Mild: outpatient service “Started under medical supervision &Continue at home”. • Sever: Hospitalization.
  102. 102. Rehydration therapy ORT Nasogastric Rehydration I.V fluid Rehydration Diet therapy Cases without dehydration Cases with dehydration Chemotherapy Bacterial diarrhea “Shigellae & Vibrios” Existing systemic bacterial infection Symptomatic Manage symptoms, especially fever ttt of Underlying Disease Nutritional deficiency diseases
  103. 103. Rehydration therapy 1st line to replace loss of fluid & electrolytes & restores fluid-electrolyte balance. a) Oral Rehydration Therapy (ORT): 5.5gm of NaCl, NaHCO (correct acidosis), KCl (correct hypokalaemia) & glucose. Dissolved in 200 ml water. b) Nasogastric Rehydration: repeated uncontrolled vomiting. c) IV fluid Rehydration: hospitalized severe cases Diet Therapy - Cases having no dehydration: usual feeding & sufficient fluid & Supplementary vit. B,C. - Cases with dehydration: Mild cases: ORS & milk, alternating, until cured. Moderate cases: initially given rehydration, with fasting (water if necessary) for some hours until dehydration improves, then milk, then other foods can be given.
  104. 104. Inflammation of the colon (large intestine). Tenesmus Abd. pain Frequent stools “Bl. & mucus”
  105. 105. Agent s Bacterial “Shigellae” Protozoa “Entamiba histolytica” Helminthis “Scistosoma”
  106. 106. Acute infectious inflammatory bacterial disease of the colon. Worldwide disease. Usually sporadic cases. Outbreaks occasionally in confined groups. Incidence is higher with seasonal breeding of flies (spring, early summer & fall).
  107. 107. Relatively resistant outside the body, but readily destroyed by heat & disinfectants. Locally: the exotoxin is enterotoxic, causing dysentery. Toxaemia: exotoxin is a neurotoxin, may be fatal Most virulent Mild disease Nocrossimmunity More than 1 attack may occur, due to different groups & serotypes. Infection is usually followed by type-specific immunity.
  108. 108. • Reservoir of Infection: Man “cases & carriers”. • Carriers: number is several times cases & forms the main reservoir of infection. They are contact, healthy & convalescent carriers. • Exit: faeces • Infectivity: usually for few weeks, sometimes longer, and rarely for one or more years. IP: 1 -7 days (usually less than 4).
  109. 109. Mild disease that may pass unnoticed. Acute cases • Sudden onset • Fever • Vomiting & dysentery “May be” • Usually self-limited • Recovery in few days. Severe fulminate disease • Dysentery • Systemic manifestations • Dehydration & complications (uncommon) due to exotoxin &toxaemia, • Fatal (May be in young, elderly & debilitated). Dysentery: tenesmus, squeezing pain of lower abdomen & frequent loose scanty stools, mainly made of fresh blood, pus & mucus.
  110. 110. PROTOZOA Amoebiasis Giardiasis Balantidiasi s Causative Agent Entamoeba Histolytica “Endemic in Egypt & many parts of the world” Giardia Lamblia “Lambliasis” Balantidium coli Infective Stage Quadri-nucleate cyst “Resistant outside body, but destroyed by heat, desiccation & UVR”. Cyst: passed with faeces “remain viable in the environment for months”. Reservoir Man: chronic cases, or asymptomatic cyst-passers. “Acute cases: non- infectious, as they pass the fragile vegetative form that perishes rapidly. Even if ingested, it is destroyed by gastric acidity & digestive enzymes”. Rats: occasionally. Man & mammals (e.g. dogs, cats, cattle, sheep) Man & Swine Mode of 1. Food borne infection: ingestion of food or water contaminated
  111. 111. Amoebiasis
  112. 112. Giardiasis
  113. 113. Balantidiasis
  114. 114. Amoebiasis Giardiasis “Lambliasis” Balantidiasi s IP 3-4 weeks 1-2 weeks 3-4 days C/P “Colon, with invasion of intestinal wall”. 1ry amoebiasis “Dysentery”: colon. 2ry amoebiasis: other parts of body. Complications: -Intestinal: severe ulceration “may cause perforation of colon & intestinal hemorrhage” and appendicitis. -Extra-Intestinal: amoebic abscesses, especially in the liver, causing amoebic hepatitis “Duodenum & Ilium, without invasion of intestinal wall”. Asymptomatic. -Gastro-enteritis of infants & young. “Terminal ileum & Colon” - Asymptomatic. -Mild colitis. -Dysentery.
  115. 115. HELMINTHES Ascaris Enterobius vermicularis Hymenolepis nana Causative Agent Ascaris Lumbricoides “Ascariasis” “Oxyuriasis pinworm Disease” most widespread helminthic infection” dwarf tapeworm Prevalence Worldwide distribution “Preschool & school children are frequently, and may be heavily, infected Infective stage Embryonated egg “resistant to desiccation & disinfectants, and remains viable & infective, under favorable environmental conditions, for 3 months”. How Ascaris eggs reach food? -Using fresh human fertilizer. -Promiscuous defecations. -Flies may have potential, least role. Egg, deposited by migrating gravid female worm in the perianal region. Eggs are relatively resistant outside the body Eggs passed in faeces, are immediately infective Reservoir Man Man & Rats “occasionally’
  116. 116. Ascariasis
  117. 117. Enterobiasis
  118. 118. Ascaris Enterobius vermicularis Hymenolepis nanaModeoftransmission Food borne Infection. Hand-to-mouth infection No Auto-infection: eggs in faeces are not infective, except after developing into embryonated egg “infected food handlers do not spread infection”. -Auto-infection: fingers & nails contaminated with eggs on scratching the anal region. -Hands contaminated with eggs: * Playing with the case. * Handling soiled fomites. *Touching soiled toilet fixtures. -Auto-infection. -Hand contaminated with eggs when playing in rat excreta-contaminated dirt. Internal Autoinfection: ova invade the intestinal wall.
  119. 119. ASCARIS ENTEROBIASIS HYMENOLEPIS NANA IP 2 months 1-2 months 2-4 weeks C/P -Mild infection may be in apparent. -Abdominal discomfort & colic. -Nutritional deficiency. -Respiratory manifestations. -Restless sleep & grinding of teeth. Perianal pruritus & scratching, usually nocturnal, causing disturbed sleep and irritability. Asymptomatic, mild or vague abdominal disturbance. Heavy infection: abdominal pain &diarrhea Diagnosis Stools examination: eggs. -Worms in anal region & stools. -Perianal swab to demonstrate eggs (using adhesive tape). -Stool examination: not diagnostic. Stools examination: eggs.
  120. 120. Ascariasis
  121. 121. TAENIASIS HETEROPHYIASIS Causative Agent T.solium (pork tapeworm) & T.saginata (beef tapeworm). Heterophyes heterophyes. Prevalence Worldwide. Man is usually infected with one worm only. Endemic in Egypt around Lakes Manzala & Borollos. Infective stage Cysticercus bovis in beef & Cysticercus cellulosa in pork Encysted metacercaria in muscles of infected brackish-water fish (e.g. Mugil cephalus & Tilapia nilotica) Reservoir Man: definitive host “discharges detached gravid segments which rupture to liberate eggs in faeces”. Egg is infective to the intermediate host (cattle for T.saginata & pig for T. Solium) where it hatches in the intestine of the animal & the embryo penetrates the intestinal wall and then carried by the circulation to various tissues (especially skeletal muscles where it becomes encysted). Period of communicability so long the worm remains in the intestine “sometimes >30 years”. T.saginata is not directly transmitted from person to person. Man: infected individuals pass eggs in faeces. Fishermen in endemic areas are particularly important for pollution of brackish water channels where intermediate hosts “Pyrenella conica” of the parasite are found. Fish-eating animals (e.g cats & dogs) are potential reservoirs.
  122. 122. TAENIASIS HETEROPHYIASISModeoftransmission Man is infected by ingestion of raw or under cooked infected beef or pork containing the infective stage. In the intestine the scolex (in the cysticercus) evaginates, attaches to the mucosa and develops into mature worm. Ingestion of the infective stage in muscles of infected brackish-water fish when eaten raw, or insufficiently cooked or grilled (Salted raw Mugil fish "fessikh", eaten before 10 days of pickling). IP 2-3 months. 1-15 days C/P -Asymptomatic “except annoyance from having segments of worms emerging from the anus”. -Nervousness, insomnia, anorexia, weight loss, however the disease is non-fatal. Chronic intermittent diarrhea, with blood and mucus in stools, abdominal discomfort and colicky pain. Diagnosis Stools examination: Gravid segment or eggs Stools examination: ova
  123. 123. FASCIOLIASIS HYDATIDOSIS Causative agent Fasciola hepatica & less commonly F. gigantica Echinococcus granulosus “Cystic echinococcosis” Prevalence Worldwide especially in sheep or cattle raising areas. “F.hepatica: Europe, America, Australia &Middle East”, “F.gigantica:common in Egypt” Endemic in the Middle East and Arab North Africa including Egypt Infective stage Encysted metacercaria on aquatic plants Echinococcus eggs Reservoir Sheep (f. hepatica), cattle (f. Gigantica), and other large herbivorous animals. The infection is maintained in a cycle between animals, water, snails and aquatic plants. Man is an accidental host “no direct man to man transmission” Dog is the definitive host. “Pass Eeggs in faeces”. Intermediate Host: Sheep, cattle&other herbivorous animals. They ingest egg- contaminated food, to form hydatid cysts in different organs, specially lung and liver. Dogs infected on ingesting hydatid cyst in animal organs. Man:Occasionally infected with eggs from dogs.
  124. 124. FASCIOLIASIS HYDATIDOSIS Modeof transmission Food-borne infection: Eating uncooked aquatic plants such as water cress bearing encysted metacercaria. Hand-to-mouth infection: usual method of infection, when the hand gets contaminated with eggs, from contact and playing with infected dogs. Food-borne infection: ingestion of food or water contaminated with excreta of infected dogs C/P -Asymptomatic - During liver invasion: Right upper quadrant pain, hepatomegaly, liver function abnormalities & eosinophilia. -After migration to biliary ducts: biliary colic or obstructive jaundice No specific picture, but manifestations of slowly growing tumor, according to location of hydatid cyst. Diagnosis Viable eggs in faeces or in bile aspirated from the duodenum “detection of non-viable eggs in faeces occurs after eating liver from infected animal” * Clinical examination & X-ray: nonspecific cystic tumor “not diagnostic, but suggestive”. * Biopsy or aspiration of cyst: is avoided, for the risk of anaphylaxis and secondary infection. * Casoni test “intradermal hypersensitivity test”.

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