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Reference
  • There’s a lot of information here about microbiology, infection control and hygiene which I’ll try to add to and keep current.

  • It’s over 35 years since my first undergraduate microbiology lecture. I’ve tried to keep my knowledge up-to-date but please accept my apologies for all the stuff I’ve missed in the intervening years – and call me out on mistakes or omissions.

  • Don’t forget nothing on this site constitutes medical advice. If you think you’re ill consult a physician, not the bloody internet…

Aeromonas

Aeromonas are Gram-negative bacteria common in water and soil. Aeromonas species are associated with rare but serious conditions including wound infections, necrosis, septicaemia and meningitis but the role of Aeromonas in food or waterborne gastroenteritis is a matter of sometimes violent debate (primarily amongst drunken microbiologists at conferences). Usually found in places faaaaaaar warmer than the UK it is part of the normal gut flora of leeches. Which are now used medicinally again. So if you are more likely to get this from having a finger reattached than from food. Unless it’s lightly-sautéed leeches.

Members of four Aeromonas groups may cause gastroenteritis: A. hydrophila, A. veronii biovar sobria, A. caviae and A. trota. A. schubertii and A. jandaei have also been isolated from faeces and some reported cases / outbreaks have been associated with consumption of food contaminated with Aeromonas. But association is not necessarily causation.

Because (a) there is no animal model for gastrointestinal infection and (b) the taxonomy of this genus is very complex, problems arise with collecting data to demonstrate a causal link between gastroenteritis and consumption of food or water contaminated with Aeromonas.

Commercial laboratory test kits are limited in their ability to identify these bacteria and most laboratories cannot routinely culture or type them. Many potential virulence factors have been identified and these may one day assist in the identification of virulent strains. But not today. Or even this week.

Aeromonas can grow at refrigeration temperatures and under both aerobic and anaerobic conditions but they are easily destroyed when food is cooked. They do not form spores. Only the bacilli and the clostridia do that.

Growth and Control

Significant inter-strain variability is reported in conditions for growth and survival.

Temperature: Optimum 28 to 35°C. Range-2 up to 42-45°C, although often < 40°C depending on the strain

pH: Optimum 7.2, Minimum 4.5, Maximum ≥ 8.7. Unlikely to grow in food below pH 6.0 and stored at low temperatures

Atmosphere: Facultative anaerobe.

Water Activity: Optimum approximately 1-2% NaCl

Survival

pH: At pH 4.5, no growth observed at 4 or 28°C

Water Activity: 4.5% (~0.975 aw) NaCl inhibited growth for >14 days at 4°C. At 28°C 5% NaCl (~0.97aw) inhibited most strains and 6% NaCl inhibited them all

Inactivation

Temperature: D45°C = 12-29 minutes. In saline (0.85% NaCl), D48°C = 2.2-6.6 minutes and D51°C = 1.2-2.3 minutes

pH: Inactivated at values <4.5

Water Activity: < 0.96 aw (~ 6 to 7% NaCl) controls all strains tested.

Disinfectants / Sanitisers: See here for guidance.

Susceptible to disinfectants, including sodium hypochlorite and quaternary ammonium compounds. Also iodophors, 2-chlorophenol and glutaraldehyde.

Clinical

It is likely that some strains of Aeromonas cause gastroenteritis, but the role of members of this genus in foodborne illness remains controversial.

Incubation

1-2 days. In an outbreak of A. caviae infections in France, the mean incubation time was 10.6 hours.

Symptoms

Broad spectrum of symptoms ranging from mild, self-limiting watery diarrhoea to dysentery. Abdominal pain, nausea, chills, headache and colitis may also occur. Symptoms last 1-7 days. Chronic diarrhoea has also been reported, usually 7-10 days. A. veronii biovar sobria has been associated with severe gastroenteritis with dysenteric symptoms. Some strains produce aerolysin, which is toxic to vero cells, and a number of haemolytic uremic syndrome cases have been attributed to such strains.

Condition: Gastroenteritis.

Dose: In one human trial where up to 1,000 cells were given, only two of 57 (healthy) volunteers developed diarrhoeal symptoms.

At Risk Groups: Immuno-compromised individuals including adults with disrupted gastrointestinal flora. Symptoms are more severe for children.

Long Term Effects: Older patients more likely to present with chronic enterocolitis.

Reservoirs / Sources

Human: Prevalence comparisons between symptomatic and asymptomatic individuals show higher values for those with symptoms, but the ranges are broad and overlapping. The organism is, however, not considered to be a normal inhabitant of the gut.

Animal: May colonise aquatic plants and animals e.g. fish, leeches and frogs. Causes disease in animals associated with water, e.g. reptiles, fish, shellfish and snails. Minor flora component of domestic animal faeces (pigs, cows, sheep, poultry). Has been isolated from houseflies, mosquitoes and ticks (Galindo and Chopra, 2007). Recently isolated from faeces of Macaca fascicularis, a primate (Harf-Monteil et al., 2004).

Food: Organism has been isolated from fresh produce (McMahon and Wilson, 2001) and foods of animal origin, such as meat, raw milk, poultry, fish, and shellfish.

Environment: Found in salt, fresh, stagnant, estuarine and brackish water worldwide. Tends more towards freshwater because as salinity increases, recovery of organism decreases (ICMSF, 1996). Also isolated from soil, sewage, and even tree bark. Its isolation from water and sediments decreases during cooler months (ICMSF, 1996). Typing data have been reported supporting water to human transmission (Khajanchi et al, 2010).

Transmission Routes: Via water and possibly by ingestion of foods including seafood, particularly oysters that receive little or no cooking during their preparation.

Plague and Pestilence

Seasonal variation observed with Aeromonas-associated gastroenteritis peaking in warmer months.

Collated information on 16 outbreaks/incidences of Aeromonas-associated gastroenteritis implicated a range of suspect foods including fish, land snails, oysters, prawns, shrimp cocktail, dried fish sauce and egg salad. Adults are the largest age group reported among cases. Larger, suspected, outbreaks include:

Oysters: Louisana, USA, 472 adult cases (A. hydrophila)

Dried fish sauce: France, 10 adult cases

Mixed meal including seafood, meat and offals: Sweden, 27 people (A. hydrophila)

Arcobacter

Arcobacter is a member of the Epsilobacteria group, which also includes Campylobacter and Helicobacter spp. It is distinguished from Campylobacter by being able to grow in the presence of oxygen (aerotolerant, as we say in the biz) and at 15ºC.

There are four species of Arcobacter currently recognised of which two, Arcobacter butzleri and Arcobacter cryaerophilus, have been associated with human disease. A. butzleri is probably the primary human pathogen. Arcobacter spp. are gram-negative, curved, s-shaped or helical non-spore-forming rods that are 0.2-0.9 μm wide and 1-3 μm long. They are motile with a single polar unsheathed flagellum. Most strains are non-haemolytic.

Growth and Control

Temperature

Optimum and range depends on the isolate and atmosphere. Optimum probably between 25 and 35ºC, range 15 to 37ºC, though some isolates may grow at 42ºC.

pH

Optimum 6.0 to 7.0 (A. butzleri), 7.0 to 7.5 (A. cryaerophilus), range 5.0 to 8.5

Atmosphere

Can grow in microaerobic conditions, but can also grow in fully aerobic conditions.

Water Activity

Inhibited below aw 0.980 (adjusted with NaCl, glycerol or sucrose).

Survival

Temperature

Survives under cold storage (4ºC) with only a gradual decrease over time. Freezing (-20ºC) causes an initial reduction in numbers, followed by little change in cell viability. Cells in the exponential phase are more cold-sensitive.

Atmosphere

Survives in aerobic and anaerobic conditions.

Inactivation (CCPs and Hurdles)

Temperature

Rapidly inactivated by heating to 55°C and above. D-values in liquid at 50°C = 5.12-5.81 min; 55ºC = 0.38-0.76 min; 60ºC = 0.07-0.12 min. D-values in pork were 18.51 min at 50ºC, 2.18 min at 55°C. Mild heat (50°C) followed by cold shock (4 – 8ºC) is more lethal than either treatment alone. A. butzleri is more heat sensitive at a lower pH or during its stationary phase.

pH

Growth inhibited below pH 5.0. Upper pH tolerance not known (probably greater than pH 9).

Water Activity

Inhibited below aw  0.980.

Preservatives

Able to grow in the presence of 3.5% NaCl, some strains can grow at 4% NaCl, and survival of some strains has been observed at 5% NaCl. A. cryaerophilus is more sensitive than A. butzleri to NaCl. Inhibited by citric acid and lactic acid at 0.2%, and by 0.5% trisodium citrate.

Sanitisers/Disinfectants

See here for guidance.

Sensitive to chlorine (inactivation within 60 seconds at 0.46 mg/L free chlorine, 0.61 mg/L total chlorine). See here for suggestions.

Radiation

Sensitive to γ irradiation, though more tolerant than C. jejuni. Reduced 10-fold in ground pork by 0.27 kGy (0.18 kGy for C. jejuni). Irradiation doses of 0.3 to 1.0 kGy (FDA-approved for pork) would reduce Arcobacter spp. by up to 3.7 log units, and probably eliminate it.

Antibiotics

Nisin alone is not significantly inhibitory, but enhances inhibition in the presence of organic acids. Vary in sensitivity to antibiotics; most are sensitive to fluroquinolones (but resistance is emerging) and imipenem and amikacin. High level of resistance to penicillins and others such as vancomycin and methicillin.

Clinical Notes

A. butzleri is more commonly associated with human disease, and serotypes 1 and 5 are primarily associated with human infection.

Incubation: Not known.

Symptoms: Patients can be asymptomatic. The most common symptom is acute watery diarrhoea lasting for 3-15 days, sometimes being persistent or recurrent for greater than 2 weeks or even as long as 2 months. Often accompanied by abdominal pain and nausea. Some patients also experience bodily weakness, fever, chills and vomiting. Coinfection with another enteric pathogen has been observed, as has infection by Arcobacter in patients with other conditions such as diabetes. Hospitalisation can occur.

Condition: Usually gastroenteritis, but occasionally septicaemia.

Toxins: Produces chemicals that are toxic to some cells, but no information on toxin production in foods.

At Risk Groups: Can affect any age group, though highest prevalence is in very young children. One Belgian study indicated that slightly more females were infected than males.

Long Term Effects: Not known.

Dose: Not known.

Treatment: Typically none, as recovery usually occurs with conservative management (e.g. administering fluids). Some cases are treated with antibiotics such as amoxicillin+clavulanate, erythromycin and ciprofloxacin, although some strains may be resistant to these antibiotics.

Human: A. butzleri is most commonly isolated from humans, and A. cryaerophilus more rarely. They are not normally found in the human intestine, and have been isolated from patients with bacteraemia, endocarditis, peritonitis and diarrhoea. Likely transmission route between people is faecal-oral.

Animal: A. butzleri, A. cryaerophilus and a third species Arcobacter skirrowii, are associated with diarrhoea and abortion in animals. The primary reservoirs are cattle, sheep and pigs, although horses may also be important. Arcobacter have been isolated from the intestine, placenta and foetus of these animals, and also cultured from raw milk during mastitis outbreaks in cattle and the faeces of chickens. A. cryaerophilus has been isolated from the preputial washings of bulls and Arcobacter have also been isolated from large numbers of clinically healthy animals.

Food: Arcobacter spp. have been detected on food of animal origin such as beef, lamb, pork and poultry. Higher prevalence has been found in chicken and pork products. Chicken carcasses are often contaminated with Arcobacter spp., and unlike Campylobacter, Arcobacter are rarely found in intestinal contents (possibly transient), but are recoverable from throughout poultry processing plants and are present on birds prior to evisceration. Genetic clustering of Arcobacter isolates with retail establishments is also evident, suggesting that in situ contamination may be important. Distribution in other foods is not known.

Water: Arcobacter spp. have been detected in drinking water reservoirs and treatment plants, and can adhere to water distribution pipe surfaces.

Environment: Excreta from infected animals may contaminate soil or water. Arcobacter spp. have been found in river and canal waters, but their ability to survive in the environment is not known.

Transmission Routes: Contaminated foods of animal origin (particularly poultry and pork) and consumption of contaminated water are likely to be the most important transmission routes to humans.

Plague and Pestilence

The number of outbreaks and incidents attributable to Arcobacter infection is unknown as this organism is not usually included in routine clinical investigations so reported incidents and outbreaks associated with Arcobacter are rare. Recurrent abdominal cramps in 10 children from a school in Italy were caused by Arcobacter infection. Arcobacter were also isolated from many Thai children suffering from diarrhoea.

Bacillus cereus
HAZARD GROUP 2

Bacillus cereus is a spore-forming bacterium that occurs naturally in many kinds of foods and can cause illness in humans. It forms spores that are resistant to heating and dehydration and can therefore survive cooking and dry storage as well as a heat-stable toxin.

Forms recalcitrant spores and a heat-stable toxin

It can cause serious illness in two different ways: after contaminated food is eaten the bacteria produce toxins in the small intestine leading to diarrhoea, cramps, and sometimes nausea (but usually not vomiting). B. cereus can also make a different toxin in (usually) rice and other starchy foods which causes nausea and vomiting in 30mins to 6 hours. Usually clears up in about a day. Both kinds of illness are generally self-limiting but can cause serious complications, although rarely in otherwise healthy people.

Refrigeration at 4°C or lower is vital – B. cereus can form spores which can germinate at higher temperatures and the more bacteria, the more toxin, and the greater the chance that you’ll get sick. When foods containing B. cereus spores are at the right (or wrong!) temperature the spores may germinate, the bacteria may grow and produce toxins that make people sick. Really sick. This is frequently linked with reheated rice but also other starchy foods of plant origin such as pasta, potatoes, pastries and noodles.

B. cereus can cause vomiting or diarrhoea and, in some cases, both. This depends on the kinds of toxin it produces.

When B. cereus grows and produces emetic toxin in food, it can cause vomiting, even if the food is cooked again and no live bacteria are eaten. This is because the toxin is not easily destroyed by heating. When food containing live B. cereus is eaten the bacteria may grow and produce another toxin – diarrhoeal toxin – in the gut. This results in – you’ve guessed it – diarrhoea.

Illness from B. cereus can be prevented by making certain that hot foods are kept hot and cold foods are stored cold. It is important to remember that re-heating food that has been ‘temperature abused’ will not make it safe.

Growth and Control

Growth

Temperature

Optimum 30-40°C

Range 4-55°C, emetic strains have a minimum of 10°C

Maximum toxin production at 20-25°C, toxin production range 10-40°C

pH

Optimum 6-7

Range 4.5-9.5

Atmosphere

Facultative anaerobe

Oxygen required for production of emetic toxin

Minimum Water Activity

With NaCl >0.93 and <0.95 aw

With glycerol 0.93 aw

Survival

Temperature

Spores more resistant to dry than moist heat, and are also more resistant in oily foods. Cooking at or below 100°C may allow spore survival.

Emetic toxins remain active after 150 min at 100°C (pH values 8.7 to 10.6)

pH

Generally vegetative cells decline rapidly in stomach acid, however some may survive depending on food and level of stomach acidity. Spores are resistant to gastric acidity (between pH 1 and pH 5.2)

Emetic toxin stable between pH 2 and pH 9

Water Activity

Spores survive long periods in dry foods e.g. population unchanged after 48 weeks in cereal (aw 0.27-0.28)

Inactivation

Temperature

Vegetative cells destroyed by frying, grilling, roasting and pressure-cooking

Spores (depends on strain and food):

D100°C = 1.2-7.5 minutes in rice

D120°C (mean of 465 datapoints) = 2.5 seconds

D120°C (mean of 19 datapoints in oily foods, e.g. pumpkin pie, soybean oil) = 3.4 min

Emetic toxins inactivated 90 min at 100°C at pH 8.6

Diarrhoeal toxin inactivated 5 min at 56°C

pH

Vegetative cells inactivated in yoghurt (pH 4.5) and fruit juice (pH 3.7, 5-6 log10 reduction within a few hours depending on temperature)

Diarrhoeal toxins unstable outside range pH 4-11 (Jenson and Moir, 2003)

Water Activity

Vegetative cells inhibited at aw < 0.91

Preservatives

Vegetative cell growth inhibited by sorbic acid, benzoate, sorbate, ethylenediaminetetraacetic acid (EDTA) and polyphosphates

Spore germination and outgrowth inhibited by nisin (NB: Nisin is not sporicidal)

Disinfectants / Sanitisers

Most food industry sanitisers destroy vegetative B. cereus cells on surfaces – but it’s the spores that are a bastard to kill.

Phenolics, QACs, alcohols, bisguanides, organic acids, esters and mercurials have little sporicidal effect. QACs are sporistatic but you really need an oxidising agent such as AntiBak– see here for suggestions.

Glutaraldehyde, formaldehyde, chlorine, iodine, acids, alkalis, hydrogen peroxide, peroxy acids, ethylene oxide, ß-propionolactone and ozone are all sporicidal at high concentrations with long contact times

Chlorine disinfectants are often recommended against spores; most bleaches contain about 5% sodium hypochlorite and are effective against vegetative B. cereus cells but not spores

Clinical

B. cereus-associated foodborne illness occurs as two distinct intoxication syndromes: emetic and diarrhoeal. Recovery is rapid for both syndromes, usually within 12-24 hours. There are usually no long-term effects, but severe consequences, including fatalities, can occasionally occur.

Emetic syndrome

Incubation: 0.5-6 hours.

Symptoms: Nausea, vomiting, malaise, occasionally followed by diarrhoea.

Dose: Large numbers in the range of 105 to 108/g viable cells are required before toxin (cereulide) becomes detectable in the food. Emetic toxin concentration in foods implicated in an outbreak in Japan ranged from 0.01 to 1.28 μg/g. An intoxication dose of 8 μg kg-1 body weight has been suggested (Paananen et al., 2002).

Diarrhoeal syndrome

Incubation: 8-16 hours

Symptoms: Abdominal pain, watery diarrhoea, occasional nausea.

Dose: 105-107 (total cells). Foods with such high populations of B. cereus may not be acceptable to the consumer.

At Risk Groups: All people are susceptible to intoxication, but intensity of symptoms varies between individuals.

Treatment: Treatment is usually not given. Fluids are administered when diarrhoea and vomiting are severe.

Sources

B. cereus is a spore former. It is widely distributed in nature and contaminates virtually every agricultural commodity. It has been isolated from soil, dust, cereal crops, vegetation, animal hair, fresh water and sediments, although it is not generally isolated from fish (ICMSF, 1996).

Human: Can be transiently carried in the intestine of healthy humans (14-43%) (Jenson and Moir, 2003). However, no person-to-person transmission has been reported.

Food: Transmission is predominantly foodborne. Most raw foods will contain B. cereus spores, as do many dried herbs, spices and dehydrated foods. Emetic illness is frequently linked with raw starchy foods of plant origin (such as rice, pasta, potatoes, pastries and noodles). In 95% of emetic cases, fried or cooked rice is implicated (Jenson and Moir, 2003). Diarrhoeal illness is often associated with meat products, soups, vegetables, sauces and milk/milk products. Dairy products may spoil through the growth of spores that survive pasteurisation.

Plague and Pestilence

Most B. cereus food poisoning incidents are from cereal-based or protein-based foods, slowly cooled and stored between 10 and 50°C. This allows surviving spores to germinate and reach numbers high enough to cause illness. Rice is frequently a culprit. Global oubreaks include:

Pancakes; (5 cases) Commercial eatery. Temperature abuse and poor storage of pancake batter.

Savoury rice, potato, mashed pumpkin (suspected); (27 cases). Food vehicles not identified.

Japan, contaminated milk in school lunch: 1877 cases (emetic).

Norway, fish soup: 20 cases (diarrhoeal). Inadequate cooling.

Denmark, meat with rice: >200 cases (diarrhoeal).

Spain, cooked noodles: 13 cases (diarrhoeal). Inadequate cooling of cooked noodles.

Norway, vanilla sauce: >200 cases (diarrhoeal). Prolonged storage at ambient temperature.

Campylobacter
HAZARD GROUP 2

Most common bacterial UK gastrointestinal disease.

The two species Campylobacter jejuni and C. coli are most often associated with disease. Grows best in reduced oxygen atmospheres and only at temperatures exceeding room temperature.

Loves meat slicers. While the 2011 FSA Guidance focussed on E. coli, EHOs had identified howling Campy counts on complex equipment – one of the principal reasons you now need separate complex equipment for raw and cooked.

Growth and Control

Growth

Temperature: Optimum 42°C, range 30.5 to 45°C. Is comparatively slow growing (fastest generation time approximately 1 hour) even under optimum conditions.

pH: Optimum 6.5 to 7.5, range 4.9 to 9

Atmosphere: Normally requires reduced levels of oxygen – optimum growth at 3-5% oxygen and 2-10% carbon dioxide. Can be adapted to aerobic growth, although the significance of this in transmission of the disease is unclear.

Water Activity: Optimum growth is at aw = 0.997 (≡0.5% NaCl), minimum aw ≥0.987 (≡2.0% NaCl)

Survival

Temperature: Survival in food is better under refrigeration than at room temperature, up to 15 times as long at 2°C than at 20°C. Can survive up to an hour on hands and moist surfaces. Numbers decline slowly at normal freezing temperatures after an initial reduction. Freezing therefore does not instantly inactivate the organism in food.

Atmosphere: Survives well in modified atmosphere and vacuum packaging. Usually survives poorly at atmospheric oxygen concentrations.

Viable but Non-Culturable (VNC) Cells: Under adverse conditions Campylobacter can undergo a transition to a ‘VNC’ state. The ability for Campylobacter to produce VNC cells is becoming widely accepted.

Inactivation (CCPs and Hurdles):

Temperature: Rapidly inactivated by heating at 55°C and above.

D50C = 1-6.3 min. D55C = 0.6-2.3 min. D60C = 0.2-0.3 min.

pH: Growth inhibited in foods at less than pH 4.9 and above pH 9. Rapid death in foods at pH <4.0 especially at above refrigeration temperatures.

Water Activity: Thought to be sensitive to drying but under certain refrigeration conditions can remain viable for several weeks.

Preservatives: Sensitive to NaCl concentrations above 1%, and death occurs slowly at 2% (D time is 5-10 hours). Ascorbic acid and several spices inhibit growth.

Sanitisers/Disinfectants: Sensitive to most sanitisers, e.g. chlorine and QACs. See here for guidance.

Radiation: Sensitive to γ irradiation. An estimated 6 D reduction would result from exposure to 2 kGy, 10 D would result from 2.5 kGy. A 2-3 kGy dose is sufficient to decontaminate meat. D values reported are 0.18 kGy in refrigerated product, 0.24 kGy in frozen product. More sensitive to ultraviolet radiation than E. coli and commercial UV water treatment units producing 30 mWs/cm2 are considered adequate.

Clinical

Incubation: 1 to 10 days (usually between 2 and 5 days) following ingestion of the bacteria.

Symptoms: Typically muscle pain, headache and fever (known as the “febrile prodrome”) followed by watery or bloody diarrhoea, abdominal pain and nausea. Symptoms may last 1 day to 1 week or longer (usually 5 days). Excretion of the organism in stools occurs on average for 2 to 3 weeks and is mostly self-limiting. Hospitalisation has been reported in 10% of cases. The attack rate is around 45%.

Condition: Campylobacteriosis. Campylobacter colonises the gut and damages the intestine. The exact mechanisms of this remain unclear.

Toxins: Toxins are not produced in foods.

At Risk Groups: Can affect any age group but most often isolated from infants (< 1 year) and young (twenties) adults. Incidence higher in males (up to 45 years of age).

Long Term Effects: Infection may occasionally be followed by arthritis (e.g. Reiter’s syndrome) or Guillain-Barré Syndrome (GBS). 1% of cases suffer reactive arthritis 7-10 days after onset. 0.1% of cases develop GBS 1-3 weeks after infection, and of these 15% recover completely, 3-8% die and the rest recover with varying degrees of impairment. A number of other less common non-enteric diseases can occur. Invasion of the bloodstream may occur in 1.5 per 100,000 cases, especially in the elderly. US data suggests a case-fatality rate of around 3 per 100,000 outbreak associated illnesses.

Dose: Consumption of 800 cells causes infection on approximately 50% of occasions, but many are subclinical (the proportion of people showing symptoms is not as high). Dose response information for numbers less than this is not available. Modelling has indicated an “optimum” dose for becoming ill is 1,000-10,000 cells.

Treatment: Supportive. Fluids may be given. Some cases warrant treatment with antibiotics. Erythromycin is the drug of choice, although resistant strains are emerging.

Reservoirs / Sources

Human: Campylobacter is not one of the organisms normally found in the human intestine. Faeco-oral person-to-person transmission (in some cases by asymptomatic carriers) has been reported.

Animal: Commonly found at high numbers in the guts of ruminant animals. Some non-ruminant animals (e.g. dogs and cats) are infected with the organism and may, or may not, show signs of disease. Flies have been implicated as vectors. Birds are considered to be a reservoir.

Food: Raw poultry is frequently contaminated, cooked chicken is rarely contaminated. Raw milk, offal, red meat, mushrooms, garlic butter, salads and shellfish have all yielded Campylobacter.

Environment: Excreta from infected animals may contaminate soil or water. Environmental survival is conventionally considered to be poor but newer information suggests it may be better than currently acknowledged. For example Campylobacter has been detected in dry beach sand. Survival in cold water is good, but reduced at temperatures above 10°C. Campylobacter is present in water and sediments more frequently and at higher numbers in the winter months. Environmental survival appears to be the opposite to human cases, i.e. survival is poorer in the warmer months.

Transmission Routes: The importance of undercooked chicken as a source of a proportion of cases of campylobacteriosis recognised, but the relative importance of other routes, e.g. other foods, recreational water, occupational exposure is unknown.

Plague and Pestilence

Outbreaks: Most cases of disease are sporadic and outbreaks relatively rare. Most outbreaks are caused by cross contamination – especially in retail butchery – or inadequate cooking. Correct refrigeration serves to aid the survival of the organism.

Associations include occupational exposure to raw meat, having a household pet with diarrhoea, ingesting untreated water from lakes, rivers and streams, travel abroad, consumption of poultry liver, consumption of poultry, consumption of sausages at a barbecue, and eating poultry that was brought into the house raw.

Clostridium botulinum
HAZARD GROUP 2

Clostridium botulinum a potent nerve toxin which vain twats inject into their faces – aka Botox. Ick.

Rare but deadly if not treated. Its toxin (sold as Botox®) causes paralysis and is one of the most potent nerve toxins ever studied. Grows well in places with low oxygen, such as cans of food that became contaminated before being sealed. Minute amounts of toxin can cause paralysis and suffocation. With antitoxin and a ventilator the paralysis usually goes away within weeks – or in severe cases, months. Can also infect babies. Constipation is often the first sign then a dull face, weak sucking, weak cry, less movement, trouble swallowing, more drooling than usual, muscle weakness and breathing problems. Children under 1 year old should never be fed honey which has been linked to infant botulism (but not to adult botulism). Wound botulism more common – principally in IV drug abusers. Ick.

Clostridium botulinum is one of the most important pathogens associated with food. The organism forms spores that are resistant to many common food process controls. Botulinum neurotoxins (BoNT) produced by vegetative cells of this Gram positive, anaerobic bacterium are among the most potent biological neurotoxins known. And some silly twats inject into their faces – it’s marketed as Botox®.

Foodborne botulism is a very severe intoxication, historically caused by eating preserved low acid, low oxygen foods (e.g. canned vegetables, meat and fish) in which C. botulinum had grown and produced BoNT. Symptoms appear between 12 and 36 hours after consuming the contaminated food with early nausea, vomiting and diarrhoea followed by paralysis of the eyes, mouth, throat and, progressively, muscles. Infant botulism is an extremely rare toxico-infection that occurs when C. botulinum grows and produces toxins in the intestines of babies; symptoms appear in 3-30 days and include constipation, lethargy, floppiness and breathing difficulties. This is why babies under a year old must not be fed honey; it’s a reservoir for botulinum spores.

Not all C. botulinum cause illness in humans. Strains produce one of seven known types of BoNT (A to G). Only those producing types A, B, E and F (rarely) cause botulism in humans. Strains are also separated into two groups based on physiological differences: Group I (can produce A, B or F toxin) are proteolytic and cause food spoilage; Group II (can produce B, E or F toxin) are non-proteolytic and may be present in foods without obvious spoilage.

Foodborne and infant botulism caused by C. botulinum in Groups I and II; more common is wound botulism in IV drug users – but as most food businesses don’t sell black tar smack as a rule we’ll stick to the foodborne disease.

Growth and Control

Normally grows in the absence of oxygen.

C. botulinum produces a fatal toxin. This toxin is reasonably heat-stable but is destroyed by heating at >80°C. While the toxin has legitimate medical uses is one of the most potent nerve toxins ever discovered yet is injected into the faces of the vain and stupid under the trade name Botox®. The medical term for such people is ‘morons’.

Like the other clostridia C. botulinum forms a spore which makes proper cooling and reheating very important. Outbreaks have been implicated in low acid canned foods such as garlic and oil preparations. In addition, outbreaks have been caused by foil wrapped baked potatoes improperly cooled and then used to make potato salads.

While botulism poisoning is very rare, the organism is common in the soil and can survive in the environment as a resistant spore which stays dormant until exposed to conditions that support growth.

There are three main types of botulism – food borne botulism, intestinal botulism (due to proliferation of the organism in the gut) and wound botulism. Wound botulism in intravenous drug users is the most common presentation. The most common food-related outbreaks of botulism are linked to incautious home preserving of foodstuffs but – rarely – other canned foods can be tainted with the bacteria. Symptoms often begin with blurred vision and difficulty in swallowing and speaking, but diarrhoea and vomiting can also occur.

Symptoms of food borne botulism usually turn up 18 to 36 hours after eating tainted food, but it can take up to 10 days for symptoms to occur. The disease can progress to paralysis. Most cases will recover, but the recovery period can be many months. The disease is fatal in 5-10% of cases; death is due to respiratory failure.

When caught early an anti-toxin is available to stop the spread of the bacteria and emetics are often used in an attempt to rid the body of tainted food particles. Those canning their own foods need to take special care with those that are low in acid. Botulism is prevented in commercially-canned food by cooking at 121°C (250°F) for 3 minutes thus killing the spores. Honey is the only known dietary reservoir of botulinum spores. This is the reason honey is not recommended for infants under 12 months.

The spores are killed by heating or by strong oxidising agents.

Clostridium perfringens
HAZARD GROUP 2

Clostridium perfringens is an anaerobic rod-shaped, Gram-positive bacterium associated with foods such as rolled meat joints, stews and gravies. This common commensal is rarely pathogenic and is usually limited to the immunocompromised and those with open wounds but can also cause food poisoning with abdominal pain, diarrhoea, vomiting is rare. In very rare cases it has been associated with tissue necrosis, bacteraemia, emphysematous cholecystitis or gas gangrene.

During cooking, vegetative cells of C. perfringens die but they form spores able to survive the unfavourable conditions. If the food is cooled slowly, the spores can germinate into vegetative cells that can then multiply to high numbers. When the highly contaminated food is eaten, although the cells are unable to grow in the gut they form spores and as the cells break to release the spore, a large amount of toxin is released into the gut. Symptoms include watery diarrhoea and abdominal pain that usually resolves itself as the diarrhoea removes the toxin from the body.

There are five types of C. perfringens based on toxin type (A, B, C, D, E). Most C. perfringens food poisoning cases reported in developed countries are caused by type A strains. Type C causes a rare, severe, necrotic enteritis. Less than 5% of all C. perfringens carry the gene responsible for the production of the enterotoxin causing Type A illness (the cpe gene). Only strains carrying this gene in a chromosome (C-cpe) cause foodborne illness. For this reason we shall stick to Type A and cpe positive C. perfringens.

Growth and Control

Isolates with chromosomal cpe have a competitive advantage over isolates with the same gene located on a plasmid (P-cpe), as they are more resistant to several food preservation procedures (e.g. heat, refrigeration, freezing).

Optimal heat shock occurs around 75°C which will activate germination of any spores in the food. Slow cooling and / or slow reheating provide germinating spores and any surviving vegetative cells with conditions (>10°C to <54°C) allowing multiplication to large numbers, particularly as competitive flora will have been killed.

Growth

Temperature

Minimum 10°C

Maximum 54°C

Optimum 43°C

Some isolates have a very short generation time (<10 min). Enterotoxin is produced only during spore formation but remains intracellular until lysis of the mother cell to release the mature spore. Toxin is not produced in significant amounts during optimum vegetative growth. Toxin production is optimum at 35-40°C.

pH

Optimum 6-7

Range 5.1 to 9.7

Spore formation occurs between pH 5.1 and 9.9 (Li and McClane 2006a).

Atmosphere

Optimal under anaerobic conditions.

Small amounts of oxygen, up to a redox potential of +200 mV can be tolerated, but generation and lag times lengthen. The redox potential of many foods, including meat, is sufficient to allow growth to start, after which the atmosphere is made more anaerobic by the organism. Growth rates are similar under carbon dioxide or nitrogen atmospheres.

Minimum Water Activity

0.93

Survival

Temperature

Concentrations of C-cpe vegetative cells decline at refrigeration temperatures, with C-cpe isolates surviving longer; D4°C of 11 days compared to 1.8 days for P-cpe isolates (Li and McClane, 2006b). Similarly, the D-20°C was 1.5 days for C-cpe cells compared to 0.6 days for P-cpe isolates.

Spores survive both refrigeration (4°C) and freezing (-20°C) with less than 1-log reduction in spore viability after 6 months at both refrigeration and freezing temperatures.

pH

Sporulation occurs between pH 6 and 8 under gut conditions. The hardy spores show less than a 1.2 log decrease in numbers after 3 months at pH 4 and pH 10.

Atmosphere

C. perfringens vegetative cells survive some exposure to oxygen (redox potentials between +200 to +300 mV).

Inactivation

Temperature

A literature review indicated a mean D70C of 23 seconds with a 95th percentile of 125 seconds (based on 146 data points).

Cooking for 2 minutes at 70°C would achieve a mean (approximate) 6-log reduction in vegetative cells, but would not kill spores. In the same review, a mean D120C of 18 seconds was calculated for spores, with a 95th percentile of 161 seconds (based on 64 data points ).

D-values for different isolates of C. perfringens vary, particularly when present as spores, and C-cpe strains appear more hardy. As spores, the D100C of six C-cpe strains was between 30 and 124 min compared with 0.5-1.9 min for P-cpe strains.

While the enterotoxin is a heat-labile protein and inactivated by heating for 5 min at 60°C, it is not generally produced in food.

pH

Vegetative C-cpe cells inactivated below pH 5 (Bates and Bodnaruk, 2003)

C-cpe spores slow inactivation below pH 5

Enterotoxin not generally produced in food

Preservatives

For the curing of meats hurdle technology is often used. For example, the use of pH (6.2), salt (1%) and sodium nitrite (50μg/ml) act synergistically to inhibit C. perfringens vegetative growth at 15°C.

Disinfectants / Sanitisers

QACs and chlorine sanitisers destroy vegetative C. perfringens cells on surfaces. See here for guidance.

Glutaraldehyde, formaldehyde, chlorine, iodine, acids, alkalis, hydrogen peroxide, peroxy acids, ethylene oxide, ß-propionolactone and ozone are all sporicidal at high concentrations with long contact times – Antibak is far quicker and less toxic – see here for further info.

Phenolics, QACs, alcohols, bisguanides, organic acids and esters have little sporicidal effect. Chlorine disinfectants such as household bleach contain 5.25% sodium hypochlorite (52,500 ppm available chlorine) are not effective against C. perfringens spores.

Clinical

Incubation: 6-24 hours, usual onset 10-12 hours.

Symptoms: Profuse watery diarrhoea with severe abdominal pain that subsides within 24 hours or less. Diarrhoea is initiated by the enterotoxins causing tissue-damage to intestinal cells. Vomiting and nausea are rare. Severity of illness is lessened by the diarrhoea flushing out both the enterotoxin and sporulating cells from the small intestine. Estimated hospitalisation and fatality rates are 0.3% and 0.05%, respectively.

Condition: Gastroenteritis or C. perfringens enteritis.

Dose: Approximately108 organisms. Large numbers of vegetative cells must be ingested. Assuming a 100g serving, at least 106/g of food is needed to cause illness.

Toxins: Illness is due to foodborne infection with toxin produced in the intestine. Rare cases of intoxication with pre-formed toxin have been reported, resulting in earlier onset of symptoms. In instances where the bacteria have multiplied to such levels that sporulation and toxin production occurs, the food is usually in an advanced state of spoilage. Up to 15% of a sporulating cell’s protein can be enterotoxin.

At Risk Groups: No specific ‘at risk’ groups.

Long Term Effects: Generally none.

Treatment: Not usually given as symptoms resolve naturally (McClane, 2007).

Reservoirs / Sources

Human: USA, Finnish and Japanese studies indicate that most healthy adults are not routinely colonised by C. perfringens C-cpe type strains but about half of all subjects studied were colonised with non-enterotoxigenic type A vegetative cells and/or spores, including P-cpe strains.

In general, counts in populations of healthy individuals of <103-104/g faeces are considered normal. The organism is more numerous in healthy neonates and the elderly than in adults. Food handlers are not thought to be a source of food contamination as the organism already exists on the at-risk foods. As levels of C. perfringens spores can be elevated in some healthy individuals (e.g. the elderly), detection of toxin in faeces is preferable to culture for diagnosis and outbreak investigation. Analysis for enterotoxin should be carried out within 48 hours of onset due to rapid elimination of toxin from the gut. PCR methods on suspected food samples are also useful because they identify the presence of the C-cpe gene.

Animal: C. perfringens can be found in the contents of virtually all animal intestines. Contamination of carcasses occurs at slaughter. Animal foods are the most common vehicles.

Food: C. perfringens can be found in raw, dehydrated and cooked foods. Type A food poisoning often involves large volumes of food, especially meat and poultry dishes, prepared and cooked (possibly undercooked) in advance then allowed to cool too slowly. Cooking creates an anaerobic atmosphere as oxygen is depleted. Rolled meats, stuffed poultry, pies, thick soups, stews, gravies and curries have been implicated in outbreaks. In the case of rolled meats, any bacteria on the outside of the meat are rolled into the centre where conditions are anaerobic and heat can be slow to penetrate. Undercooking of foods is a major factor for survival of vegetative cells. Heating activates any spores while slow cooling promotes germination and growth.

The most effective way to prevent C. perfringens food poisoning is to prevent its growth in food, i.e. strict controls on cooling and on storage temperatures.

Environment: Spores of C. perfringens are resilient and are widely distributed in soil, dust and vegetation.

Transmission routes: Primarily ingestion of food with high levels of C. perfringens vegetative cells (>106/g).

Plague and Pestilence

No particular seasonal patterns. Outbreak investigations commonly reveal control point failures including preparation too far in advance (implying temperature abuse), undercooking, inadequate cooling, poor reheating and improper hot holding.

Outbreaks have been associated with inadequate cooling or refrigeration, reheating, improper hot holding.

Cronobacter

Enterobacter sakazakii was recently reclassified into eight distinct taxa of a new genus – Cronobacter. All have been linked retrospectively to clinical cases in adults and infants. To avoid confusion the organism will be referred to here as Cronobacter spp. (E. sakazakii). This confusion is caused by microbiologists renaming stuff while pissed at conferences to irritate clinicians. Just as we continue to do with classifying strep.

Anyway, the bacterium is Gram-negative, motile, non-spore-forming rod and will grow in aerobic and anaerobic conditions. It is considered an opportunistic pathogen. Enterotoxin-like compounds are produced by some strains.

Principal Risk: Baby Formula

Powdered formulae (PF) can be used to supplement or replace human breast milk. As a powder, it has advantages of cost and storage over the liquid form, however liquid (ready-to-use) infant formula is commercially sterile and is rarely implicated in human illness. PF includes all types of powdered formulae for infants and young children, including powdered infant formulae (PIF) and infant formulae for special medical purposes, follow-up formula (FUF), and human milk fortifiers used to supplement breast milk.

In general, PF products have been identified as high-risk foods for the growth of Cronobacter spp. (E. sakazakii) although only PIF has been implicated in cases of Cronobacter spp. (E. sakazakii) infection.

PIF is intended for newborns to weaning infants. Its composition closely resembles human breast milk. It is subject to stringent hygiene controls and microbial criteria in its manufacture. Current international standards (CAC, 2008) require Cronobacter spp. (E. sakazakii) to be absent in 30 samples of 10 grams.

Follow up formula (FUF) is a liquid food (derived from milk and/or other constituents of animal/plant origin) that is suitable for weaning infants from their 6th to 12th month. FUF may contain a wider variety of dry-mix ingredients that diversify the diet, e.g. cocoa powder, fruit/vegetable powders or flakes and flavours. FUF generally has a higher protein, iron and mineral content and a higher renal solute load compared to PIF.

International evidence suggests that FUF has been consumed by infants <6 months old, and occasionally <1 month old. A general consensus has been reached by the Codex Alimentarius Commission not to establish a microbial criterion for Cronobacter spp. (E. sakazakii) in FUF. This is mostly due to a lack of evidence associating illness with FUF, but also because feeding FUF to infants <6 months old contradicts manufacturers’ directions. Unintended use or misuse of FUF has led to calls for clearer labelling and education of caregivers and healthcare professionals regarding the appropriate preparation and use of PIF and FUF.

Growth and Control

Growth

Temperature: Range 5.5-45°C. Optimum 39.4°C. Generation time 5 h at 10°C, 40 min at 23°C, 20 min at optimum. It has been shown to grow in breast milk and breast milk with fortifiers (calorie and/or nutrient supplements) at 23°C and 37°C. The addition of fortifiers slowed growth at both temperatures, the effect was especially pronounced at 10°C.

pH Minimum 3.89. Optimum 5-9. No maximum value found in the literature.

Atmosphere Grows in aerobic and anaerobic conditions.

Water Activity Maximum salt concentration permitting growth: 9.1% (Lambert and Bidlas, 2007).

Survival

Favoured in PIF at low aw and temperature. In a long-term survival experiment the organism was inoculated into PIF to achieve a final reconstituted concentration of 106 cfu/ml and the PIF stored in screw-capped bottle at room temperature for 2 years. A final concentration of approximately 300 cfu/ml was measured in the reconstituted product (a 3.4 log10 reduction). Most of the reduction occurred in the first 5 months.

Temperature Survived 6 months of freezing in reconstituted PIF without a decrease in concentration. Ten strains did not grow in reconstituted PIF stored at 4°C but could be detected by enrichment 72 h after preparation.

pH Ability to survive moderate acid conditions is pH-dependent. Ten of twelve strains reduced by less than 1 log10 during a 5-hour challenge at pH 3.5 (at 36°C).

Water Activity Survives in PIF (aw = 0.2). Survived better in PIF at aw 0.25-0.30 than in PIF at aw 0.43-0.50 at both 21°C and 30°C

Exponential-phase cells are more sensitive to drying than stationary-phase cells in low Water Activity environments. Dried stationary phase cells survived 46 days at 25°C and 47°C, reducing by around 2 log10 CFU/ml in the first 20 days then remained stable.

Inactivation

No synergistic interactions between inhibitory factors such as weak acids, pH, salt and temperature.

Cryptosporidium

Cryptosporidium parvum and Cryptosporidium hominis are intracellular protozoan parasites that may produce gastrointestinal symptoms when ingested by humans. Up until 2002 C. parvum was named C. parvum genotype 2 (cattle genotype) and C. hominis was named C. parvum genotype 1 (the human genotype). They are now recognised as different species based on genetic distinctions, but care should be taken when reviewing pre-2002 literature for this reason. There are a further thirteen recognised species of the genus Cryptosporidium. C. parvum and C. hominis are the most widespread and most frequently associated with human infections (C. parvum infects cattle too; other spp infect other mammals and birds but not humans.

C. hominis and C. parvum are transmitted person-to-person. C. parvum is also transmitted animal-to-animal or animal-to-human (zoonotically). Both organisms move between hosts in an environmentally-resistant oocyst form that is excreted with faeces. An oocyst is the resting stage of the protozoan, similar to a bacterial spore, and may facilitate transmission of the organism via contaminated water or food.

Growth and Control

N.B. Viability refers to whether the organism is still alive, infectivity relates to the organism’s ability to infect a host.

Growth

The organism does not replicate outside the intestines of hosts.

Survival

Temperature

Oocysts remain infective in water at:

67.5°C for 1 minute

-5°C for up to 8 weeks

-10°C for up to 7 days

-15°C for up to 24 hours

-20°C for up to 5 hours.

pH

Viable C. parvum oocysts were detected after 14 days, in media based on citric acid (pH 4.6, 3.6 and 2.6), acetic acid (pH 3.6) or lactic acid (pH 4.6) held at 4°C or 22°C.

Water Activity

Oocysts survive on wet stainless steel (93.1% viable after 30 minutes).

Inactivation

Temperature

Oocysts become non-infective when:

Pasteurised (71.7°C, 15 seconds)

Held in water at 64.2°C for 2 minutes

Frozen in de-ionised water (-20°C for 24 hours and -70°C for 1 hour)

Frozen in liquid nitrogen (-196°C)

Frozen in ice-cream (-20°C for 24 hours)

pH

pH <4 or >11 results in minor viability loss. Ammonia can enhance inactivation at low and high pH values. Fruit juice organic acids inhibit oocyst infectivity.

Water Activity

Oocysts are sensitive to air drying (e.g. at ambient temperatures). Viability on stainless steel after 10 minutes = 81%, 1 hour = 69%, 2 hours = 45%, 4 hours = 5%. At aw 0.85, 99.9% are non-infective after 24 hours at 28°C, or 1 week at 7°C. At aw 0.95, 99.99% are non-infective after 1 week at 28°C, or 2 weeks at 7°C.

Radiation

Sensitive to UV from sunlight and UV lamps. Under strong sunlight for 8 and 12 hours, oocyst viability reduced from 98% to 11.7% and 0.3%, respectively. A synergistic effect occurs at temperatures greater than 45°C.

Disinfectants / Sanitisers

Oocysts are resistant to chlorine and monochloramine. Swimming pool transmission has been problematic for this reason.Few disinfectants tested were effective with short exposure. These were:

Ammonia 5% for 120 minutes or 50% for 30 minutes

Formalin 10% for 120 minutes

Hydrogen peroxide 10 vol; 3% for 30 minutes

Ozone (25°C, 1ppm) renders oocysts non-infective after 3 minutes (90% decrease), 5 minutes (99%) and 10 minutes (99.9%).

Clinical

Incubation: Time from ingestion to illness usually 3-5 days, up to 2 weeks.

Symptoms: Copious watery non-bloody diarrhoea, vomiting, anorexia, fever, malaise, abdominal cramping and weight loss.

Usually self-limiting. Symptoms typically last 2-4 days but can last up to two weeks. Infectious oocysts usually excreted for 6-9 days, but can be excreted by asymptomatic carriers for up to 2 months or longer following infection. The respiratory system may also be adversely affected by the illness.

Condition: Cryptosporidiosis.

Dose: Healthy human volunteer studies have shown that the infectious dose varies depending on the isolate used. The dose needed to infect 50% of the population ranged from 9-1042 oocysts (Chappell et al., 2006; Okhuysen et al., 1999).

At Risk Groups: Children aged under 1 year and immunocompromised people are more susceptible (Carey et al., 2004).

Long Term Effects: Immunocompromised patients (e.g. AIDS patients or those receiving immunosuppressant drugs) develop severe symptoms that can last months or years and the condition can be fatal. The infection may also spread to other parts of the body in immunocompromised patients, such as the respiratory tract.

Treatment: There is no specific treatment for cryptosporidiosis currently available, but some antibiotics (e.g. spiramycin) are effective.

Reservoirs / Sources

Human: Person-to-person transmission occurs with C. parvum and C. hominis. More than 108-1010 oocysts can be excreted daily in the faeces of infected hosts.

Animal: C. parvum has been identified in 155 species of mammal including domestic animals. Pre-weaned ruminants, especially calves, are especially vulnerable to infection. Shedding of oocysts increases in calves to a peak at day 12 (excreting approximately 4×1010 oocysts). Flies are potential vehicles of transmission as oocysts can pass unaltered though their gastro-intestinal tract and be deposited in fly faeces, but flies have never been linked to an outbreak.

Around 80% of oocysts remain in an infected host’s gut and can autoinfect the host. The remaining 20% develop thick (trilaminar) cell walls and are released in the faeces of the infected host into the environment. This can lead to subsequent infection of a new host.

Food: Oocysts have been detected in raw milk, raw meat, raw fruits and vegetables. Foods suspected as acting as vehicles of disease include raw milk, green onions, apple cider, sausage, fruit/vegetables and frozen tripe.

Environment: Oocysts in the environment are particularly resilient, especially under cool, moist conditions. Infectivity can be retained for months, especially in low water temperatures (<5°C but above freezing) (Fayer, 2004). The long term viability of oocysts in animal faeces is unclear. A study of a variety of slurries, soil types, pH ranges and temperatures found that acid to neutral soils at 4°C were most conducive to oocyst survival (still viable after 162 days).

Transmission Routes: Three main routes of transmission are person-to-person, zoonotic, and via faecally-contaminated water or food.

Enteric Viruses (non-Hep A / Noro)

Enteric viruses other than hepatitis A virus and Norwalk-like viruses have occasionally been implicated in foodborne disease. These include rotaviruses, astroviruses, hepatitis E virus, picornaviruses, adenoviruses and parvoviruses.

Most of the enteric viruses contain RNA rather than DNA, the exceptions being adenoviruses and parvoviruses. Foodborne enteric viruses are inert particles which do not replicate in food. They require human cells to multiply. Enteric viruses can pass through the gastrointestinal tract and are resistant to environmental stresses, including heat and acid. Most enteric viruses are stable at pH 3.0 (so are not inactivated by stomach acid) and in the presence of lipid solvents. They resist freezing and drying. All foodborne viruses are transmitted by the faecal-oral route and are human–specific (although animal strains of the same virus may also exist).

Rotaviruses

Rotaviruses are the major cause of childhood gastroenteritis world-wide. In developing countries, deaths are common among children < 5 years. Although the disease occurs in all age groups, it is mild and usually asymptomatic in adults.

Infection is generally not recognised as foodborne but outbreaks associated with food and water have been reported in a number of countries. Many rotaviruses can be grown in cell culture. Rotaviruses infect both humans and animals; some human strains are closely related to animal strains.

Infectious dose: < 100 virus particles.

Survival: Human rotavirus can survive for several weeks in river water at 20ºC and at 4ºC.

Inactivation: Heating at 50ºC for 30 min reduces infectivity by 99%, and infectivity is rapidly lost at pH levels < 3.0 and > 10.0. Normal cooking temperatures should be sufficient to inactivate rotaviruses.

Sources of infection: contaminated water, care-givers, food handlers, general adult population.

Astroviruses

Astroviruses infect animals and humans and cause gastroenteritis. Some strains replicate in cell culture. Generally associated with infection in young children <1 year although they may also cause a mild infection in adults. Epidemiological evidence of transmission by foods is limited, but infections via contaminated shellfish and water have been reported.

Infectious dose: < 100 virus particles.

Survival: Astroviruses survive heating for 30 min at 50ºC.

Hepatitis E Virus

Hepatitis E virus belongs to the calicivirus group and is non-culturable. It occurs widely in Asia, Africa and Latin America, where waterborne outbreaks are common. It has rarely been identified elsewhere.

The virus infects the liver and symptoms of hepatitis are produced following a 22-60 day incubation period. The disease is self-limiting and does not progress to a carrier or chronic state. Transmission is generally via faecally–contaminated water and evidence for foodborne transmission has not been documented.

Picornaviruses

This group includes poliovirus, Coxsackie B viruses and ECHO viruses, many of which are culturable. They do not cause gastroenteritis but are transmitted by the faecal-oral route and excreted in faeces. Polioviruses were the first to be recognised as foodborne. Wild strains are now rare and NZ is a registered WHO polio-free zone.

Outbreaks of foodborne illness associated with Coxsackie virus and ECHOvirus have been reported.

Adenoviruses

Of the many types of adenovirus, only two types, 40 and 41, are generally associated with faecal–oral spread and gastroenteritis (especially in children). Most infections are subclinical or mild. The enteric adenoviruses, types 40 and 41, are difficult to grow in cell culture, whereas most other non-faecal types can be cultured.

Transmission is generally via faecally–contaminated water and evidence for foodborne transmission has not been documented.

Parvoviruses

The role of parvoviruses in human gastroenteritis is uncertain, although clearly documented in many animal species. There is limited evidence of parvovirus association with foodborne disease but it has been linked with consumption of contaminated shellfish.

Parvovirus was identified in all stools examined from a large UK gastroenteritis outbreak of >800 cases. This outbreak was attributed to consumption of contaminated cockles. BUT ASSOCIATION IS NOT CORRELATION. Parvo is largely something that infects Domestic Fluffy Vermin so being seropositive means fuck all – but it might be like toxo in cats making you crash your car. Who knows what our Microbial Overlords are up to?#

Escherichia coli
VTEC STRAINS: HAZARD GROUP 3 | STRAIN O157 NOTIFIABLE TO LA

E. coli: Many strains, mostly harmless. The pathogenic strains can be very nasty and potentially fatal. E. coli was behind the S Wales outbreak that resulted in the Pennington Report and wholesale changes to food hygiene law so here we’re talking strains like O157 and the other non-O157 Shiga Toxin-Producing STEC jobs.

The FSA 2011 Guidance post-Pennington was all over this and the latest iteration of that guidance is due out soon. These organisms form a diverse group of Escherichia coli that are capable of producing shigatoxin(s), as is E. coli O157:H7. However, they are of widely differing pathogenic potential, varying from those that can cause disease similar to that produced by E. coli O157:H7 to those that have never been associated with disease.

There are many strains of E. coli and almost all are completely harmless. It is one of the most common of the gut flora, but some strains can cause nausea, diarrhoea (often bloody), severe abdominal cramps and can lead to haemolytic uraemic syndrome (HUS) and death. 5 – 10% mortality in children under 5 years of age.

Between 10 and 100 organisms of E. coli O157 are sufficient to cause infection compared to over 1,000,000 required for other pathogenic E. coli strains.

By definition all STEC must produce one of two toxins (denoted Stx1 and Stx2), but other factors are also involved in pathogenicity and it is the possession of these that seems to determine the virulence of any one serotype. Other factors known to be involved include the ability to adhere to intestinal cells, and the ability to produce a haemolysin. An isolate possessing the ability to produce either Stx in the absence of other virulence determinants is unlikely to be a major pathogen. Individual members are denoted by their O and H serotypes.

Growth and Control

Growth

The behaviour of these organisms is largely the same as for serotype O157:H7. Only basic information is given below as data on specific characteristics of individual serotypes are lacking. Refer to the E. coli O157:H7 RectoBugWiki tab for more detail.

Temperature: Optimum 37°C, minimum 7-8, maximum 46°C. Doubling time approx. 0.4h at 37°C.

pH: Optimum 6-7, range 4.4 to 9.0 or 10.0. The limit at the low pH end depends on the acidulant used. Mineral acids such as HCl are less inhibitory than organic acids (e.g. acetic, lactic) at the same pH. Growth was inhibited in the presence of 0.1% acetic acid (pH 5.1).

Atmosphere: Can grow in the presence or absence of oxygen. E. coli can grow at 8 and 9°C on beef under vacuum-packaged conditions, but not under 100% CO2.

Water Activity: Optimum growth is at aw =0.995 minimum aw = 0.950 (about 8% NaCl).

Survival

Temperature: Survives well in chilled and frozen foods.

pH: Dies at pH values outside the range allowing growth. However, when exposed to low pH at low temperature, cells may survive for some time.

Inactivation (CCPs and Hurdles)

Temperature: Rapidly inactivated by heating at 71°C. D time at 54.4°C = 40 min D time at 60°C = 0.5–0.75 min D time at 64.3°C = 0.16 min Freeze thawing can lead to a reduction in numbers but the effect is strain dependent. D times may increase if the organism is heat shocked prior to heat treatment.

pH: Inactivated at pH values outside the range allowing growth at rates dependent on the conditions encountered. Inactivation is generally more rapid at warmer temperatures at low pH.

Clinical

For information on Haemorrhagic Colitis (HC), Haemolytic Uraemic Syndrome (HUS) and thrombocytopaenic purpura (TTP) see the E. coli O157:H7 page.

Treatment: Dialysis, maintenance of fluid balance and treatment of hypertension in cases of HUS.

Reservoirs / Sources

Human: Some serotypes appear to be restricted to man, e.g. O1, O55:H7 and H:10 and O148:H21.

Animal: Ruminant animals, notably bovines, seem to be a natural reservoir of many of the non-O157 STEC that cause disease in humans. Food, environment, transmission routes: Little is known about the distribution of these organisms in food and the environment. However, it seems likely that the situation will be similar to that for serotype O157:H7. Non-O157 STEC are likely to be much more common than serotype O157:H7 in foods, but only a small proportion of the isolates appear to be pathogenic to humans.

Non-O157 STEC has been detected in beef, pork and lamb mince, and unpasteurised milk. It has been estimated that 85% of cases are foodborne.

Plague and Pestilence

Pennington.

Foodborne Pathogens

All About Bugs and Food

Our Microbial Overlords are wonderful and some are even tasty. But they can bugger up your food business in a heartbeat. The Foodborne FAQs concentrate on bugs relevant to food so you can get them before the bastards get you. There are also other dubious resources – from food alerts to guidance on legislation – all listed under the ‘Food’ tag.

Disclaimer: I’m a microbiologist, not a clinician. These resources mention stuff bugs can do to you or your customers but for medical advice consult a bloody doctor, not the Internet. Especially not this site.

Chances are I don’t know what I’m talking about anyway and if you have any of the symptoms described here stop twatting about on the Interwebs and see a medic. Refer to the full legal nonsense here, don’t run with scissors, stick your tongue into plug sockets, attempt surgery on yourself etc etc.

Remember more can impact the survival of bugs in food than the variables listed here so the this is a guide only. If you work in food it’s your responsibility to ensure your food is safe, not mine.

Using the Rectofossal Resources

The RectoBugWiki is a resource primarily aimed at people working in food and so has a lot of geeky, technical stuff. If you want a general rant about any particular organism please contact me and I’ll happily write one; our Microbial Overlords are relentlessly fascinating so there’s plenty to write about.

Various bugs associated with (principally) foodborne illness are listed here; the conditions they like (pH, temperature etc) and how to piss them off (with heat, chemicals etc). I also list those that are notifiable to Local Authority Proper Officers in the UK.

Because this is intended to be a resource for people working in food the entries also talk about things like…

Water Activity (aw)

Water Activity is (basically) the energy state of water in a system. Microbial growth is dependent on Water Activity, not water content and higher aw substances tend to get more bugs growing on them.

Bacteria usually require at least 0.9 and fungi at least 0.7. It’s useful in food safety as a critical control point both for HACCP programs and in food design because water migrates from areas of high aw to areas of low aw so if honey (aw ≈ 0.6) is exposed to humid air (aw ≈ 0.7), the honey will absorb water from the air.

If smoked salmon (aw ≈ 0.965) is exposed to dry air (aw ≈ 0.5), it will dry out. Especially at weddings.

This is important when designing foods for a long shelf life – mixing ingredients with markedly different aw is usually avoided. You can find lost of aw values here.

D-Values

This relates to how good something is at killing bugs. It is the time taken to kill 90% of a given bug by a certain means, so if a population is reduced by 1 D, 10% of the original organisms remain, 2D 1% remain, 3D 0.1% remain. It’s a log scale for those of you with a mathematical bent.

Different organisms have different D-values at different temperatures so you might see D80C = 45s – or that organism is reduced by 90% after exposure to temperatures of 80°C for 45 seconds.

Notifiable to Local Authority

Some diseases are notifiable (to Local Authority Proper Officers – EHOs) under the Health Protection (Notification) Regulations 2010 due to the danger they present to public health.

Note that various syndromes are also notifiable as well as organisms – for example, E. coli O157 is notifiable in its own right but Salmonella isn’t – but ‘food poisoning’ is, as is infectious bloody diarrhoea. (Incidentally, bloody diarrhoea is never a good look – always see a doctor).

The full list is:

Acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS – from some E. coli), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox.

Hazard Groups

Organisms are classified by the WHO and HSE into four Hazard Groups. Some foodborne bugs are in Group 2, in Group 3 we have Salmonella typhi, SARS, VTEC E. coli, Hep B, C and D (the bloodborne ones) and Hep E (turd-to-tongue route and in 10% of sausages).

Group 4 is principally stuff like viral haemorrhagic fevers where you bleed to death via every orfice you can think of as well as a few you can’t. Don’t start any long books.

  • Hazard Group 1: Unlikely to cause human disease.
  • Hazard Group 2: Can cause human disease and may be a hazard to employees; it is unlikely to spread to the community and there is usually effective prophylaxis or treatment available.
  • Hazard Group 3: Can cause severe human disease and may be a serious hazard to employees; it may spread to the community, but there is usually effective prophylaxis or treatment available.
  • Hazard Group 4: Causes severe human disease and is a serious hazard to employees; it is likely to spread to the community and there is usually no effective prophylaxis or treatment available.
Giardia

Giardia intestinalis (formerly G. lamblia) is a protozoan parasite that produces gastrointestinal symptoms when ingested by humans. The organism is most likely to be present in the food as a cyst, the protozoan resting stage equivalent to a bacterial spore. In the older literature this organism is referred to as Giardia lamblia.

Growth and Control

Growth: The organism does not grow outside of the animal reservoir so controls designed to restrict the growth of bacteria will be ineffective. There is very little information on the survival of the organism on foods or on how cysts present on foods may be destroyed.

Survival: In general the cysts are stable and can last for long periods (months) in the environment. Cool moist conditions favour survival.

Cysts have been shown to survive on herbs for 8 days.

Temperature: Cyst survival in water is better at lower temperatures. Survival was 77 days in distilled water at 8°C, but only 4 days at 37°C. 0.1-25% survived in river water for up to 56 days.

Inactivation (CCPs and Hurdles): Temperature: Heating cysts to 60-70°C for 10 min inactivates them. Alternatively heating to boiling for 3 min will achieve the same result. Milk pasteurisation is sufficient to inactivate cysts. Cysts may be inactivated when frozen in water for long periods.

Sanitisers / Disinfectants:

Relatively resistant to ozone requiring 0.17 mg-min/l at 25°C or 0.53 mg-min/l at 5°C to reduce viability by 99%. Chlorination at levels required to inactivate E. coli is not sufficient to inactivate Giardia cysts. The protozoan requires <15 mg-min/l at 25°C and 90-170 mg-min/l at 5°C for inactivation.

Ct values: chlorine 93 to 121, chloramine 1,470, chlorine dioxide 17, ozone 1.3.

Physical removal, e.g. passing through an 8 μm pore size filter, will remove cysts from water.

Commercial phenol-based disinfectants are effective at inactivating the organism.

Radiation: Cysts are resistant to UV radiation. Doses of 42,000 to 63,000 μW-s/cm2 resulted in only a 90% loss of viability. Ct for UV 80 mJ cm-2.

Clinical

Incubation: One to 3 weeks after infection.

Symptoms: Immunocompetent people who are infected may be asymptomatic or experience gastrointestinal disease. In the immunocompromised the results may be more serious (severe diarrhoea, dehydration and loss of weight), and occasionally life threatening. Malabsorption may be quite severe in diarrhoeal cases.

Symptoms may last from 4 to 6 weeks, and consist of diarrhoea followed by flatulence, foul-smelling stools and cramps. The mean attack rate is 44%.

Condition: Giardiasis.

Toxins: Toxins are not formed in food by this organism.

At Risk Groups: Any one may become infected, but the disease is more serious in those who are immunocompromised. Infants and children are more susceptible to infection than adults.

Long Term Effects: Can be fatal in those unable to fight the disease. Lactose intolerance can be induced in 40% of cases for some time after symptoms have ceased.

Dose: As few as 10 cysts can cause an infection when ingested.

Treatment: Most cases are self-limiting, but chemotherapy can be used.

Reservoirs / Sources

Human: Asymptomatic carriers may excrete the organism for years. The asymptomatic carriage rate has been estimated at 3-20% in the USA.

Animal: The organism is found in mammals, birds, reptiles and amphibians. However isolates from these sources are not necessarily pathogenic to humans.

Food: Agricultural products that have directly or indirectly been subjected to faecal contamination may be a source of cysts. Giardia has been isolated from root crops, lettuces, herbs and strawberries irrigated with wastewater.

Environment: Cysts are found in waters which have been faecally polluted.

Transmission Routes: Transmission to humans may be via water, food contaminated by water or a food handler, or person-to-person.

Plague and Pestilence

Outbreaks: Few well documented outbreaks have been reported, and this may be due to the long incubation period.

Hepatitis A
Hazard Group 2 | Notifiable to Local Authority if acute

Hep A and Hep E are foodborne: A via the faeco-oral (‘turd to tongue’) route, E from swine flesh (mmm!) too – 10% of sausages contaminated…

Hepatitis A virus (HAV) causes hepatitis A, a severe food and waterborne disease that is primarily transmitted by the faecal/oral route. It is the only notifiable foodborne viral disease. It is a single-stranded RNA virus belonging to the Picornaviridae family and now classified in a distinct genus, Hepatovirus. HAV has a single serotype. Seven genotypes, four of which are found in humans, have been identified. These genotypes can be useful for tracing outbreak sources.

Growth and Control

Growth: Hepatitis A virus is culturable in primate cell lines but wild type strains are difficult to culture and generally do not produce cell changes so are not easy to identify by culture alone. It will not grow in food or water.

Survival: HAV is very stable, shows high resistance to chemical and physical agents such as heat, acid and solvents and has been shown to survive in the environment for over 3 months.

Inactivation

Temperature: HAV integrity and infectivity were retained after 60 min incubation at 60°C and the virus was only partially inactivated after 10-12 hours at 56°C. Infectivity was retained after 10 min at 80°C in 1M MgCl2 but for only 5 min in phosphate buffered saline. HAV heat resistance is reported to be greater in foods and shellfish.

HAV inoculated into oysters was not fully inactivated after heating in a can for 19 min at 60°C.

MAFF recommend a heat treatment of 1.5 min at 90oC to inactivate HAV in cockles.

Under refrigeration and freezing conditions the virus remains intact and infectious for several years.

pH: Stable at acid pH. At pH 1.0 and 25°C, HAV retained high infectivity after 2 hours and was still infectious after 5 hours.

Drying: Infectious for >1 month at 25°C and 42% humidity. Greater resistance to inactivation at low humidity and temperatures.

Sanitisers/Disinfectants: Infectivity is decreased by exposure to 70% alcohol. Resistant to chloroform, Freon, Arklone and 20% ether. Not inactivated by 300mg/l perchloroacetic acid or 1g/l chloramine at 20°C for 15min.

HAV is inactivated by chlorine: 99.99% reduction in 6.5 min at pH6 and 49.6 min at pH10 (estimated Ct values under conditions described are 1.8 and 12.3 respectively.

Hypochlorite: 3-10mg/l at 20°C for 5 to15min.

Iodine: 3 mg/l for 5 min at 20°C

Formalin: 1:4000 for 72 hours at 37°C or 3% for 5 min at 25°C.

Radiation: Inactivated by UV irradiation after 1 min exposure to 1.1W or 197μW/cm2 for 4 min. Gamma irradiation has not been found to be effective for inactivation of HAV on fresh fruits and vegetables.

Clinical

Incubation: 2-6 weeks, average 28 days.

Symptons: Initially non-specific symptoms – fever, headache, fatigue, anorexia, nausea and vomiting, then viraemia, jaundice and hepatitis symptoms appear 1-2 weeks later. Virus is present in the blood at weeks 2- 4, and is shed in faeces (>106 particles/g) from the latter 2 weeks of the incubation period for up to 5 weeks. Jaundice is usually evident from weeks 4 to 7, and virus shedding generally continues throughout this period. Overall debility lasting several weeks is common and relapses may occur. Acute hepatitis is usually self-limiting but can occasionally cause fulminant disease that results in death.

Estimated hospitalisation rate is 13%.

Condition: HAV infects hepatocytes, causes elevation of liver enzymes and inflammation of the liver. The cytotoxic T cell immune response destroys infected liver cells. Virus particles are released into the bile duct and excreted in faeces. The virus is believed to initially enter the liver via the bloodstream and it is not clear if intestinal replication occurs. The gastrointestinal tract is not a required route for infection.

Toxins: None produced in foods.

At Risk Groups: All age-groups. The disease is milder in young children under 6 years than older children and adults. Case-fatality risk increases with age so risks are higher for unexposed older people.

Long Term Effects: Overall case fatality rates in the US are 0.3% (0.003 per 100,000) and range between 0.004% for 5-14 years to 2.7% in people > 49 years. HAV has not been associated with chronic liver disease.

Treatment: Rest and an appropriate low-fat diet. Post-exposure prophylaxis may be recommended for certain groups such as day-care centre staff, military and food industry staff. Prevention is possible via HAV vaccination for at-risk groups including overseas travellers and for food handlers when situations warrant it.

Reservoirs / Sources

Human: Human faeces are the major reservoir. Eat poop, get Hep A.

Animal: HAV infects primates including chimps and some species of monkeys. Non-primates are also infected but disease is milder. Transmission via these hosts is unlikely.

Food: Contaminated bivalve shellfish, salads, fresh fruits and vegetables, water, and any manually prepared food products. HAV survived in crème-filled cookies for >1 day at 21ºC. Poor hygiene practices and poor sanitation are major risk factors. Presymptomatic foodhandlers excreting HAV pose a risk. Food is rarely available for analysis because of the long incubation period.

Environment: Survival of HAV in the environment (fresh and seawater, wastewater, marine sediments, soils and shellfish), is prolonged (>12 weeks) at 25°C. Excreta from infected humans may contaminate soil or water. Human faecal pollution from sewage discharges, septic tank leachates and boat discharges has caused contamination of shellfish beds, recreational water, irrigation water and drinking water.

Transmission Routes: The faecal/oral route is the established route of transmission and infection occurs following ingestion of faecally-contaminated food and water. Viral contamination of fresh fruits and salad vegetables through the global marketplace is becoming a significant route of exposure, especially in countries with low levels of hepatitis A.

Person to person transmission is also important especially among young children in overcrowded living conditions, day-care centres or institutions. Parenteral transmission occurs in the drug-using population and via contaminated blood products.

Plague and Pestilence

Outbreaks: Most cases of disease are outbreak related. Large outbreaks have been reported in developed countries where there is little immunity. Secondary transmission may account for 20% of cases in an outbreak.

Listeria
Hazard Group 2

Listeria can grow at fridge temperatures. And it’s nasty. A cause of serious food poisoning causing flu-like symptoms, fever, diarrhoea and a risk of miscarriage in pregnant women. It is fatal in 20% of cases. Listeria is particularly dangerous as it can multiply at fridge temperatures, albeit slowly.While disease caused by this organism is uncommon, the clinical consequences are often serious. Two forms of disease are now recognised; a serious invasive disease and a non-invasive gastroenteritis. It grows at refrigeration temperatures in the presence or absence of air.

Growth and Control

Growth

Temperature: Optimum 37°C, range -1.5 to 45 °C.

pH: Optimum 7.0, range 4.4-9.4.

Atmosphere: Grows optimally under microaerophilic conditions but grows well both aerobically and anaerobically. Can grow in relatively high (e.g. 30%) CO2, but is inhibited under 100% CO2. Growth was not retarded by a 5-10% CO2 atmosphere.

Water Activity: Minimum aw permitting growth = 0.92 (≡11.5 % NaCl). Will grow in media containing up to 10% NaCl.

Survival

Temperature: Survives freezing very well.

Atmosphere: Not influenced by atmosphere.

Inactivation (CCPs and Hurdles)

Temperature: Rapidly inactivated at temperatures above 70°C. D time at 50°C can be in the order of hours, at 60°C 5-10 min, 70°C approximately 10 sec.

pH: Inactivated at pH values less than 4.4 at rates depending on the acidulant and temperature. Organic acids, such as acetic, are more effective than mineral acids (e.g. hydrochloric). Inactivation proceeds faster at higher temperatures.

Water Activity: Can remain viable in dry environments for long periods.

Preservatives: Inactivated on vegetables by lysozyme (100 mg/kg), 0.2% sodium benzoate at pH 5, 0.25- 0.3% sodium propionate (pH 5, less effective at lower temperatures), and 0.2-0.3% potassium sorbate (pH 5.0).

The addition of nitrite to salami-type meat batter minimally affected survival of the organism at 37°C (pH was the primary factor). The use of appropriate starter cultures results in the elimination of the organism from salami.

In other meats at around pH 6-6.3, nitrite (70-140ppm) did retard growth, and sodium ascorbate (0.042%) in combination with the nitrite retarded growth further. Ascorbate had no effect in the absence of nitrite.

Lactate and ALTA 2341 (shelf life extender) lengthened lag times in poultry but effectiveness decreased as temperature increased. Inhibited by 100 ppm monolaurin or 1000 ppm eugenol.

Sanitisers/Disinfectants:

See here for guidance.

Gaseous acetic acid did not disinfect all samples of inoculated mung beans.

Sanitisers/disinfectants (aldehydes, alcohols, ethanol/phenols, substituted phenols, disochlorine, quaternary ammonium compounds (QACs)) are generally effective in the absence of organic matter.

Clinical

There are two types of disease associated with the organism; invasive and non-invasive. The invasive disease normally occurs in people with weakened immune systems, while the non-invasive disease can occur in anyone if a high number of L. monocytogenes cells is consumed.

Incubation: Invasive: 1-90 days, mean 30 days. Non invasive: 11 hours to 7 days, median 18 hours.

Symptoms: Invasive: Include flu’-like symptoms (e.g. fever, headache), diarrhoea, vomiting, meningitis, septicaemia, spontaneous abortion. Non-invasive: Diarrhoea, fever, muscle pain, headache, and less frequently with abdominal cramps and vomiting. Attack rate reported to be 74%.

Condition: Invasive: Listeriosis. A mortality rate of approximately 30% is associated with the disease. Hospitalisation rate: 92%. Non-invasive: Has been termed non-invasive febrile gastroenteritis.

Toxins: No toxins are produced in foods.

At Risk Groups: Invasive: Those at risk include pregnant women and their foetuses, new born children, the elderly and those with compromised immune systems, e.g. AIDS patients. Non-invasive: Will affect anyone consuming high numbers of cells.

Long Term Effects: In one outbreak neurological problems (cranial nerve palsies) developed in 30% of the survivors of meningitis. Pre-term infants may suffer from excess fluid in the brain, requiring surgery, and partial paralysis.

Dose: Invasive: The estimate of the number of cells that need to be ingested to cause disease is open to debate. A general consensus seems to be that 100- 1,000 cells are normally required. Non-invasive: Outbreaks have been attributed to foods containing >105 cells/g, and in one case the median consumption of cells was estimated to be 1011.

Treatment: L. monocytogenes is susceptible to a number of antibiotics, but penicillin and ampicillin optionally with an aminoglycoside (e.g. gentamicin) is considered to be the combination of choice.

Reservoirs / Sources

Human: L. monocytogenes is carried asymptomatically in the faeces of 2-6% of the population. Person-to-person spread (other than mother to foetus) not often recorded but has been recognised. Up to 30% of case contacts may carry the organism. Is shed in high numbers (≥ 104/g) in the faeces of infected people.

Animal: Can cause disease in animals, and veterinarians were originally considered to be the at risk group. Listeria present in animal faeces can contaminate red meat. Improperly made silage can be a source of domestic animal infection.

Food: Should be considered as potentially present in all raw foods and ingredients. May be present in cooked foods as a result of post-cooking contamination. Risk posed is likely to be greatest in ready-to-eat cooked foods with long shelf lives. Has been isolated from a wide variety of ready-to-eat and raw foods but is generally considered to be usually present in low numbers (<10/g) on foods, although it has been detected at numbers far in excess of this.

Environment: Is widespread in the environment including soil, vegetation, water and sewage. Has been isolated from toothbrushes and other domestic environments.

Transmission Routes: One study estimates that 1/3 of cases are foodborne. Other reports describe foodborne transmission as the primary source of human infections. Alternative routes include infections acquired in hospital and occupational exposure (e.g. vets).

Plague and Pestilence

Outbreaks: Most cases of invasive listeriosis are sporadic, but large outbreaks have occurred. Outbreaks feature prominently in the media because of the associated high case fatality rate.

Non-invasive listeriosis has been recognised because of the outbreaks of disease that have resulted from the ingestion of large numbers of the organism.

Epidemiological studies: Factors reported include consuming unpasteurised milk, uncooked hot dogs, undercooked chicken, soft cheeses and foods purchased from delicatessen counters.

Mycobacterium bovis

This is one of two species of the ‘tubercle bacilli’ (the other is M. tuberculosis) that are able to cause tuberculosis. Unlike M. tuberculosis, M. bovis infects cattle and other animals, and so the disease can be spread to humans via contaminated milk and meat. We gave TB to cows 40-50,000 years ago. From the same genus as leprosy – which diverged from it 40m years ago, Before there were humans to get it…

Growth and Control

Growth

It is a characteristic of the organism that it is very slow growing, and so given the shelf life of foods that it has been associated with, e.g. unpasteurised milk and raw meat, growth in foods is unlikely to be significant. The organism is a microaerophile.

Survival

Temperature: Survival is better under cool conditions, e.g. survived in cow faeces for 5 months in winter and 2 months in summer.

Water Activity: Survives dry conditions well.

Inactivation (CCPs and Hurdles):

Temperature

Inactivated by normal pasteurisation. An inoculum of 105 / ml cells became undetectable after 30 minutes at 63.5oC in whole milk (low temperature, long-time pasteurisation). In meat products the D time at 61°C was 1 min, while at 55°C it was approximately 10 min. Treatment at 65°C for 5 min gives a 5 D kill.

Sanitisers/Disinfectants

Ortho-phthalaldehyde applied at the minimum effective concentration resulted in a 6 log reduction in numbers in 5 minutes.

A study of 14 hospital disinfectants found chlorine dioxide, 0.8% hydrogen peroxide plus 0.06% peroxyacetic acid, glutaraldehydes (2% alkaline and 2% acidic, a phenolic and chlorine (approx. 1,000 ppm) and an iodophor were effective, some quaternary ammonium compounds and 0.13% glutaraldehyde plus 0.44% phenol plus 0.08% phenate were ineffective. On their own chlorhexidine diacetate and cetylpyridinium chloride are relatively ineffective, but their action may be improved in the presence of ethambutol.

Radiation: Inactivated by sunlight.

Clinical

Incubation: In airborne infections and in immunocompetent people the incubation period can be years, while in the immunosupressed it may be months. Cases of the gastrointestinal form can occur after reactivation of infections that must have occurred many years earlier.

Symptoms: Fever, chills, weight loss, abdominal pain, diarrhoea or constipation. Other symptoms depend on the organs infected. Symptoms may last for months or years. The organism enters the body via the intestinal tract in foodborne infections, and primary infection is set up in the associated lymph nodes to form ‘tubercles’. The infection is often contained at that point, but it can also spread to other parts of the body to cause illness. The reverse can be true in that pulmonary disease can spread to the intestinal region.

Condition: Intestinal tuberculosis or tuberculous enteritis.

Toxins: Does not produce toxins.

At Risk Groups: Immunosupressed people are especially at risk of either acute infection or reactivation of an infection acquired in the past. In countries where infection is uncontrolled children are at greater risk of infection.

Long Term Effects: The course of the disease is long term and may result in death.

Dose: The infectious dose for organisms ingested (as opposed to inhaled) is probably very high (millions of organisms).

Treatment: Multiple antibiotic treatment is required to be administered over protracted periods. This is because the organism may have antibiotic resistance and this will not be apparent for long periods because of the slow growth of the organism. The antibiotics currently used are rifampicin, isoniazid and ethambutol. Infected lymph nodes can be removed.

Multiple drug resistant forms have caused outbreaks among AIDS patients that resulted in deaths of all those infected.

Reservoirs / Sources

Human: Humans are a reservoir of the organism, but human to human infection occurs only rarely.

Animal: Cattle and other animals are the main reservoirs of the organism.

Food: Meat and milk derived from infected animals may contain the organism. Tubercles are detectable post-mortem in food animals, and infection can also be detected using an immunological test.

Environment: Can persist and remain infective in the environment for long periods.

Transmission Routes: Can be by respiratory aerosols between humans and animals. To a lesser extent also transmitted by milk and meat derived from infected animals. Apparently not transmitted by the waterborne route.

Plague and Pestilence

Outbreaks: No recent reports of foodborne outbreaks of M. bovis infection that I can find. The last outbreak attributed to contaminated milk occurred in the UK in 1959.

Epidemiological Data: A study in Ireland on disease caused by M. bovis between 1983 and 1992 found that most cases could be attributed to the prior consumption of milk in the pre-pasteurisation era.

Norovirus
Hazard Group 2

Human noroviruses (NoV) are now the most common cause of outbreaks of epidemic non-bacterial gastroenteritis world-wide.

Highly infectious, nightmare to control, 100 billion virus particles per gram of faeces.

Previously known as Norwalk-like viruses (NLVs) and small round structured viruses (SRSVs), these viruses belong to the Caliciviridae family and are 26-35 nm non-enveloped single stranded positive-strand RNA viruses. That’s really, really small.

Each virus is ~30nm wide. Visible light has wavelengths between 300-700nm. Eeek!

The noroviruses are probably the single most infectious agents known. Their low infectious dose (1-10 virions), resistance to most chemical agents, prolific faecal shedding in those infected (100×109 per gram of stool) – which can continue for two months after symptoms have ceased – all militate towards making this a right little bastard to keep on top of. If it gets into a food business it’s a nightmare to get rid of it.

Noroviruses are divided into 5 genogroups, GI-V, of which GI, GII and GIV are known to infect humans. Over 25 different human genotypes are now recognised. Since 2002, genotype GII.4 strains have been the most common cause of outbreaks. Recombinant NoV strains have also been identified. Norwalk virus, GI.1, is the prototype strain. Norovirus identification has been difficult prior to development of molecular methods because human noroviruses cannot be cultured, and their wide genetic diversity limits the use of traditional immunology and serotyping assays.

Growth and Control

Growth

Human norovirus has not been grown in vitro and there is still no suitable animal model. This makes it difficult to study. The murine norovirus strain is readily culturable but not ideal. NoV detection is carried out using conventional or – better – real time RT-PCR. This is accurate but seriously expensive and is only likely to be used to investigate a serious outbreak. The illness is self limiting and the clinical diagnosis is accurate enough. There is an ELISA test but it’s pretty crap.

Survival

It’s reasonably stable on surfaces but not hugely so; a week is a reasonable assumption as you need a rare confluence of circumstances for it to last longer.

Inactivation

High-level oxidsers or 10,000ppm chlorine. Standard disinfectants ineffective.

Temperature

The virus retains infectivity after incubation at 60°C for 30 min pasteurisation is not sufficient to eliminate it and resistance is reported to be greater in foods and shellfish. Steaming of bivalve shellfish is unlikely to inactivate NoV – and any cooking process that will would render the shellfish pretty much inedible. 100°C for 5mins will do it.

Under refrigeration and freezing conditions the virus remains intact and viable for several years.

pH

Resists gastric acids at pH 3-4. The virus retained infectivity after exposure to pH 2.7 for 3 hr at room temperature. Believed to be sensitive to pH >9.0 (but unproven cos you can’t really test) so the pH in commercial dish wash detergents will render it inactive.

Water Activity

Based on data for other enteric viruses and virus indicators, it is likely that NoV persist in waters for extended periods (possibly weeks/months). NoV has caused many waterborne outbreaks and are often detected in environmental waters.

Drying

Infectious NoV has been detected on environmental surfaces, including carpets, for up to 12 days after NoV outbreaks.

Preservatives

Unknown but likely to be resistant.

Sanitisers/Disinfectants

Dose-response studies shows that NoV is resistant to inactivation following treatment with free residual chlorine of 0.5 to 1.0 mg/ml – the level of free chlorine consistent with that generally present in a drinking water supply.

Clinical Notes

Incubation: 10-50 hours (mean 24h) following ingestion of the virus.

Symptoms: Vomiting, often projectile, is generally the predominant symptom and is present in > 50% of cases. Stomach cramps, watery non-bloody diarrhoea, abdominal pain, low-grade fever and headache are other common symptoms. The duration of illness is usually between 24-60 hr. Diagnostic criteria are often used in the absence of virological confirmation.

Excretion of the virus in stools occurs from onset for up to 8 weeks following infection, with peak excretion rate at 4 days. Noroviruses are frequently discharged in vomit. The disease is generally mild and self-limiting. Hospitalisation is not generally required, but has been reported in some outbreaks. Attack rates are high, generally around 40-60% and sometimes as high as 80%.

Condition: Gastroenteritis. Norovirus colonise the proximal region of the small intestine and cause development of mucosal lesions with broadening and shortening of the microvilli. Short-term maladsorption of fats and some sugars has been reported. Abnormal gastric motor function is believed to be the cause of associated nausea and vomiting. The exact mechanism of pathogenesis remains unclear. Susceptibility or resistance to certain strains of HuNoV appears to be associated with human histo-blood group antigens (HBGA) Immunity is generally short lived, and is not sufficiently cross-reactive to protect against different norovirus strains.

Dose: Infective dose is estimated at 1-10 particles. Consumption of 1 virus particle may cause infection in 50% of occasions in susceptible people.

At Risk Groups: Affects all age groups, but the elderly and the immuno-compromised are particularly susceptible.

Long Term Effects: There is no evidence of any long-term sequelae following norovirus infection. Fatalities, which mostly occur in elderly patients, are rare in the developed world.

Treatment: Usually none, but fluids may be given to reduce the risk of dehydration.

Reservoirs / Sources

Human: The only known direct source for human NoV is human faeces or aerosolised vomit. Other indirect sources are shellfish, contaminated foods, water, fomites and the environment.

Animal: Bovine, feline, ovine and porcine noroviruses have been identified but there are no reports of cross-species transmission to humans as yet. Overseas, human GII NoV sequences have been identified in swine. Other caliciviruses have been found in various animal species.

Food: Contaminated bivalve shellfish, fresh produce (eg. herbs, lettuce, salads), water, ice and manually prepared ready-to-eat foods (including bakery items). Poor hygiene practices by food harvesters, processors and food handlers are a significant source.

Environment: Faeces from infected humans may contaminate soil or water. Faecal pollution from sewage discharges, septic tank leachates and boat discharges has caused contamination of shellfish beds, recreational water, irrigation water and drinking water. NoV are believed to survive for long periods in the environment and have been detected in shellfish 8-10 weeks after contamination.

Transmission Routes: The faecal/oral route is the established route of transmission. Infection occurs following ingestion of faecally-contaminated food and water. Another important route is person-to-person spread via aerosolised vomit following projectile vomiting. Direct transmission via contaminated surfaces, especially carpets, is also now considered a significant route; These routes contribute to the explosive outbreaks that cannot be attributed to faecal/oral spread alone. They generally occur in semi-closed communities such as rest homes, cruise ships and camps where there is close quarter living and often there may be reduced hygiene levels. There is evidence that asymptomatic food handlers can also cause infection and may excrete high numbers of NoV in their faeces.

Plague and Pestilence

Because of the relatively high attack rate, large numbers of people are often infected and most cases of disease are outbreak-related. Most foodborne outbreaks are ascribed to cross contamination via a food handler or inadequate cooking of previously contaminated foods. However, any food that becomes contaminated can act as a vehicle. Uncooked or lightly cooked bivalve shellfish such as oysters and mussels present a risk to health if grown in faecally contaminated waters.

Salmonella (non-typhoidal)
Hazard Group 2 | S. typhi is Hazard Group 3

This group of bacteria of is comprised of a large number of different serotypes of the species Salmonella enterica. However, in general, a few serotypes tend to dominate those identified as causing disease. These serotypes are normally denoted as a non-italicised specific name, e.g. Salmonella Enteritidis. Which drives microbial taxonomists nuts. You never capitalise the specific name, FFS.

So, there’s lots of Salmonella. These are bad enough, this one is really bad.

Serotypes are often associated with particular geographical areas.

Growth and Control

Growth

Temperature: Minimum 7°C, growth greatly reduced at <15°C. Maximum 49.5°C. Optimum 35-37°C. Some evidence for growth at 5.2°C exists, but this is serotype specific and the data are still not universally accepted.

Water Activity: Minimum 0.94, optimum 0.99, maximum >0.99.

pH: Minimum 3.8, optimum, 7-7.5, maximum 9.5. The minimum pH is influenced by other factors such as temperature, the acid present, and the presence of nitrite etc. For example at 10°C the minimum pH allowing growth was 4.4-4.8 (13 isolates tested), while at 30°C it was 3.8-4.0.

Atmosphere: Can grow in the presence or absence of air. Growth under nitrogen is only slightly less than that under air. Grows at 8-11°C in the presence of 20-50% CO2. Growth at low temperatures is retarded in the presence of 80% CO2 compared to air.

Survival: Salmonella is known to survive well in foods and on surfaces.

Temperature: Survival for >10 weeks in butter held at –23 and 25°C has been noted. Salmonellae can survive for 28 days on the surfaces of vegetables under refrigeration. In essence Salmonella can survive for long periods under refrigeration.

Water Activity: Survival in dry environments is a characteristic of these organisms. For example can survive in chocolate (aw 0.3-0.5) for months. Exposure to low aw environments can greatly increase the subsequent heat resistance of these organisms.

pH: Salmonella are less acid resistant at low pH than – for example – E. coli.

Inactivation (CCPs and Hurdles)

Death can occur during the freezing process, but those that survive remain viable during frozen storage. Freezing does not ensure the inactivation of salmonellae in foods.

D times

60°C usually 2-6 min. 70°C usually 1 min or less.

N.B. Extremely high D times have been reported for experiments with milk chocolate. Values reported were up to 1,050 min at 70°C, 222 min at 80°C and 78 min at 90°C. This also applies to other low water content foods. Some rare serotypes (e.g. S. senftenberg) are significantly more heat resistant than the others which are not particularly resistant to heat.

pH: Inactivation at sub-optimal pH depends on many factors including the type of acid present and the temperature. For example inactivation is more rapid in commercial mayonnaise at 20°C than it is at 4°C.

Water Activity: Decline in numbers is reduced at lower aw values.

Preservatives: Growth was inhibited in the presence of 0.1% acetic acid (pH 5.1).

Sanitisers/Disinfectants:  not resistant to disinfectants used in the food industry.

Radiation: D value around 0.5 kGy, up to 0.8. D times are higher in drier foods such as desiccated coconut.

Clinical Notes

Incubation: 6-48 hours (usually 12-36 hours).

Symptoms: Diarrhoea, abdominal pain, vomiting, nausea and fever lasting 1-7 days. Hospitalisation rate estimated at 22.1% cases fatality rate 0.8%.

Condition: Salmonellosis.

Toxins: Toxins are not produced in foods.

At Risk Groups: The young, old, and immunocompromised are particularly at risk. In addition people of less privileged socioeconomic groups and those living in higher population densities are more at risk.

Long Term Effects: Septicaemia and subsequent non-intestinal infections can occur. Reactive arthritis may occur 3-4 weeks after gastrointestinal symptoms.

Dose: The dose required to cause disease varies with many factors. Low attack rates have been observed in one outbreak where 4-45 cells were consumed, and another where the dose was 6 cells. Different serotypes will have different dose responses, and generally recognised doses to cause disease at high attack rates are in the range of 105 to 106 cells. Foods with high fat content, like chocolate or peanut butter may protect cells from gastric juices so permitting a lower dose than usual to cause infection.

Treatment: The infection is usually self-limiting although fluid replacement may be required. Antibiotic treatment seems to be either ineffective or results in relapse or prolonged faecal shedding. Certain groups, e.g. neonates, may benefit from antibiotic treatment.

Reservoirs / Sources

Human: Some serotypes are confined to humans (e.g. S. typhi and S. paratyphi B). Faeces of infected people contain large numbers of the organism and shedding may continue for up to 3 months. The median period for shedding is 5 weeks, <1% become chronic carriers.

Animal: Some serotypes are confined to particular animal reservoirs, but many are capable of crossing between species to cause disease in man, often via food. Most Salmonella infections in animals are asymptomatic. Poultry and pigs are regarded as major reservoirs of the organism. Animal feeds made from animal products may be contaminated by Salmonella. Salmonella can also be found in fish, terrapins, frogs and birds.

Food: Meat or other products derived from infected animals are important vehicles of salmonellosis. Other animal products, e.g. re-contaminated pasteurised or raw (unpasteurised) milk can act as vehicles. Which isn’t surprising as raw milk is – microbiologically speaking – fucking sewage.

Environment: Salmonella shed in faeces can contaminate pasture, soil and water. It can survive for months in the soil. Contamination in the environment can serve to act as a source of infection of other animals.

Transmission Routes: May be transmitted to humans via contaminated food or water, animal contact, or from a contaminated environment.

Plague and Pestilence

Foods identified by epidemiological studies as acting as outbreak vehicles include poultry meat and eggs (in the USA and UK), mung bean sprouts, paprika flavoured potato chips and salami sticks.

Salmonella typhi
S. typhi is Hazard Group 3 | Others are Hazard Group 2 | Not notifiable (but bloody diarrhoea is)

S. typhi is the causal organism of typhoid (or enteric) fever, representing a more serious form of Salmonella infection than the other salmonellae.

Growth and Control

The characteristics of this species are essentially those of other non-heat resistant Salmonella. Full details are given on the entry for non-typhoid salmonellae. This is the abridged version appears with S. typhi-specific data given where available.

Growth

Temperature: Minimum 7°C, growth greatly reduced at <15°C. Maximum 45°C. Optimum 35-37°C.

Water Activity: Minimum 0.94, optimum 0.99, maximum >0.99.

pH: Minimum 3.8, optimum, 7-7.5, maximum 9.5. The minimum pH is influenced by other factors such as the acid present, and the presence of nitrite etc.

Atmosphere: Can grow in the presence or absence of air. Growth under nitrogen is only slightly less than that under air. Grows at 8-11°C in the presence of 20-50% CO2.

Survival

Temperature: Survival can be quite good, for example the organism was viable for 190 days when inoculated onto chocolate biscuits, and for 230 days on sweets. S. typhi can survive for 4 days in shellfish stored at 10-13°C, and in ice for in excess of 90 days.

Viable but Non-Culturable (VNC) Cells: This organism is thought to undergo transition to the VNC state in water.

Inactivation (CCPs and Hurdles):

Water Activity: Inactivated within 1 day when exposed to 30% NaCl.

Sanitisers/Disinfectants

Treatment of S. Typhi contaminated bean sprouts with 200 mg/l sodium hypochlorite only reduced the count by 1.5 log cycles (i.e. ineffective).

Clinical

Incubation: 7-28 days (average 14)

Symptoms: Fever, malaise, anorexia, spots on trunk. These occur commonly with pea-like diarrhoea or constipation. Patients may become delirious. Recovery is slow, taking from 1 to 8 weeks. Hospitalisation rate estimated at 75%, case fatality rate 0.4%.

Condition: Typhoid, or enteric, fever.

Toxins: Toxins are not produced in foods.

At Risk Groups: In non-endemic areas children between 0-5 years are at the greatest risk.

Treatment: Quinolone and cephalosporin antibiotics may be used. Vaccines are available.

Reservoirs / Sources

Human: Humans are the sole reservoir of this organism. Carriers may harbour the organism in their gall bladders.

Animal: Does not infect animals.

Food: Foods may become contaminated from food handlers or via the use of contaminated water during processing. Shellfish grown in polluted waters may also accumulate the organism within their tissue.

Environment: Water that has been contaminated by human faecal pollution is a transmission route. Survival in seawater for up to 9 days, and in sewage for weeks have been recorded. Survival in groundwater was better than in pond, stream or lake water and this was attributed to less grazing pressure by protozoa.

Transmission Routes: Mainly from water or from human carriers.

Shigella

This genus includes four species; S. dysenteriae, S. flexneri, S. boydii and S. sonnei, which are able to cause bacillary dysentery. They are very similar to Escherichia coli and are serologically cross reactive but have remained separate species for clinical reasons.

Growth and Control

Growth

Very little is known about the growth and survival of the organism in food. S. sonnei is more robust than S. flexneri (data for S. sonnei given). It has been shown to be able to grow on foods (e.g. parsley).

Temperature: Minimum 6-7°C, maximum 45-47°C.

Will grow on sliced fruits at room temperature.

Water Activity: Maximum 5.2% NaCl.

pH: Minimum 4.8-5.0 in 3.8-5.2% NaCl, 5.5 in the presence of 300-700 mg/litre NaNO2. Maximum 9.3 in the presence of 5.2% NaCl.

Atmosphere: Able to grow in the absence of oxygen.

Survival

Temperature: In general they survive best at low temperatures (subzero and refrigeration). Can survive storage in butter for more than 100 days at –20°C and 4°C. Can survive storage on soil, cheesevand herbs for 50 days, in orange juice for 1-6 days and in white cheese, cheese curd and salad with mayonnaise from 19-32 days. Persisted for 11-20 days on salads, depending on salad type.

Survives heating to 63°C for 2-3 min.

Water Activity: In general they survive better in low moisture foods. Some strains can survive 15% NaCl for 1 day.

pH: Despite its relatively high minimum pH for growth, Shigella is among the most acid resistant of foodborne pathogens. Some strains can survive exposure to pH 2.5 or 3.0 for 2 hours, and for a few hours to a day in fruit juices of various pH values. Organic acids are more inhibitory than mineral acids.

Inactivation (CCPs and Hurdles)

Temperature: Rapidly inactivated at temperatures above 65°C.

pH: Are inactivated at pH values <4.0 (but can persist for some time, see above).

Water Activity: Numbers decline slowly (over days/weeks) at 6% NaCl. Two of 21 isolates survived for 4 days in 10% NaCl.

Preservatives: S. flexneri is inhibited by plastic containing 1,500 ppm of triclosan. At pH 5.5 450ppm nitrite was required to inhibit S. flexneri but 700ppm was required to inhibit S. sonnei.

Sanitisers/Disinfectants: QACs or chlorine. 90% inactivation was produced by sodium hypochlorite at a concentration 0.5-1.5 mg/litre free chlorine and at 4°C. A 6D reduction was achieved on inoculated parsley with 5.2% acetic acid or 200 ppm free chlorine after 5 minutes exposure at 21°C. Treatment with 7.6% acetic acid or 250 ppm chlorine increased the kill to >7D.

Radiation: Sensitive to γ radiation, a dose of 3 kGy results in a 7D kill. D values are of the order of 0.2-0.4 kGy.

Clinical

Incubation: 12 hours to 4 days. In outbreaks incubation times of up to 36 hours are observed.

Symptoms: Abdominal pain, diarrhoea, fatigue, malaise and fever. Mucus and occasionally blood appear in the faeces. The illness may progress to the colonic phase within 1-3 days where the symptoms are intense cramps as well as frequent and painful bowel movements. Lasts for 3 to 14 days. Estimated 13.9% hospitalisation rate, 0.16% case fatality rate.

Condition: Bacillary dysentery or shigellosis.

Toxins: Toxins are not produced in foods.

At Risk Groups: Some groups are more predisposed to infection: children under 6 in day care centres, people in nursing homes or prisons, men who have sex with men.

Long Term Effects: Septicaemia sometimes occurs in the immunocompromised host with an associated high fatality rate. May rarely cause haemolytic uraemic syndrome.

Dose: The dose required to cause disease is small at 10-100 cells.

Treatment: Antibiotic treatment is possible, but is not required in milder cases. Oral replacement of fluids may be required. Antibiotic resistance is common. No effective vaccine exists.

Reservoirs / Sources

Human: Humans and the higher primates are the reservoir for this organism. The organism can be found in the faeces for weeks after symptoms have ceased. It can survive in human faeces for days if the samples remain moist.

Animal: Not carried by animals other than primates.

Food: Foods can become contaminated by water or soiled hands.

Environment: Water that is contaminated by sewage may act as a vehicle for this organism.

Transmission Routes: Person-to-person spread (during convalescence) is important, but in many countries food and waterborne transmission are more significant. Most meals implicated in causing shigellosis comprise cooked food that is served cold and that has been contaminated by a food handler. Food can become contaminated by flies carrying sewage or faeces.

Plague and Pestilence

Associated with dips, lettuces, parsley, salads generally. Control measure failures are likely faecal contamination of ready-to-eat food / possible contamination by sick food handler / contaminated water and ice.

Staphylococcus aureus

Staphylococcus aureus is very common in the environment and can be found in soil, water, and air, and on everyday objects and surfaces. It can live in humans and animals.

Everyone immediately thinks of MRSA but don’t forget staph is also found in foods and can make toxins (enterotoxins) that might not be destroyed by cooking, although the bacterium itself can be destroyed by heat. These toxins can cause nausea, stomach cramps, vomiting, and diarrhoea. In more severe cases, the toxins may cause dehydration, headache, muscle cramps, and temporary changes in blood pressure and heart rate. Its toxins are fast‐acting; they cause symptoms within 1 to 7 hours after contaminated food is eaten. Outbreaks often have been linked to foods that require a lot of handling when they’re being prepared.

Growth and toxin production is best in the presence of oxygen but can grow anaerobically. It is not regarded as a good competitor with other bacteria. Infected food handlers are a significant cause of food poisonings.

Growth and Control

Growth

Temperature: Optimum 37°C, range 6-48°C. Upper limit of growth can be extended above 44°C by addition of NaCl, monosodium glutamate (MSG) and soy sauce.

pH: Optimum pH for growth is 7.0-7.5. Minimum pH for growth is 4.2, maximum 9.3. Growth is inhibited in the presence of 0.1% acetic acid (pH 5.1).

Atmosphere: Grows best in the presence of oxygen. Capable of growing anaerobically. Growth is retarded in the presence of 80% CO2 compared to growth in an air atmosphere.

Water Activity: The low aw at which S. aureus grows is particularly significant. The organisms are resistant to drying and may grow and produce enterotoxins in foods with aw as low as 0.85. Can grow in up to 25% NaCl. Grows well in 7-10% NaCl. Optimum aw for growth is 0.99. Its ability to grow at low aw means that it has a competitive advantage on low aw foods.

Toxin Production: Combinations of different inhibitory factors (e.g. NaCl content and pH) can be used to control toxin production (and growth), i.e. multiple hurdles can be used. Basically organisms exposed to an extreme of one inhibitory factor become more susceptible to others.

Temperature: Optimum 35-40°C, range 10-45°C.

pH: Optimum pH for toxin production is 5.3-7.0, minimum 4.8, maximum around 9.0. Toxin production is inhibited more effectively when the pH is reduced by lactic acid rather than hydrochloric acid.

Atmosphere: Greatest toxin production is in the presence of oxygen. Less toxin is produced under anaerobic conditions.

Water Activity: Optimum for toxin production is ≥0.90 aw. Range 0.86 ≥0.99.

Survival

Temperature: The organisms is usually readily killed at cooking and pasteurisation temperatures. Heat resistance is increased in dry, high-fat and high-salt foods. Survives frozen storage.

Toxins are extremely resistant to heat. For example the D time of enterotoxin B at 149°C is 100 min at an aw of 0.99, and 225 min at an aw of 0.90.

pH: S. aureus can survive in foods down to pH 4.2 but this is dependent on the type of acid present.

Atmosphere: Cells survive longer under anaerobic conditions.

Water Activity: Survives for long periods in dried foods.

Inactivation (CCPs and Hurdles)

Temperature: D60 is approx. 2 min. However, the D60 for salty foods, e.g. cheese, bacon and ham, is considerably longer (can reach >50 min). Heat resistance is reduced at high and low pH.

pH: Rapid destruction of S. aureus has been demonstrated in lemon and lime juices at pH 2.3. During food fermentations, lactic acid bacteria produce substances that are inhibitory to S. aureus including lactic acid, hydrogen peroxide and bacteriocins.

Water Activity: Withstands desiccation well.

Preservatives: S. aureus shows no unusual resistance to common food preservative methods except for its osmotolerance (permits survival and growth in high concentrations of NaCl). Cells grown in high salt foods at high temperatures are less sensitive to some food preservatives. When reduced pH and aw are used in combination to control S. aureus, less stringent levels of these parameters can be applied. Sorbate and benzoate are effective inhibitors of S. aureus with a minimum inhibitory concentration at pH 6.1 of 1000 mg/kg. The effectiveness of these preservatives increases as pH is reduced.

Methyl and propyl parabens are also effective.

High concentrations of CO2 substantially reduce growth.

Sanitisers/Disinfectants: See here for guidance. Most chemical sanitisers used routinely in the food industry, such as chlorine, other halogens, and quaternary ammonium compounds will destroy S. aureus on surfaces with ease.

Radiation: Relatively resistant to ionising radiation, but not to UV irradiation, when compared with other non-sporulating bacteria such as Salmonella and E. coli. D value of 0.45 kGy.

Clinical

Incubation: 30 min to 7 hours after eating food containing enterotoxins (mean 2-4 hours).

Symptoms: Symptoms usually include nausea, vomiting and abdominal cramps and may be followed by diarrhoea. In severe cases, headaches, sweating and fever may occur. In mild cases there may be nausea and vomiting without diarrhoea, or cramps and diarrhoea without vomiting. Recovery is rapid, usually within 2 days.

Estimated hospitalisation rate = 18%, case fatality rate = 0.02%.

Condition: Staphyloenterotoxaemia; enterotoxin causes inflammation of the intestinal tract lining. Staphylococcal food poisoning is seldom fatal but fatalities have been reported occasionally in young children and elderly.

Toxins: Illness results from consuming toxins in foods.

At Risk Groups: All people are believed to be susceptible to staphylococcal intoxication, but the intensity of symptoms may vary depending on the amount of food ingested and the susceptibility of the individual to the toxin.

Long Term Effects: None.

Dose: Less than 1.0 μg of toxin in contaminated food can produce symptoms. This toxin level is reached when S. aureus populations exceed 105 per gram. Small numbers of S. aureus in food are not a direct hazard to health.

Treatment: Usually no treatment is given. Fluids may be administered when diarrhoea and vomiting are severe.

Reservoirs / Sources

Human: Humans are the main reservoir for staphylococci involved in human disease. Human contamination of food can occur by direct contact, indirectly by skin fragments, or through respiratory tract droplets.

Animal: Animals and poultry carry S. aureus on parts of their body which can lead to infections. Cows udders and teats, tonsils and skin of pigs, and skin of chickens and turkeys are known sources.

Food: S. aureus competes poorly with other bacteria and therefore seldom causes food poisoning in raw products. Unpasteurised milk may cause food poisoning if numbers of organisms are very high, such as when a cow has mastitis. Foods which present the greatest risk are those in which the normal flora has been destroyed (e.g. cooked meats) or inhibited (e.g. cured, salted meats). Staphylococci grow well in cooked foods which are high in protein, sugar or salt, low in acid, or food with moist fillings.

Environment: May colonise food-processing equipment in areas that are difficult to clean. Often found in ventilation system dust.

Transmission Routes: Ingestion of contaminated food.

Plague and Pestilence

Outbreaks: Most outbreaks are caused by eating foods in which enterotoxin has been produced because of time and temperature screw ups following preparation. Control measure failures include contamination of food by handler, inadequate re-heating and hot holding of cooked foods, inadequate thawing prior to cooking, inadequate cooling of cooked product, prolonged storage at ambient temperature.

Vibrio cholerae

The species is divided into serotypes on the basis of the O antigen. Cholera is typically associated with O1, but serotype O139 has also been the cause of many cases of cholera in Asia. There are subgroups of O1; classical and El Tor. The classical biovar is responsible for a more severe form of cholera.

Growth and Control

Growth

Temperature: Optimum 37°C. Range 10-43°C.

pH: Optimum 7.6. Range 5.0-9.6. The organism can grow relatively quickly under optimum conditions.

Atmosphere: Grows with or without oxygen, but growth is optimal under aerobic conditions.

Water Activity: Optimum aw 0.984 (0.5% NaCl). Range aw 0.940-0.988 (0.1-4.0% NaCl). Does not require the presence of salt for growth.

Survival

Temperature: Survives better under refrigeration than at ambient temperatures. Also survives freezing.

Viable but Non-Culturable (VNC) Cells: These organisms have been shown to undergo a transition to a VNC state.

Inactivation (CCPs and Hurdles)

Temperature: D60C = 2.7 min. D71C = 0.30 min. pH: Rapidly inactivated at pH values <4.5 at room temperature.

Water Activity: Sensitive to drying.

Sanitisers/Disinfectants: QACs and hypochlorite are effective disinfectants in the absence of protein. Quaternary ammonium compound quite effective at 50 ppm. Isoproponol used to disinfect hands was effective.

Radiation: A dose of 0.5 kGy is optimal for inactivating this organism. D value of 0.11 kGy in frozen prawns.

Preservatives: Freshly squeezed lemon juice has been found to inactivate the organism after 5 minutes exposure. Lime juice has also been shown to inhibit growth.

Depuration: Not effective for the removal of Vibrio from shellfish.

Clinical

Incubation: 12 to 72 hours.

Symptoms: Cholera: Initially mild diarrhoea progressing to diarrhoea characterised by the production of copious pale grey (“rice water”) stools. Other symptoms include low blood pressure, nausea, abdominal cramps and occasionally fever. The loss of fluids requires rehydration and if this does not happen death by fluid loss can occur. Recovery within 1-6 days in healthy people is normal.

Non-O1/O139: The diarrhoea is milder but may be bloody, and is accompanied by abdominal cramps and fever. Can last 6-7 days. Extraintestinal infections may also occur, e.g. in wounds exposed to contaminated water.

Condition: Cholera. Six worldwide pandemics of cholera originating in India are known to have occurred. In the seventh pandemic type O1 El Tor originated from Indonesia. The emergence of type O139 from southern India can be regarded as the eighth pandemic. The hospitalisation rate from cholera has been estimated at 34% and the case fatality rate at 0.6% in the USA.

Non-O1/O139: In the developed world most cases are due to non-O1/non-O139 serotypes. Such incidents are normally associated with the consumption of contaminated seafood.

Toxins: Cholera toxin and a related adherence factor produced in the intestine are essential components for cholera to occur. A number of other factors are also important.

Non-O1/0139 serotypes do not produce these toxins.

At Risk Groups: Cholera: Usually between the ages of 2 and 9 years in endemic areas. When people become exposed to new serotypes adults are also susceptible to infection.

Non-O1/O139: Diarrhoea may occur in anyone eating contaminated shellfish. Septicaemia can occur in people with liver cirrhosis or who are immunocompromised.

Long Term Effects: Prevented by rehydration.

Dose: Approximately 100 cells when ingested with food in healthy adults, less in those taking antacids.

Treatment: Cholera: Rehydration and electrolyte replacement. Antibiotics shorten the duration of the illness.

Non-O1/O139: Usually self-limiting. Antibiotics shorten the duration of the illness.

Reservoirs / Sources

Human: Believed to be the primary reservoir of the organism. Asymptomatic carriers are known to occur.

Animal: Aquatic microscopic animals living in contaminated marine waters become contaminated themselves. O1 strains have been shown to colonise zooplankton at >104 cells per animal. Cholera organisms can be carried by domestic animals, but not for long periods. Non O1/O139 strains are normal inhabitants of the marine environment.

Food: Food becomes contaminated from food handlers or contaminated water. The most commonly implicated foods are seafood, including shellfish, fish and crustaceans. Grains, legumes, meat, fruits and vegetables have also acted as vehicles. Fruits and vegetables may be irrigated with contaminated water and consumed raw. Other foods may be contaminated by infected food handlers.

Environment: Whether there is a natural aquatic reservoir for O1 and O139 is still under debate, although the weight of evidence suggests that there is. Cholera serotypes have been isolated from Asian, American and Australian waters.

Other serotypes are associated with marine, brackish and freshwater aquatic environments.

Transmission Routes: By food that has been in contact with contaminated water. Non O1/O139 cases are associated with the consumption of raw oysters.

Plague and Pestilence

Outbreaks in non endemic countries (mainly USA): Frozen coconut milk (imported from Thailand): (O1) 3 cases, 1 hospitalisation. Control point failure not identified, although insufficient final cooking occurred. Canned palm fruit (imported from El Salvador): (O1 El Tor) 4 infected, 2 symptomatic, both hospitalised. Control point failure: probably incorrect processing of the home canned fruit. Seafood salad (airline meal): 75 infected out of 336 exposed, 10 hospitalised, 1 died. Control point failure: not identified.

Raw Oysters: (non-O1) 4 cases. Control point failure: not identified but presumably harvesting contaminated shellfish and/or temperature cock up.

Rice: (O1 El Tor) 15 cases. Control point failure: rice washed in contaminated water after cooking, temperature cock up.

Vibrio parahaemolyticus

A marine Vibrio normally associated with food poisonings involving seafood consumption. Especially oysters. It is a major cause of food poisoning in Asian countries. Certain strains (Kanagawa phenomenon-positive, KP+) are primarily involved with human disease.

Growth and Control

Growth

Temperature: Range 5-43°C, optimum 37°C. Growth is very rapid under optimum conditions.

pH: Optimum 7.8-8.6. Range 4.8-11. Minimum pH for growth decreases as the incubation temperature increases towards the optimum. Growth was inhibited in the presence of 0.1% acetic acid (pH 5.1).

Atmosphere: Can grow in the presence or absence of oxygen, but grows optimally under aerobic conditions.

Water Activity: Grows in NaCl concentrations from 0.5-10%. Optimum = 3%. aw range is 0.940 to 0.996, with an optimum of 0.980.

Survival

Temperature: Survives freezing, although number reduced 10-100 fold.

Inactivation (CCPs and Hurdles)

Temperature: The organism dies at temperatures of 0-5°C. Cooking to an internal temperature of 65°C effectively inactivates this organism. D time at 65°C < 1 min, at 55oC 2.5 min. A low temperature pasteurisation of 10 minutes at 50°C has been suggested for shellstock oysters.

pH: Thermal D time increases as pH increases from 5.0 to 8.0.

Water Activity: Very sensitive to drying. Fresh water inactivates the organism.

Preservatives: The organism is highly sensitive to 50 ppm butylated hydroxyanisole. It is inhibited by 0.1% sorbic acid.

Sanitisers/Disinfectants: D time of 15 seconds when exposed to chlorine or iodophor at 13 ppm.

Radiation: A dose of 3 kGy has been recommended for the elimination of Vibrio from frozen shrimps. Quite sensitive to irradiation; D value of <0.1 kGy in fish at 24°C.

Depuration: Not effective at removing Vibrio from shellfish.

Clinical Notes

Incubation: 4-74 hours, mean 12-46 hours.

Symptoms: Abdominal cramps and watery diarrhoea. Sometimes nausea, vomiting and fever. Symptoms last from 1 to 7 days, occasionally longer. Mean duration 2.5 days. Hospitalisation is required in approximately 7% of cases. Usually self-limiting. Extraintestinal infections can occur.

Condition: Primarily gastrointestinal infection.

Toxins: The KP+ factor is a haemolysin. Expression of this haemolysin seems to be responsible for the symptoms. However other virulence factors, such as a shiga-like toxin are also likely be involved.

At Risk Groups: No at risk groups reported for gastroenteritis.

Long Term Effects: Reactive arthritis has been reported.

Dose: Ingestion of 2 x 105 – 3 x 107 cells is required to cause disease in healthy adults, but it may be lower in the presence of antacids or food.

Treatment: Gastroenteritis is usually self-limiting. Appropriate antibiotics may reduce symptoms.

Reservoirs / Sources

Human: Asymptomatic carriers are known to occur. Carriers act as a source of environmental contamination.

Animal: Occurs in marine animals including mammals, fish, shellfish, crustaceans and plankton.

Food: Foods of marine origin may harbour this organism. Levels may approach 103/g in fresh seafood and may be greater in the warmer months, but are more typically present at around 10/g. Large proportions (60-100%) of seafood samples in the USA were found to contain the organism.

Environment: A normal inhabitant of the marine environment. The presence of the organism in the environment is heavily influenced by the season, occurring at the highest levels in the warmer months. However, typically > 99% of isolates from seawater are not of the human pathogenic kind.

Transmission Routes: Usually via seafood with crappy temperature control.

Plague and Pestilence

Seafoods are the food group most often associated with outbreaks.

Yersinia enterocolitica

Yersinia enterocolitica and Yersinia pseudotuberculosis are bacteria known to cause foodborne gastroenteritis in humans. The pathogen can cause diarrhoea and pain that may be mistaken for appendicitis. More invasive illness occasionally occurs, and post-infection arthritis may occur in a small proportion of cases.

Not all Y. enterocolitica strains can cause human illness. Six biotypes can be differentiated using biochemical tests, and this forms a useful investigative tool for determining pathogenicity. Pathogenic biotypes are 1B, 2, 3, 4 and 5. Foodborne yersiniosis can be avoided by following standard food safety and hygiene advice.

Growth and Control

Note: Isolation of Y. enterocolitica is notoriously difficult; no single method is suitable for all serotypes. Y. enterocolitica is thought to compete poorly with spoilage organisms.

Growth

Temperature: Optimum 25 – 37°C. Range -1.3 – 42°C

pH: Optimum 7.2. Minimum 4.2 – 4.8 depending on temperature and acidulant. Maximum 9.6-10.

Atmosphere: Facultative anaerobe. 100% N2 and CO2/N2 gas mixes inhibitory (more so at refrigeration temperatures).

Water Activity: Minimum 0.96 aw. Growth in 5% salt, not in 7% salt.

Inactivation

Temperature: Pasteurisation effective. D55°C = ~ 2 min, D60°C = ~ 0.5 min, D65°C = ~ 2 sec.

pH: Below pH min, bactericidal activity order is: Acetic acid >lactic acid > citric acid > sulphuric acid.

Water Activity: 0.945 aw (7% NaCl) was bactericidal on all of 4 strains tested, when incubated at 3°C but at 25°C both bactericidal and bacteriostatic effects were observed. At 9% NaCl and 25°C, all 4 strains were killed.

Preservatives: Growth is retarded by potassium sorbate up to 5,000 ppm at pH 6.5 in a dose-dependent manner. At pH 5.5 concentrations above 1,000 ppm virtually eliminate growth or cause inactivation depending on dose. Sodium nitrite at a concentration of 150 ppm retarded growth on bologna.

Disinfectants / Sanitisers

Treatments with ozone (1.4 and 1.9 ppm) and with ozonated water (1 min exposure) reduce pathogen loading.

Clinical

Incubation: Approximately 7 days, range 1-11 days.

Symptoms: Usually manifests as a self limiting gastrointestinal infection. Symptoms generally last 2-3 days but duration may extend to 3 weeks. More serious illness occurs less commonly. Common symptoms include diarrhoea (watery / mucoid in young children), enterocolitis, pseudoappendicitis syndrome in 5 yrs – adolescents, particularly with more virulent strains. Caused by acute inflammation of the terminal ileum or mesenteric lymph nodes in right lower quadrant, with little or no diarrhoea. Pharyngitis. Post infection autoimmune sequelae.

Less common: septicaemia, visceral abscesses, skin infections, pneumonia, endocarditis, osteomyelitis, peritonitis, meningitis and eye infections.

Condition: Yersiniosis.

Dose: Insufficient data are available to ascertain dose response.

At Risk Groups: Highest notification rates for <5 age group, followed by >60 age group, more common in males than females. Immunosuppression, blood disorders, malnutrition, chronic renal failure, cirrhosis, alcoholism, diabetes mellitus and acute/chronic iron overload states.

Long Term Effects: Enterocolitis may persist for several months. Acute inflammatory, arthritic syndromes may develop 7-21 days after infection. Other symptoms, e.g. urethritis and skin lesions, can occur in adults.

Treatment: Antibiotics do not reduce severity or duration of gastrointestinal illness, but are of use in more serious manifestations of the disease.

Reservoirs / Sources

Infections are zoonotic, those sub-types that occur in humans also occur in domestic animals.

Human: Person-to-person transmission can occur.

Animal: Isolated from mammals, birds, frogs, flies, fleas, crabs and oysters. Associated with pigs, especially the tongue and tonsil area. Pigs are the only animal from which Y. enterocolitica biotype 4 and serotype O:3 are frequently isolated and this is the group commonly associated with human illness. Serotype O:3 is common in pigs globally and may also be carried by companion animals.

Food: Foodborne transmission is the primary route for infection and may be associated with pork, beef, lamb and poultry and has also been isolated from fruit, vegetables, tofu, pastries, sandwiches and pasteurised milk.

Environment: Terrestrial and freshwater ecosystems harbour the pathogen, including soils, vegetation, lakes, rivers, wells and streams. Extended survival periods at low temperatures.

Plague and Pestilence

Pasteurised milk: Vermont, USA, 1995; 10 cases, 3 hospitalised, 1 appendectomy. Control measure failure: likely post pasteurisation contamination.

Pork chops and pork brawn: Norway, 2006; 11 cases, 4 hospitalised, 2 died. Control measure failure: Unidentified.

Chitterlings (boiled pig intestine): Chicago, USA, 2002. 9 cases. 6 hospitalisations. Control measure failure: Probably poor handling practices in the home.

Ingestion of raw or undercooked pork is considered to be a major risk factor. Yersiniosis has been associated with consumption of pork products (including intestines), sausages, eating raw food or food cooked rare, and the consumption of untreated water.

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