6695029 Food Borne Diseases New One

8/14/2019 6695029 Food Borne Diseases New One

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Food borne diseases

By Dr. Nihal Salah Shihab Professor of Public Health


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Definition What are food borne diseases ? Ingestion of contaminated food or water Infections Intoxications


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Classifications I-DISEASES WITH MAINLY SYSTEMIC MANIFESTATIONS * ENTERIC FEVERS (TYPHOID AND PARATYPHOID FEVERS). *BRUCELLOSIS * POLIOMYELITIS * EXTRAPULMONARY T.B. * VIRAL HEPATITIS TYPES A & E *Anthrax A- NON-INFECTIVE DIARRHEAL DISEASES B- INFECTIVE DIARRHEAL DISEASES ,INCLUDING: * BACTERIAL FOOD POISONING * DYSENTERIES * GASTROENTERITIS * CHOLERA*PARASITIC AND PROTOZOAL DISEASES

II- DIARRHEAL DISEASES (with GIT manifestations)


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TYPHOID FEVER Causative Organism: Salmonella typhi (gram negative,typhoid bacilli):- it isone of the salmonella species (group D salmonella), It has a big number ofserotypes >2000 It has O,H and Vi (polysaccharide capsule ,envelop) antigens.

Many serotypes have the same O & H ant. but not the Vi ant. Whish is importantfor phage typing during epidemics. it produces a potent endotoxin (part of the cell wall).

Resistance: It can remain viable in the environment (water, ice, milk, ice-cream, and otherfoods) for weeks, but is easily destroyed by heat and disinfectants.


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Major habitat for the typhoid bacilli After ingestion,The organism invades the mononuclear phagocytic cells In thelymphoid tissue of small intestine (peyers patches) and mesenteric lymph nodes(multiplicates intracellular), also it is localised in the reticuloendothelialsystem: In the liver, gall bladder; spleen; bone marrow. In the kidney. Theymigrate from the GIT to the mesenteric lymph nodes to the thoracic duct then tothe systemic circulation.


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Exit of infection In Stool mainly In Urine


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Reservoir of Infection: Man: All cases: clinical, missed and ambulatory. Carriers (all types ofcarriers). About 10% of convalescents become carriers, either temporary or chronic. Chronic carriers, according to the age, from about 1 to 5% in typhoidpatients. Carrier state Varies from 2 weeks (as incubatory) to 2-3 months (inconvalescence) and even up to years (in chronic carriers).


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Infectivity : from the last days of incubation period till convalescence. Causes of chroniccarrier states: Chronic carrier state of typhoid is favored by existingcholecystitis (fecal carriers), and urinary lesions due to shistosomal infection(urinary carriers)..


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Severity of infection It depends on: Infecting dose of organism and virulance

Host factors Use of some medications as,antiacids. Evidence of helicobacter pylori infection, leads to increased risk ofacquiring typhoid infection


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Why in Typhoid fever and Brucellosis, there is a tendency to relapses andchronicity? 1- Because organisms tend to be intracellular in the phagocytes in blood andreticuloendothelial system. Thus, the role of antibiotics is difficult to assess(in brucellosis and typhoid f). 3- Due to Drug resistance. 2- Sometimestyphoid like picture develop by some other serotypes of non typhoidal salmonellathat could be mistaken in case of relapses (in Typhoid fever).


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Pattern of the disease spread in Egypt: it is endemic with sporadic casesthroughout the year (any age). Outbreaks may occur during summer months.

Modes of Transmission: 1-Ingestion of contaminated food and water . 2-Directhand-to-mouth infection . 3- contaminated articles and fomites IncubationPeriod : 14-17 days, usually, from 2-3 weeks.


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Clinical Picture:Picture of Classical TyphoidProdromal stage: (the 1st week) :

(A): Systemic manifestation: Bacteraemia, Gradual rise of temperature (stepladderrise), which is usually higher in the evening; Pulse is relatively slower totemperature; Malaise, severe Headache, Body aches.


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(B): GIT: Anorexia, vomiting, diarhea (in children) or constipation (inadults), abdominal distension, furred tongue. Rash of few macular rosy spotsappears on the abdomen, back, and chest, on the 6th or 7th day. (bacterial emboliin the abdom. Capillaries.) Enlarged liver, spleen


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Figure 1.

Bal, S. K. et al. CMAJ 2004;170:1095

Copyright 2004 CMA Media Inc. or its licensors


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2- Advance stage : 1 or 2 weeks:High fever with worse physical and : mental state as apathy and mental confusion.GIT: deterioration with subsequent appendicitis or cholisystitis in some cases.

3- Decline stage 4th week):uncomplicated cases show a drop of temp, and gradual improvement.

4- Convalescence:

it may take 2-3 months with possible disccharge of the organism. Relapses arecommon with untreated cases.


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Complications: Intestinal, intestinal ulcers & perforation, hemorrhage,cholecystitis, appendicitis ,thrombophlebitis (of femoral vein, usually)myocarditis, meningitis, pneumonia, osteomyelitis, bone abscesses, and others. Fatality: may reach up to 10% in untreated cases and 2% in treated cases)


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Diagnosis:

1-clinical picture: in classical type 2-Laboratory Diagnosis A) By cultures: during stage of bacteraemia (the firstweek). It takes from 18 hours up to 4 days such as: Bone marrow aspiratesculture: The most sensitive. Blood Culture: It is sensitive. It is positive in40-80% of patients.


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Urine & stool culture : during the 2nd & 3rd weeks. Only done for carrier statesand in surveys. B) Felix Widal Test: It is serological agglutination test : Itis done initially then repeated after one week , a rising titer is diagnostic (inabout 40-60% of patients). It is a low specific test (with high false positiveresults) because all gp. D salmonella share the same O & H antigens. Also the H Abtiter remain eleveted for long periods after infection or immunization. It is oflow sensitivity: ( high false negative results).


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The causes of low sensitivity and specificity of widal test: The widal test is influenced by: a- Tab vaccination & repeated subclinicalinfection. b- Stage of illness. c-Chemotherapy d Anamnestic reaction(2nd immuneresponse) which is due to any related organism enhances the AB titre alreadyexisted from previous vaccination or infection. (it has cross reacting epitopeswith other enterobacteriacae)


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C) PCR (polymerase chain reaction): highly sensitive & specific. It takes 16 hoursin Lab. (D) New serological test techniques Tubex test: it can detect IgM O9antibodies from patients within few minutes. Typhidot test : can detect IgM, IgGwithin three hours.


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Prevention I- General prevention: 1- Environmental sanitation including: Food+water+milk Insect control & safe waste & sewage disposal Food handlers:a- Examination+ stool & urine culture for subjects, supervision at work place,health education. b- Exclude the carriers from food handling practice, then repeatculture until two consecutive negatives.


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2- Health education II- Specific Prevention: a) TAB vaccine: heat-killed, phenol-preserved vaccine, for Salmonella typhi andSalmonella paratyphi A and B bacilli. Primary Immunization: two doses of 0.5and 1.0 ml, Subcut., 4 weeks apart. Booster Doses: when necessary, a boosterdose of 1.0ml is given every 3 years. Efficiency : (50-75%). Side effects: local& systemic in 25-50% of persons.


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b) New vaccines in USA and Europe: 1- Oral live attenuated Ty21a: Dose:Primary, a series of 4 capsules given in 4 doses.one every other day, anda booster every /3-5 years. Side effects: rarely, GIT troubles and urticaria. Efficiency (85-95%) If the person is taking antimalarial drus, stop treatmentfor two days before vaccination


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2-Itramuscular Vi-polysaccharide vaccine: (from S Typhi strain Ty2)

Dose: primary, a single dose, 25-ug and a booster every /2 years. Sideeffect: It rarely causes fever and headache Efficiency: 55%-74%.


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Indications for vaccinations 1- In travelers to and from endemic areas. 2- In contacts especially in, thoseimmunocompromized. 3- In some at risk groups as workers in sewage and wastedisposal, lab. Workers, in military troops, in nurses (if contacts) or confinedgroups on outbreaks and food handlers.


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Why chemoprophylaxis or seroprophylaxis are unfeasible in Typhoid fever? 1- Theorganism tend to be intracellular along its course of illness [Antibiotics aredifficult to assess]. 2-Low Cost-benefit effectiveness. 3-Long incubation periodso either resistant strains or lowered body immunity develop. 4-The diseaseendemicity may pay already a suitable immune level at many people ??


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Control measures: 1- Case finding: 2- Control of cases: Notification, Isolation(at home), Disinfection Treatment : general, & specific as chloramphenicol,amoxicillin,ciprofloxacin. Release : after 3 negative cultures of stools andurine, 24 hours or more apart. The first sample is taken two weeks after drop oftemperature to normal (to exclude possibility of relapse).


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Remember: The organism shows a high tendency to develop resistant strains toantibiotics. So, a sensitivity test should be done before chemotherapy. Whatmeasures could be done for chronic carriers? Health education; No license forthose working in food handling In ch. Gall bladder carrirs, give chemotherapy(1-3 months) or cholecystectomy.


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In urinary bladder carriers: surgical management 3- Measures for contacts: A)Family and Household Contacts : *Surveillance for two weeks, from date of lastexposure to the case, for case-finding. *Active Immunization: protection ofcontacts is doubted. It may be given, during seasonal spread or outbreak, to bevaluable against subsequent exposure.


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If the contact was food handler? He must be excluded from work andbacteriological examined until prove not to be carriers. b) Nursing Personnel:active immunization, personal cleanliness and precautions on nursing the case, andnot to handle or serve food for the others .


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4.Epidemic Measures: Strict Sanitary measures, Health education of the publicVaccination of at-risk group or population (who ?) Epidemiologic study, to tracesource(s) and channel (s) of infection.


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Paratyphoid fever The causative organism is Salmonella paratyphi A (serogroup A), Salmonellaparatyphi B (serogroup B) . Reservoir: human reservoir cases. Basicepidemiologic features are similar to those of typhoid but: It is a milder form. Incubation period is shorter; complications are rare. Typhoid vaccine (TAB) isdoubtful in prevention of paratyphoid fever. Other vaccines are non effective . Rate of typhoid/ paratyphoid fever is 10/1


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Brucellosis (Malta fever, intermittent or undulant fever) Definition: It is systemic bacterial infection with an acute or insidiousonset. It is a zoonotic, and occupational disease. It is an economic disease{abortions in cattle and physical incapacity in humans}.


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Causative Organisms: [gm ve coccobacilli ,nonspore forming, with an endotoxinin the cell wall]

Brucella abortus in cattle (causing abortions in cattle). Brucella melitensis in sheep, the most virulent Brucella suis in pigs (usually associated with chronicity) Brucella canis in dogs. Occurence: In North & East Africa, Central & South America and South Europe.

Male/female ratio is 1.6 /1 due to occupationalexposure.


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resistance The organism is killed by pasteurization of milk or boiling for 15-20 minutes. Sensitive to acids, so it is absent in sour milk.


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Reservoirs of Infection: Only animals: infected cattle, goats, sheep and pigs.No man-to-man infection . Organisms are found in excreta, discharges, tissues,meat, milk, and the fetus, placenta and vaginal discharges of aborted animals.


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Modes of Transmission: Mainly from Animals man

It is not recorded from man to man.


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Continue modes of transmission 1. Food borne Infection: Ingestion ofinsufficiently cooked meat or heated milk (the common route). 2. ContactInfection: through skin (with abrasions) and mucous membranes. It is usuallyoccupational (farmers, veterinarians.lab.workers). 3. Airborne Infection: inand around the infected farm, on inhalation of dust of dried animal excreta.


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Man is rarely recorded to be infected on accidental injection with the animallive attenuated vaccine.


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Other modes of transmission possible theoritically to occur from man to man.

Blood transfusion Transplantations such as in kidney and bone marrow transpl. Sexual transmission in semen.


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Pathogenesis: After ingestion, the organism passes from GIT to lymphaticchannels and lymph nodes, thoracic duct blood then to parenchymatous organs. Theorganism tend to be intracellular, Where as Granulomatous formations in thetissues, as the liver, bone marrow, lymph nodes and spleen {epitheloid cells,lymphocytes, monocytes and fibroplasts. Sometimes necrosis with pus in B.Suis}. Abscess can occur in any tissue (spines, lymph nodes).


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Incubation Period: varies, usually 5-21 days . Clinical Picture: In-apparentinfection:- (detected by brucellin skin test) Acute Disease: abrupt onset,intermittent fever, weakness, headache, sweating, arthralgia, weight loss andgeneralized aches. Chronic disease: for months or years Relapses may occur.


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What are the causes of relapses or chronicity1. Intracellular organism 2. Drug resistance 3. Host factors: (such as:Immunodeficiency and immunocompromised subjects, .


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Complications: Osteoarticular , with big joint affection (sacroiliitis) in 20-60% of cases ending with disability.

Genitourinary involvement in:2-20% of cases. [ pyelonephritis, orchitis, epididimitis ,oophoritis.

Endocarditis: may cause fatality in 2% of cases especially in B. melitensis.


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Continue other rare complications Neurological: Cerebral: as cranial neuritis, (papillodema), meningo-encephalitis. Spinal: asspinal cord compression. Peripheral: as sciatica.


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Brucellosis infection in pregnant female dosent produce abortion. Why ? Due to absence of Erythritol hormone which is present in animal placenta andstimulate the growth of brucella.


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Diagnosis:1- Clinical picture 2- Laboratory: *Culture is diagnostic (blood, urine, lymphnodes and bone marrow aspirates ). *Serological agglutination tests as antibodyrising titre is diagnostic. *Intradermal skin test [ brucellin test for surveystudies] for past or present infection.


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Brucella skin testing It is an unreliable diagnostic test and is rarely used. (may be used for surveystudies) Intradermal injection of a protein brucella extract, is followed within24 hours with erythema, edema and induration in some infected individuals.


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Prevention: A): For Animals 1-Proper environmental

sanitation and proper Veterinary care: Animal sheds and stables (place,.. ProperCleaning Aborted tissues are soaked with formalin or burned . Veterinary care


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2- Animal disease Eradication:

Agglutination test: if the animal is infected, the disease is eradicated eitherwith: segregation, sluphtering, Immunization: with live attenuated Rev-1 strain ofB.Melitensis or with 19-D strain of B.abortus. Treatment.


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3- International measures:

Quarantine measures for imported animals to prevent Brucellosis.


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For man 1-

Prevent ingestion infection, mainly by H.E, of public and particular occupationsabout meat, milk and food sanitation.


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2- Prevent inhalation infection mainly by environmental sanitation in the stablesand animal sheds with proper ventilation. 3-Prevent contact and occupationalinfection Mainly by washing hands, wearing gloves, boots, special clothes forhunters or butchers or those handling infected animals. Care for disposal ofcarcass or fetal tissues.


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Why we cannt use animal vaccines for human? Because it can induce human brucellosis as they are live attenuated.


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A review article by WHO, 1997


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Control 1-Case finding 2-control of cases

Notification, No isolation, disinfection specially in the animal field.,treatment by combination of rifampin (600-900 mg daily) and doxycycline (200 mgdaily), (There is no immunizations for the contacts).


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Poliomyelitis Causative organism : Poliovirus, which is one of the enteroviruses group thatbelongs to picorna virus group. It has three antigenic types. Type I, thecommonest in epidemics, type II, in endemic areas, and type III the leastcommon. Poliovirus is a Neurotropic virus.


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Resistance Polioviruses can survive for long time under suitable conditions (up to -20c)but are readily destroyed by: Heat , (at 55 c for hour) Pasteurization Disinfectants as chlorine at 0.1 ppm. Ultraviolet radiation can inactivate thevirus(for enough time)


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Immunity Immunity is permanent to the type causing infection . There is no crossimmunity, but There may be a low degree of heterotypic resistance induced byinfection, especially between type I and type II. Passively administeredantibodies lasts only 3-5 weeks.


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Reservoir of Infection : Man, cases and carriers . Cases : all clinical forms ofthe disease. Carriers: all types of carriers except chronic carriers (healthycarriers are the most frequent due to polluted environment). Age of incidence (

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6695029 Food Borne Diseases New One