Food Borne Diseases One

‫بسم ال الرحمن الرحيم‬

Food borne diseases

By Dr. Nihal Salah Shihab Professor of Public Health

Definition • •  

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

Classifications • I-DISEASES WITH MAINLY SYSTEMIC MANIFESTATIONS • • • • • •

* ENTERIC FEVERS (TYPHOID AND PARATYPHOID FEVERS). * BRUCELLOSIS * POLIOMYELITIS * EXTRAPULMONARY T.B. * VIRAL HEPATITIS TYPES A & E * Anthrax

• II- DIARRHEAL DISEASES (with GIT manifestations) • • • • • • •

A- NON-INFECTIVE DIARRHEAL DISEASES B- INFECTIVE DIARRHEAL DISEASES , INCLUDING: * BACTERIAL FOOD POISONING * DYSENTERIES * GASTROENTERITIS * CHOLERA *PARASITIC AND PROTOZOAL DISEASES

TYPHOID FEVER • Causative Organism: • Salmonella typhi (gram negative,typhoid bacilli):- it is one of the salmonella species (group D salmonella), It has a big number of serotypes >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 important for 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 other foods) for weeks, • but is easily destroyed by heat and disinfectants.

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

Exit of infection • In Stool mainly • In Urine

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

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

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 of acquiring typhoid infection

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

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

• Modes of Transmission: • 1-Ingestion of contaminated food and water . • 2-Direct hand-to-mouth infection . • 3- contaminated articles and fomites • Incubation Period : • 14-17 days, usually, from 2-3 weeks.

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

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

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

Figure 1.

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

Copyright ©2004 CMA Media Inc. or its licensors

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 are common with untreated cases.

• 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)

• Diagnosis:

• 1-clinical picture: in classical type • 2-Laboratory Diagnosis • A) By cultures: during stage of bacteraemia (the first week). It takes from 18 hours up to 4 days such as: • Bone marrow aspirates culture: The most sensitive. • Blood Culture: It is sensitive. It is positive in 40-80% of patients.

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

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

C) PCR (polymerase chain reaction): highly sensitive & specific. It takes 16 hours in Lab. • (D) New serological test techniques • Tubex test: it can detect IgM O9 antibodies from patients within few minutes. • Typhidot test : can detect IgM, IgG within three hours.

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 repeat culture until two consecutive negatives.

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

• 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, and a booster every /3-5 years. • Side effects: rarely, GIT troubles and urticaria. • Efficiency (85-95%) • If the person is taking antimalarial drus, stop treatment for two days before vaccination

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

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

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

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

• • • • • •

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 and urine, 24 hours or more apart. The first sample is taken two weeks after drop of temperature to normal (to exclude possibility of relapse).

• Remember: The organism shows a high tendency to develop resistant strains to antibiotics. So, a sensitivity test should be done before chemotherapy. • What measures could be done for chronic carriers? • Health education; • No license for those 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 last exposure to the case, for case-finding. • *Active Immunization: • protection of contacts is doubted. • It may be given, during seasonal spread or outbreak, to be valuable against subsequent exposure.

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

• • • •

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

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

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

• Causative Organisms: [gm –ve coccobacilli ,nonspore forming, with an endotoxin in 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 occupational exposure.

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.

• 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.

• Modes of Transmission: Mainly from Animals

man

It is not recorded from man to man.

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

• Man is rarely recorded to be infected on accidental injection with the animal live attenuated vaccine.

• 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.

• Pathogenesis: • After ingestion, the organism passes from GIT to lymphatic channels and lymph nodes, thoracic duct blood then to parenchymatous organs. The organism tend to be intracellular, Where as Granulomatous formations in the tissues, 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).

• • • •

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

What are the causes of relapses or chronicity 1. Intracellular organism 2. Drug resistance 3. Host factors: (such as :Immunodeficiency and immunocompromised subjects, .

• 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.

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

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

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

Brucella skin testing • It is an unreliable diagnostic test and is rarely used. (may be used for survey studies) • Intradermal injection of a protein brucella extract, is followed within 24 hours with erythema, edema and induration in some infected individuals.

• Prevention: •

A): For Animals

• 1-Proper environmental

• • • •

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

• 2- Animal disease Eradication:

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

• 3- International measures:

• Quarantine measures for imported animals to prevent Brucellosis.

For man

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

1-

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

Why we cann’t use animal vaccines for human? • Because it can induce human brucellosis as they are live attenuated.

Human vaccines are under trial: • Trials are directed to production of a vaccine which can elicit a powerful cell-mediated response (beside the antibody response), why? • Because as the organism is facultative intracellular so, the type of immunity to brucella infection is mainly cell-mediated while humoral immunity in a lesser degree. • So, DNA vaccines are under trial. (from brucella DNA antigen)

A review article by WHO, 1997

• 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 mg daily), • (There is no immunizations for the contacts).

Poliomyelitis • Causative organism : • Poliovirus, which is one of the enteroviruses group that belongs to picorna virus group. • It has three antigenic types. • Type I, the commonest in epidemics, • type II, in endemic areas, and type III the least common. • Poliovirus is a Neurotropic virus.

Resistance • Polioviruses can survive for long time under suitable conditions (up to -20°c) but are readily destroyed by: • Heat , (at 55° c for ½ hour) • Pasteurization • Disinfectants as chlorine at 0.1 ppm. • Ultraviolet radiation can inactivate the virus(for enough time)

Immunity • Immunity is permanent to the type causing infection . • There is no cross immunity, but There may be a low degree of heterotypic resistance induced by infection, especially between type I and type II. • Passively administered antibodies lasts only 3-5 weeks.

• • • •

Reservoir of Infection : Man, cases and carriers . Cases : all clinical forms of the disease. Carriers: all types of carriers except chronic carriers (healthy carriers are the most frequent due to polluted environment). • Age of incidence (< 5 years) • Pattern of spread: endemic disease. Sporadic cases and or epidemics is possible.

• Period of Infectivity: (6-8 weeks), In throat swabs, the virus appear about 1.5 days after exposure up to 1-2 weeks. • In stool, it appears 3 days after exposure up to 3-6 weeks or longer.

• Modes of Transmission. 1- Direct by:

2- Indirect:

a- Pharyngeal (Oral-Oral route), common in industrialized countries b- Fecal-oral route (hand-to-mouth Food-borne infection (a vehicle)

• Incubation Period : 7-14 days, it may be extended up to one month.

Pathogenesis • After oral ingestion or the organism in the mouth, it can multiply in the oropharynx (tonsils),lymph nodes, or the peyers patches in the small intestine. • The virus invades blood within few days after exposure (2-5 days ) • The virus spread along axons of peripheral nerves to the CNS, invades nerve cells, damage them. It damage anterior horn cells of spinal cord, in the brain, it invades the reticular formation, vestibular nuclei, deep cerebellar nuclei

Clinical picture and Squeale of Polio Infection: 1- Inapparent infection: • it is associated with acquired immunity. 2- Clinical poliomyelitis: either • (a) Abortive poliomyelitis with moderate fever and either upper respiratory or gastrointestinal manifestations, then clears up and gives immunity.

• (b) Major illness with involvement of the CNS: • Few days after subsidence of abortive disease, a small % of cases shows: • *Non-paralytic cases : (from 2-to-10 days) • with meningeal irritation (fever, headache, vomiting, neck rigidity, stiffness in the back with severe pain in the back and limbs and pleocytosis.

• Continue, CNS involvement • *Paralytic poliomyelitis : • affects the nerve cells of motor nerves, in about 1% of cases, causing flaccid paralysis. • Appear 7-10 days from onset of disease. Sites: • Paralytic poliomyelitis may be spinal (e.g.lower limbs), bulbar (cranial nerves e.g, dysphagia, dysphonia, diplopia diplopia) or bulbo-spinal.

• Complications: • Respiratory infections, myocarditis, urinary infection, soft tissue and bone deformities, and others. Exposure in pregnancy lead to increase risk for abortion, prematurity or still birth. • fatality: (2-10%) due to respiratory muscles paralysis. • Post- Polio syndrome: • After a latent period of 15-20 years after paralysis, exacerbation of muscle pain with more muscle weakness and paralysis. • It is more common in females.

What are the predisposing factors for enhancing polio major illness during epidemics ? • The followings accelerate invasion of the CNS after exposure to infection: • Mouth and throat surgery, • Giving inoculations (SC or IM), • Excessive muscular activity & • fatigue and • Pregnancy (especially in non endemic areas).

• Diagnosis:

1-Clinical diagnosis: Poliomyelitis is suspected only when CNS involvement occur. 2-Laboratory diagnosis: Suspected cases can be confirmed by isolation of the virus from throat washing or stool, or serologic testing for neutralizing antibodies (rising titer is diagnostic).

• Prevention: 1- general: for both routes of transmission 2- Specific:

(a)- Oral polio (Sabin vaccine): • Nature is trivalent live attenuated polioviruses, Route of administration: oral • Dose is 2-3 drops in the mouth. • Indications : for mass vaccination in infants and young children.

• Primary Immunization:. •

• •

•

•

3 doses are protective. In Egypt, they are given to infants at 0 dose , 2, 4, and 6 months. For children (aged from 7 to 18 years) who have not been previously immunized, two doses of oral polio (6-8 weeks apart) and the third dose given 6 months later. Booster Immunization: booster doses are given at 18-24 months, and at entry to school. Effectiveness: Immunity is usually

• Advantages of Oral Immunization: Immunity Natural immunization • What ? 2 types Easy, safe, low cost

• Rare side effect: [VAPP], Vaccine Associated Paralytic Polio. Incidence, 1/3 million dose of vaccine. • N.B. If the alimentary tract of the child is infected with another enterovirus at the time the vaccine is given , the establishment of immunity is blocked.

• ii) Salk vaccine: trivalent inactivated (killed) by formalin. • Primary Immunization: different schemes. The commonly used scheme gives 4 doses, 1.0 ml each, (6-8) weeks apart, then the 4th dose 7 months thereafter. In Egypt , it is used with oral polio vaccine

• Booster Immunization: booster dose is given at school age, and when necessary (e.g. whenever an epidemic or outbreak threatens).

• Protective Value: Salk vaccination prevents more than 80% of paralytic cases, and lowers severity of paralytic effect in the affected . It dosent prevent local multiplication in the gut.

• • • •

Application of Salk vaccination : in some countries, Mass immunization of infants and children During pregnancy, to provide the newborn with maternally acquired immunity. • At-risk groups, during polio outbreaks . • Susceptible travelers going to visit endemic areas.

What are the causes of failure of Oral polio V in preventing poliomyelitis, sometimes? • 1- Error in the cold chain cycle. • 2- In immuno-compromized or with HIV infants. • 3- Due to exposure to more frequent concurrent enterovirus infections [ affects antibody titre ]

Eradication of Poliomyelitis in Egypt: • Strategies of Eradication: • 1- The MOH expanded program on immunization:• Sabin vaccine is given to all infants at the usual scheme primary and booster. • A zero dose is given soon after birth or with BCG vaccination. • Another dose is given with measles vaccine at 9 months. • One dose of salk vaccine is given either at the age of 2, 4 or 6 months. • Any time the child comes to the center, give him one dose of the oral vaccine.

• 2- National poliomyelitis campaign: • 3. Case investigation and recording: • Any case of acute onset of paralysis in a person aged 0-15 years with no apparent reason, or at any age and suspected to be of poliomyelitis should be investigated as follows:-

• Data collection, Collection and storage of stool specimens for laboratory diagnosis, follow up of the case, and determine if paralysis continued for more than 2 months. • Inform the district officers and the regional officers about the suspected cases of polio. • 4. Surveillance. [ active and passive ]

Control • 1. Case-finding: • 2. Control of Cases: • Notification, isolation at home (of little value) or hospital (with enteric precautions). Concurrent disinfection and terminal cleaning . Medical care and rehabilitation of paralytic cases.

• 3.Control of Contacts : • Examined for case-finding , seroprophylaxis (not in Egypt) and immunization, if necessary.

• 4. Epidemic Measures:

Seroprophylaxis in other countries • Intravenous injection of 0.3 ml/kg . • It is effective only if shortly given before exposure to infection. • It can provide a protection for 3-5 weeks against paralytic polio but don’t prevent subclinical infection (the virus can multiply in the gut).

remember • Q1 • If a vaccine dose is missed, does the entire series need to be restarted in a mutiple-dose regimen ? • Answer: • No.., the series should be completed without starting over. Except for Oral

Typhoid vaccine, it needs to be started for the missed doses.

remember

• Q: • Can vaccines be given all at once or, do they need to be given at separate times? • Answer: • Injected live virus vaccines administered at least 28 days apart. • Oral live vaccines can be administered at the same day but preferred in some occasions to be separated by few hours.

• Any immunoglobulin should not be given within 2 weeks of MMR vaccination and Varicella vaccines [ but not yellow fever vaccine], because we may need to repeat vaccinations.