Risks
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1. What are the risks for fresh unprocessed whole milk, including all types of risks, such as adverse consequences, intolerance and allergens?

2. Where do these risks originate?

3.  Is there a difference in the nature of utilization of fresh unprocessed whole milk and pasteurized milk?

*The Michigan Fresh Unprocessed Whole (FUW) Milk Workgroup topic discussion participants included Ted and Peggy Beals, Susan Esser, Katherine Fedder, Frank Fear, Rosanne Ponkowski, Joe Scrimger, and John and Patti Warnke, Howard Straub and Elaine Brown.

Discussion Summary:

The workgroup follows a set of Topics and within each Topic a set of questions.  For Topic 3 Risk,  the workgroup combined questions 1. What are the risks for fresh unprocessed whole milk, including all types of risks, such as pathogens, adverse consequences, intolerance and allergens? and question 2. Where do these risks originate?  They deferred question 3. Is there a difference in the nature of utilization of fresh unprocessed whole milk and pasteurized milk?;  until the discussion of Topic 6.

They reviewed each of the 4 groups of bacteria that are considered important causes of current foodborne illnesses in this country: Campylobacter jejuni, Listeria monocytogenes, Salmonella and the O157:H7 subtype of Escherichia. coli. They also reviewed the bacteria that cause human illnesses that dominated the public health concerns in the past. And they reviewed information on noninfectious adverse reactions to milk.  The reviews resulted in 12 documents that are posted on the website under Topic 3:

• Each of the 4 organisms of current interest has a Pathogen Summary (which present in systematic outline pertinent characteristics of the specific bacteria) 
  • Campylobacter jejuni
  • Listeria monocytogenes
  • Salmonella
  • Escherichia. coli O157:H7
• Each of the 4 has a Scenario for transmission to people (which systematically outline patterns of spread of illness with emphasis on routes of transmission that pertain to milk consumption). 
• A discussion of infectious dose.
• A narrative on the illnesses of historical interest.
• A document on noninfectious adverse conditions. 
• Recognizing that some of the terms in these documents might need explanation, the group developed a table of such terms, with a description (not dictionary definitions) to help the reader understand the terms in the context of the documents.

MILKBORNE BACTERIAL HUMAN PATHOGEN SUMMARIES

Campylobacter jejuni

Scientific Name:
genus: Campylobacter
species:  jejuni
abbreviated:  C. jejuni

Recognized Subtypes within the species:
There are several commonly used systems of subtyping with from 60 to 100 recognized subtypes using these different techniques. [1] [2] [3]

General:

• Gram negative, rod shaped, motile bacterium. Only natural habitat is the intestinal tract of many warm blooded animals.  But is widespread in the natural environment when persistent animal fecal contamination occurs. Also common as a transient contaminant in home kitchens, water and food manufacturing facilities.
• Easily cultured and detected when present in large numbers (such as in human diarrhea specimens). However, it is specifically difficult to culture from unpasteurized milk because of the multiple conditions listed below.
• Conditions that promote growth/survival:  Optimal growth is within living cells.  Growth is optimal at 108 °F. Survive best in warm wet conditions.
• Conditions that inhibit growth/survival: Generally described as “fragile”, this bacteria is sensitive to air (oxygen), drying, acidic environments and grows poorly, if at all, at room temperatures and does not grow well outside of warm blooded animal hosts. Does not compete well with other bacteria and usually isolation techniques require inhibiting those other bacteria. The numbers decline over time in unprocessed milk; particularly when refrigerated or exposed to air.  Unprocessed milk with other bacteria tends to become acidic because of the growth of the other bacteria. Specific research on fate of Campylobacter jejuni isolated from human cases inoculated into unpasteurized milk under laboratory conditions, documented inactivation over several days. [4]

Disease Description:

Animals: Present in healthy birds and other animal intestines (carrier state) but rarely causes disease.

Humans:

• Acute gastroenteritis with diarrhea categorized as campylobacteriosis.   Nearly all human infections are from C. jejuni, but a few are from C. coli.
• The most common foodborne illness in the US with two million cases per year (1 illness per 150 people each year).
• Interval from consumption to symptoms is 3-5 days. Illness is usually self-limiting (get well without antibiotics) lasting for 3-12 days. However, in untreated cases individuals may continue to shed infectious bacteria for 7 weeks. A true persistent carrier state (colonizing in intestine without illness) in humans is rare.
• Because of huge numbers of bacteria present in diarrhea, culturing in the medical laboratory is a practical means of making the diagnosis.
• There are at least four virulence steps necessary for human illness (1. adhers to intestinal cells, 2. grows in the intestine, 3. enters the cell and proliferates, and 4. produces toxin). 
• During 2009 there were 911 reported cases of campylobacter gastroenteritis in Michigan.  Frequency of illnesses in humans is seasonal, highest in June, July and August.

Category of human disease: 

• Causes acute enteritis with nausea, abdominal cramps, severe diarrhea which may be bloody and mild fever.
• Infectious dose:  from 500 to 10,000 virulent bacteria depending on foods consumed and health of the person. 
• Immunity results from frequent direct contact with farm animals.

Complications of human infection: 
Rare; a form of Guillian-Barre Syndrome occurs in about 1 out of 1,000 human cases of campylobacteriosis.  This inflammatory neurologic syndrome has been associated with a number of other viral and bacterial infections.

Reservoir (potential source):

• Humans with campylobacter enteritis shed 1,000,000 bacteria per gram of diarrhea.
• All warm blooded animals, particularly birds, become exposed in infancy and persist as carriers of campylobacter in their intestines throughout life.
• Chickens shed 1,000,000 or more colony-forming-units per gram (cfu/gram). [5]
• Water, contaminated from animal manure.
• Cows whose intestines are temporarily colonized with C. jejuni shed comparatively low numbers in feces. [6]
• Shedding directly from an infection into the milk does not occur.
• A study in rural Michigan found that poultry husbandry carried the greatest risk of human campylobacter enteritis. [7]

Food implicated in outbreaks:
Surveys show that 20-100% of retail chicken packages are contaminated. It is estimated that one drop of fluid from fresh packaged chicken contains an infectious dose.  
           
Outbreaks:
Most campylobacter foodborne outbreaks are limited to a few cases of illness; however some outbreaks from contaminated water supplies have sickened thousands.

• FUW milk in Michigan 1999-2011 [8] – 36 illnesses
• FUW milk USA 1999-2011 [8] – Total 383 illnesses  (average 31.9 per year)
• For all foods, estimated annual illnesses from Campylobacter spp. in the USA, based on data collected in 2006-2008 – 845,0249 [9]

References:
Unless referenced separately most of the comments are from the FDA “Bad Bug Book”  Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. www.cfsan.fda.gov/~mow/chap1.html

[1] "Campylobacteriosis". Center for Infectious Disease Research and Policy. Academic Health Center University of Minnesota, 2008.

[2] "Assessing Health Benefits of Controlling Campylobacter in the Food Chain". European Food Safety Authority Scientific Colloquium Summary Report 12, 2008 Rome Italy.

[3] Common Somatic O and Heat-Labile Serotypes among Campylobacter Strains from Sporadic Infections in the United States. Patton, et al, 1992. Journal of Clinical Microbiology; 31(6): 1525-1530. (CDC)

[4] Prevalence and Survival of Campylobacter jejuni in unpasteurized milk. Doyle and Roman. Applied and Environmental Microbiology 44 (5): 1154-1158, 1982.

[5] Campylobacter in primary animal production and control strategies to reduce the burden of human Campylobacteriosis. Wagenaar, et al. Rev. sci. tech. Off. int. Epiz. 2006, 25(2):581-594.

[6] Chronic shedding of Campylobacter species in beef cattle. Inglis, et al. 2004, Journal of Applied Microbiology 97:410-420.

[7] Risk Factors for Sporadic Campylobacter jejuni Infections in Rural Michigan: A Prospective Case-Control Study. Potter, Kaneene, Hall. American Journal of Public Health, 2003; 93 (12): 2118-2123.

[8] Illnesses enumerated for outbreaks were obtained from a comprehensive listing of incidents with official reports for the period, January 1, 1999 to March 30, 2011. All incidents were entered into the database from news releases and public reports from national and state agencies, media articles, published listings from public interest groups and litigation websites, scientific publications, as well as from personal information. Numbers displayed in the Pathogen Summary documents include both confirmed and presumed illnesses given in final reports without any evaluation of the way the officials made their determination. There is no judgment on the manner of the investigation nor on the strength of the conclusions. Only incidents within the USA were included, and only when the investigation specified consumption of fluid fresh unprocessed milk as the presumed source. Both cow and goat dairies that were specifically operated for the purpose of supplying fresh unprocessed milk to consumers were included. 

[9] Foodborne Illness Acquired in the United States --- Major Pathogens, Elaine Scallan, R.M. Hoekstra, F.J. Angulo, R.V. Tauxe, M. Widdowson, S.L. Roy, J.J. Jones and P.M/ Griffin, Emerg. Infect. Dis. 2011. Table 2, pg. 16. Note that the numbers are specific for domestically acquired illnesses. 

Listeria monocytogenes

Scientific Name:    Listeria monocytogenes
Abbreviated:   L. monocytogenes

General:
Gram positive, motile, small rod shaped bacterium.  This organism is widely found in nature. In nature it multiplies under a broad range of conditions including -2 to 80°F, and in the presence or absence of oxygen.  It is capable of survival over long intervals and under adverse conditions. Its ability to multiply and survive under adverse conditions (particularly refrigeration) gives it a competitive advantage.  However, growth is very slow with a doubling time of 1-2 days at 39°F. Some strains are able to form biofilms.  Strains are remarkably stable; one persisted in a processing plant for 12 years.

In addition to its presence in the environment some subtypes are capable of entering living animal cells and altering their growth requirements thus enabling them to rapidly multiply and spread between cells resulting in illness.

Recognized Virulent Subtypes within the species:
This is an extremely well studied and complex organism.   There are more than 13 documented serotypes using the H (flagellar) and O (somatic) characteristics. The commonly used serotyping (1/2a, 1/2b, 1/2c, 3a etc.) are based on “O” antigens.  Three lineages have been used to categorize this species; each with different patterns of serotypes and characteristic environmental niches.

Most human illnesses are associated with the serotypes 1/2a, 1/2b and 4b. [1]

Disease Description:
Perhaps best understood as an accidental pathogen in humans but primarily a source of disease in a large number of non-human animals. [2]

Humans
There are several different disease patterns. Within individual outbreaks there is a dominant pattern.

Disease patterns:
1. Systemic:  Spreads to organs in the body. In these cases the virulent pathogen circulates in the blood (bacteremia).  The most common locations for organ infections are: brain, liver and the pregnant uterus.  These illnesses tend to be severe, hospitalization and mortality common.
2. Perinatal illnesses:  The pregnant woman may have only a mild gastroenteritis or flu-like episode. However, if bacteria enter the blood stream, infection during pregnancy is most likely localized in the uterus; resulting in disease in the embryo, placenta, or newborn.  The transmitted disease is often severe with high mortality.
3. Gastroenteritis:  Mild, self limiting illness.                        

• The infectious dose is extremely variable, ranging from 100 to 1,000,000 or higher bacteria [1].  It is believed that many people (and animals) are occasionally exposed, some with very high doses, without evidence of illness.  The incubation period in human illnesses varies from several days to many weeks.
• 98% of human illnesses are with serovars 1/2a, 1/2b and 4b
• The most common serotype virulent in humans with systemic listeriosis is 4b; the most associated with gastroenteritis is 1/2a. 
• There are widely spaced outbreaks with many ill people; suggesting that there are epidemic clones.
• Most human cases, not related to pregnancy, are in adults and are acquired by ingestion of contaminated food. Only 7% of cases occur in the healthy general public. The other cases have an underlying immunocompromizing condition (cancer, HIV/AIDS, immunosuppressant medications).  Spread between humans is uncommon.
• Although of public health importance, “it appears that L. monocytogenes represents an opportunistic human pathogen and that human infections are likely to contribute little if anything to the ecological success or dispersal of L. monocytogenes.” [2]  

Classification of illness caused by Listeria monocytogenes

Animals
Predominately in ruminant animals (sheep, cattle, goats and occasionally pigs) but also in non-ruminants,  birds, fish and reptiles. The pattern of diseases is very similar to those described above for humans. Except that in domestic ruminants, infection may spread through the herd and can be severe.  Manure from cattle with listeriosis (circling disease) and from infected products-of-abortion contain very high concentrations of L. monocytogenes. And as with humans, there is evidence that animals may be exposed without illness.  Transient colonization is common. Incidence in cattle is reducing, generally attributed to awareness of risk from poorly managed silage (containing as many as 1,000,000 organisms per gram) as a major source of listeriosis.

Category of pathogen.  For all animals.

• Causing acute enteritis with nausea, abdominal cramps, and mild diarrhea.
• Causing systemic diseases localizing predominately in the liver, brain, and pregnant uterus.
• Uterine infections in pregnancy resulting in infections of the embryo or newborn.

Complications of human infection: 
Hospitalization with the systemic disease is common.  Death rate following systemic infections is high.

Reservoir:
Widely found in the environment and animals. Has a competitive advantage in salty or cold environments. Although much is known about the growth and survival in various ecosystems, transmission and principle sources are poorly understood, perhaps because it has developed different mechanisms in different systems. It appears that Listeria monocytogenes represents an opportunistic human pathogen and that human infections are likely to contribute little if anything to the ecological success or dispersal of Listeria monocytogenes.

Colors in Diagram above added by T. Beals. 
References for diagram. [3]

Foods implicated in human outbreaks:
Fresh, undamaged or unprocessed foods do not support the growth of this organism.

By all measures, ready-to-eat meats (such as deli meats) are the most frequently associated with outbreaks.  Contamination in these products occurs in the processing plant environment, including the processing equipment.  Because of the association with processing environments, the list of implicated foods is very long including processed meats such as pâté, salami, hot dogs, processed fish, cheeses, processed vegetables and salads. Specific foods associated with outbreaks are related to trends in food consumption and processing rather than to the individual foods themselves.

Foodborne human illness is mostly associated with those processed foods which ordinarily have a long self-life at refrigerated temperatures.

Outbreaks for Listeria monocytogenes:

• FUW milk in Michigan 1999-20114 – 0 illnesses
• FUW milk USA 1999-2011 4 – 0 illnesses
• For all foods, estimated annual illnesses from Listeria monocytogenes in the USA based on data collected in 2006-2008 – 1,591. [5]

General References:

FDA Bad Bug Book  Foodborne Pathogenic Microorganisms and Natural Toxins Handbook                  
http://www.fda.gov/food/foodsafety/foodborneillness/
foodborneillnessfoodbornepathogensnaturaltoxins/badbugbook/ucm070064.htm

Advisory Committee on the Microbiological Safety of Food’s Draft Report on Increased Incidence of Listeriosis in the UK.  2008

Epidemiological and Experimental Studies of Listeria Infection, with special reference to fecal excretion in ruminants, contamination of raw milk, presence in silage and growth at low temperatures., Jaana Husu, [Definitive thesis and associated published articles; Helsinki, 1990]

Risk assessment of Listeria monocytogenes in ready-to-eat foods. Microbiological Risk Assessment Series 4. WHO/FAO, 2004

Footnotes:

[1] Wiedmann, M. Molecular Subtyping Methods for Listeria monocytogenes. J. of AOAC International   85(2):524-532. 2002

[2] Oliver, Wiedmann and Boor. Environmental Reservoir and Transmission into the Mammalian Host. Chapter 6 pp 122-148. In Listeria monocytogenes: Pathogenesis and Host Response. ed. Goldfine and Shen. Springer 2007

[3] Ivaneck, R., et al. Listeria monocytogenes in Multiple Habitats and Host Populations: Review of Available Data for Mathematical Modeling. 2006. Foodborne Pathogens and Disease 3(4):319-336.

[4] Illnesses enumerated for outbreaks were obtained from a comprehensive listing of incidents with official reports for the period, January 1, 1999 to March 30, 2011.  All incidents were entered into the database from news releases and public reports from national and state agencies, media articles, published listings from public interest groups and litigation websites, scientific publications, as well as from personal information.

Numbers displayed in the Pathogen Summary documents include both confirmed and presumed illnesses given in final reports without any evaluation of the way the officials made their determination.  There is no judgment on the manner of the investigation nor on the strength of the conclusions.  Only incidents within the USA were included, and only when the investigation specified consumption of fluid fresh unprocessed milk as the presumed source.  Both cow and goat dairies that were specifically operated for the purpose of supplying fresh unprocessed milk to consumers were included. 

[5]  Foodborne Illness Acquired in the United States --- Major Pathogens, Elaine Scallan, R.M. Hoekstra, F.J. Angulo, R.V. Tauxe, M. Widdowson, S.L. Roy, J.J. Jones and P.M/ Griffin,  Emerg. Infect. Dis. 2011. Table 2, pg. 16.  Note that the numbers are specific for domestically acquired illnesses. 

Salmonella

Scientific Name:    Salmonella spp.

General:
Salmonella are gram negative, rod shaped, motile bacteria. Their normal habitat is the intestinal tract of many warm and cold-blooded animals.  But with widespread fecal contamination it can be found throughout the environment. It is also identified as a contaminant in, water supplies, food manufacturing facilities, and home kitchens.  It survives for long times in the environment, but does not generally multiply in the environment.  However, some animal feeds and processed foods that are high in protein can support their growth when not refrigerated. Salmonella does not compete well with other bacteria and is inhibited in acidic conditions.  Studies indicated that the few serovars that cause disease in humans and the equally small number that cause disease in cows are distinctly different. Essentially all of the subtypes of salmonella have been initially discovered from illnesses in different animals.  The general opinion is that this organism has “host adapted” to many animals over time.

Recognized Subtypes (Serovars):
Two species are generally listed: enterica and bongori. Enterica is divided in 6 subspecies: enterica, salamae, arizonae, diarizonae, indica and houtenae. Most of the human public health interest is in the subtype, Salmonella enterica subtype enterica. [1]

Recognized Virulent Subtypes:
Species have a confusing naming system, and many names were derived from specific animals or disease outbreaks.  Some species or named serovars contain human virulent strains. Although some serotype names imply specific animals, many are widely distributed in other animals and the environment.  Salmonella enterica Typhi causes typhoid, but this is not a significant pathogen in the USA today because the human disease has been controlled (See the History topic).  There are more than 2,500 documented serotypes; of these only about 50 have been associated with human illness.  Many different virulence factors have been identified. The virulence factors differ between subtypes, and sometimes even within specific serotypes. Even if a specific named serotype has been associated with human illness, this does not mean that any strain of that specific named serotype found in another animal or as a contaminant in food is capable of causing illness in humans.

Disease Description:

Animals:  Most animals that are clinically ill with salmonella subtypes have gastroenteritis. Systemic infections and abortions are known to be associated with specific subtypes and animals. Like typhoid in humans, some of the named serotypes are a significant health problem in specific animals.  There are “host-adapted” subtypes most of which cause specific diseases and in specific animal hosts. Such host-adapted subtypes commonly develop carrier states. The more generalized subtypes isolated from many different animals, may cause severe illness in a specific animal host, but cause gastroenteritis in the other animals. Most salmonella found in cows are long-term colonizers.

Humans:  Salmonellosis is the most common bacterial foodborne illness in the US; occurring mostly as sporadic cases with acute gastroenteritis. The interval from consumption to symptoms is shorter than for other milkborne gastroenteritites (12 hours to several days).  A human carrier state is recognized for typhoid which is host-adapted to humans.  Some studies indicate a small number of people with non-typhoidal salmonella gastroenteritis become carriers.  Among many of the named serovars isolated from humans somewhere in the world, only a few are seen with any frequency; most have not been isolated from humans for decades. Although the FDA gives an infectious dose of 15-20 cells for Salmonella spp., a USDA review of minimal infectious dose studies using human volunteers list ranges from 100,000 – 1,000,000,000 for specific serovars. [2]

Category of pathogen. 
Essentially all subtypes cause illness in some animal. Most cause a mild acute enteritis with nausea, abdominal cramps, and mild diarrhea, that last for a short time and generally does not require treatment.  However, specific subtypes cause severe systemic disease in specific animals.

Complications of human infection:  Rare

Reservoir:

• All birds and many amphibians may shed large amounts of bacteria in feces
• Water, contaminated from animal sources
• Cattle and cows, temporarily colonized, shed low numbers in feces. 
• Contaminated feed is a significant source of recolonization within herds.

Other food implicated in outbreaks:
            Most human cases are from eggs, packaged fresh poultry and meat and foods prepared from these items.

Outbreaks for Salmonella:

• FUW milk in Michigan 1999- 2011 [3] – 0 illnesses
• FUW milk USA 1999-2011 [3] – Total 39 illnesses  (average 3.3 per year)
• For all foods, estimated annual illnesses from Salmonella spp. in USA based on data collected in 2006-2008 [4] – 1,027,561

References:

FDA Bad Bug Book  Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. www.cfsan.fda.gov/~mow/chap1.html

Uzzau, et. al..2000. Review: Host adapted serotypes of Salmonella enterica. Epidemiology and Infection 125:229-255

Footnotes:

[1] Semenov, 2008. Doctoral thesis:  Ecology and modeling of Escherichia coli O157:H7 and Salmonella enterica serovars Typhimurium in cattle manure and soils.

[2] Kothary, M. and Babu, U., 2001. Infective Dose of Foodborne Pathogens in Volunteers: A Review. Journal of Food Safety 21: 49-73.

[3] Illnesses enumerated for outbreaks were obtained from a comprehensive listing of incidents with official reports for the period, January 1, 1999 to March 30, 2011.  All incidents were entered into the database from news releases and public reports from national and state agencies, media articles, published listings from public interest groups and litigation websites, scientific publications, as well as from personal information.

Numbers displayed in the Pathogen Summary documents include both confirmed and presumed illnesses given in final reports without any evaluation of the way the officials made their determination.  There is no judgment on the manner of the investigation nor on the strength of the conclusions.  Only incidents within the USA were included, and only when the investigation specified consumption of fluid fresh unprocessed milk as the presumed source.  Both cow and goat dairies that were specifically operated for the purpose of supplying fresh unprocessed milk to consumers were included. 

[4]  Foodborne Illness Acquired in the United States --- Major Pathogens, Elaine Scallan, R.M. Hoekstra, F.J. Angulo, R.V. Tauxe, M. Widdowson, S.L. Roy, J.J. Jones and P.M/ Griffin,  Emerg. Infect. Dis. 2011.    Table 2, pg. 16.  Note that the numbers are specific for domestically acquired illnesses. 

Escherichia coli

Scientific Name:
Genus  Escherichia              
species: coli
abbreviated:  E. coli

General Description and Information:
Gram negative, rod shaped bacterium, many but not all are motile. They grow well in oxygen containing or depleted environments. Its natural habitat is the intestinal tract of most warm-blooded and some cold-blooded animals. But with fecal contamination it is widespread in the natural environment.  E. coli can also be found as contaminants in home kitchens, water and food manufacturing facilities. Optimal growth is at 99°F.  Easily cultured and detected. However, due to the diversity of these bacteria there is no universal growth media for laboratory isolation.  It is widely publicized that E. coli grows extremely rapidly, doubling in less than one half hour. These growth rates are under laboratory conditions in optimal growth media and at 98.6°F.

Nearly all E. coli are benign and some are extremely beneficial and participate in digestion and metabolism in the intestinal tract.

Recognized Subtypes within the species:
There are a number of commonly used systems for distinguishing forms of E. coli resulting in hundreds of recognized subtypes based on different characteristics. The “O” antigen types and the “H” antigen types (also used in the subtyping of other bacteria) yield subtypes using differences in molecules on the surface of the bacteria.  The designation of the most publically recognized subtype, E. coli O157:H7, relies on differences in both of these subtyping systems (Identified as #157 in the growing list of 181 different “O” antigens and #7 in the list of 53 “H” antigens).  

Nearly all E. coli are benign and some are extremely beneficial and participate in digestion and metabolism in the intestinal tract.  E. coli is probably the most thoroughly researched bacterial species. Some of the research is prompted by the bacteria’s important role in digestion.  Other researchers are prompted by the rare but important subtypes associated with illnesses.  Even within the studies on those subtypes that can cause disease there are different category schemes.  Illness results from a number of different and often sequential behaviors, and this has led to some commonly used ways to distinguish categories of E. coli.

Categories of those subtypes virulent in humans:

Virulence factors:
At least 3 virulence factors are commonly recognized. A factor that damages lining cells (intestine, other organs, and blood vessels).  A factor that damages red blood cells (hemolysis). And toxins (resembling the shigatoxins produced by the bacteria Shigella dysenteriae. [1] 

Many of the human illnesses are the result of bacterial toxin production.  Subtypes that produce this toxin are collectively referred to as: Shiga Toxin E. coli (STEC).  There are hundreds of subtypes of STEC only a few have been associated with human illnesses. The equally small numbers of isolates that are shed from cows are mostly different from those found in humans. [2]

The more general “O” and “H” subtyping schemes are not based on the ability to cause illness.  They are convenient and widely used when describing the E. coli subtypes.  This does result in the important fact that simply because the subtype is E. coli O157:H7 does not categorize the subtype as one that causes disease in humans.  There are people ill from E. coli infections, which have a subtype that is not O157:H7. Furthermore, not all E. coli O157:H7 are able to infect humans and cause illness.

Another commonly used way to categorize the virulent subtypes of E. coli is based on the nature of the disease they produce.  The FDA’s Bad Bug Book separates the virulent subtypes into four principle categories based on the nature of the injury accompanying infection. 

1. Enterohemorrhagic (EHEC). [Hemorrhagic Colitis]These are the most well known of the categories of current significance in public health. They are characterized by the breakup of red blood cells when there is infection.  The E. coli O157:H7 subtype belongs in this category.
2. Enteropathogenic (EPEC). [Most common infantile diarrhea] This category cause watery diarrhea but the E. coli in this category do not produce any of the typical toxins seen in the other categories.
3. Enteroinvasive (EIEC). [Often referred to as bacillary dysentery]  This category causes a mild form of dysentery.
4. Enterotoxigenic (ETEC). [Gastroenteritis or traveler’s diarrhea] This category produces a mild form of illness with watery diarrhea. Worldwide “traveler’s diarrhea” is caused by this category. They produce toxins related to those produced by a different bacterial genus Shigella. However, destruction of red blood cells is not prominent.

With the current widespread public awareness of foodborne illnesses from the specific subtype E. coli O157:H7 tests were developed to easily identify this subtype in clinical laboratories. Unlike most forms of E. coli, this subtype was not able to utilize sorbitol as an energy source in laboratory cultures. Widely available, and FDA approved, procedures for distinguishing the O157:H7 subtype using antibody mixtures enable confirmation quickly and inexpensively. One of the consequences of the ready availability of the tests for the specific subtype O157:H7 is that other categories and subtypes causing diarrheal illness are not being recognized by hospital laboratories.

The enteropathogenic (EPEC) category of E. coli was once prominent in childhood diarrheal illness.  During the 1960s and 70s illness from this category became uncommon in the USA.3  This maybe the result of acquired public immunity.

Disease Description:

Animals:  E. coli rarely causes illness in wild or domestic animals. However, subtypes that cause illness in humans may reside as temporary intestinal colonizers in domestic animals. It is commonly accepted that cattle feces are a major reservoir of E. Coli O157:H7in the USA.

Humans:  Acute, usually self limiting gastroenteritis. The interval from consumption to symptoms is shorter than other foodborne enteritis, usually only a couple of days.  Reviews show 100,000 illness, 3,000 hospitalizations and 90 deaths annually in the USA from the subtypes with shigatoxins (STEC). [4]  The frequency of different E. coli serotypes isolated from humans with illness varies significantly in different regions of the world.
     
Because there are multiple virulence factors, research discloses considerable variety of strains with variation in human virulence and severity of illness. [5]  The variation in the incidence of hemolytic uremic syndrome in infants in different outbreaks is in part related to different forms of virulence factors and the types of shigatoxins produced by the specific subtype causing the diarrhea. 

The prevalence of E. coli O157:H7 has been extensively studied.  Human illnesses and cow colonization increase during warm months.  Prevalence of colonization and shedding is higher in calves than adult cows.  Changes in feed causes changed prevalence in cows.

The normal intestinal microflora contains about 1,000,000,000 bacteria per gram of feces. Of these as many as 1,000,000 colony forming units (cfu) are beneficial E. coli.  Cows with transient colonization with E. coli O157:H7 usually shed about 500 cfu per gram of feces.  There are reports of “super-shedders” that may be more persistently colonized and shed higher numbers of organisms.

Category of pathogen. 
The rare virulent forms of E. coli generally cause self-limiting acute enteritis with nausea, abdominal cramps and mild diarrhea that can be bloody. The severity and pattern of symptoms varies considerably with various categories of virulent forms. As the general public is exposed to specific subtypes, immunity is acquired and the illness pattern shifts to other subtypes. The usual route of infection is oral following consumption of food/drink or hand-to-mouth transfer.

Infectious dose:  With the numerous subtypes and virulence forms it is difficult to give a specific infectious dose for the group.  Reports range from 10 organisms to 100,000,000 organisms.  

Complications of human infection:  The most significant complication is hemolytic uremic syndrome (HUS).  This complication has been studied extensively and has received considerable public attention.  The true incidence is unknown but in the subset of hospitalized infants with bloody diarrhea caused by E. coli O157:H7 about 15% develop some degree of HUS. The syndrome includes damage to red blood cells and associate renal damage that can result in renal failure. [6]

Reservoirs:

Water does not naturally contain E. coli.  However, water contaminated with E. coli from animal (including human) sources is very common.
Cattle can become temporarily colonized by forms that are virulent in humans. These colonies shed in low numbers intermixed with the normal E. coli in the feces.  Contaminated feed, drinking water and contact with other cattle shedding the virulent forms of bacteria are significant source of recolonization within the herd.
Humans are the ultimate source of human virulent forms of E. Coli.

Other foods implicated in outbreaks:
Ground beef is the most frequently implicated food source (USDA FSIA 5/10). Other foods include:  leafy greens, seed sprouts, unbaked cookie dough, nuts, and fresh fruit juices.
 
           
Outbreaks for E. coli 0157:H7:

• FUW milk in Michigan 1999-2011 [7] – 0 illnesses
• FUW milk USA 1999-2011 [7] – Total 50 illnesses (average 4.6 per year)
• For all foods, estimated annual illnesses from E. coli O157:H7 in the USA based on data collected in 2006-2008 -63,153. [8]

General references:

FDA Bad Bug Book  Foodborne Pathogenic Microorganisms and Natural Toxins Handbook: www.cfsan.fda.gov/~mow/chap1.html.
Note: the FDA Bad Bug Book includes different sections based on the category of E. coli categories rather than as a unified chapter.

S.J. Bach, et al. Transmission and control of Escherichia coli O157:H7 – A review. Can. J. of Anim. Sci., 82:475-490, 2002

Specific references:

[1] CDC MMWR Oct, 16, 2009 58(RR12);1-14 www.cdc.gov/mmwr/preview/mmwrhtml/rr5812a1.htm?s_cid=rr5812a1_x

[2] Baker, et al. 2007.  Differences in Virulence among Escherichia coli O157:H7 Strains Isolated from Humans during Disease Outbreaks and from Healthy Cattle., Applied and Environmental Microbiology, 73 (22):7338-7346. http://aem.asm.org/cgi/content/short/73/22/7338

[3] Crane. 2010 Lessons from Enteropathogenic Escherichia coli. available online: www.microbemagazine.org/index.php?view=article&catid=
365%3Afeatured&id=1410%3Alessons-from-enteropathogenic-escherichia-coli&tmpl=component&print=1&layout=default&page=&option=com_content&Itemid=437

[4] Gould et al. 2009 MMWR Oct. 16,2009/58:1-14. www.cdc.gov/mmwr/preview/mmwrhtml/rr5812a1.htm

[5] Manning et al. 2008. Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks.,  Proceedings of the National Academy of Science. www.pnas.org/cgi/doi/10.1073/pnas.0710834105

[6] Desch and Motto, 2007.  Is There a Shared Pathophysiology for Thrombotic Thrombocytopenia Purpura and Hemolytic-Uremic-Syndrome? J. Am Soc. Nephrology 18:2475-2460.

[7] Illnesses enumerated for outbreaks were obtained from a comprehensive listing of incidents with official reports for the period, January 1, 1999 to March 30, 2011.  All incidents were entered into the database from news releases and public reports from national and state agencies, media articles, published listings from public interest groups and litigation websites, scientific publications, as well as from personal information.

 Numbers displayed in the Pathogen Summary documents include both confirmed and presumed illnesses given in final reports without any evaluation of the way the officials made their determination.  There is no judgment on the manner of the investigation nor on the strength of the conclusions.  Only incidents within the USA were included, and only when the investigation specified consumption of fluid fresh unprocessed milk as the presumed source.  Both cow and goat dairies that were specifically operated for the purpose of supplying fresh unprocessed milk to consumers were included. 

[8] Foodborne Illness Acquired in the United States --- Major Pathogens, Elaine Scallan, R.M. Hoekstra, F.J. Angulo, R.V. Tauxe, M. Widdowson, S.L. Roy, J.J. Jones and P.M/ Griffin,  Emerg. Infect. Dis. 2011. Table 2, pg. 16. Note that the numbers are specific for domestically acquired illnesses. 

SCENARIO FOR TRANSMISSION

Scenario(s) for transmission of virulent Campylobacter jejuni to people

Key requirements for transmission

• Must be virulent form of C. jejuni.
• Most be in adequate numbers (500 or more bacteria)
• Person must be susceptible (does not have full immunity), but not immunocompromised
• Must get into the intestinal tract of person (ingestion)

It’s all about numbers.  Microbiologists have worked hard to develop techniques/conditions that enable C. jejuni to multiple in large numbers in the laboratory.  However, in nature C. jejuni does not multiply outside of living cells of the animal intestine.  During infection virulent forms will multiply in the intestine. However, the principle of infectious dose is based on the observation that there must be a large enough mass of healthy virulent bacteria before infection happens. Becoming ill requires ingestion of adequate numbers of virulent C. jejuni. So nearly all circumstances of foodborne C. jejuni illness involve contamination with large numbers so that enough survive the interval and conditions prior to ingestion.   

Source and/or vehicle for transmission
 Items identified in Bold are factors with the greatest potential for leading to illness.

• People
  • People ill with diarrhea- the bacteria multiply and shed very high numbers of virulent C. jejuni in stool. Shedding persists after illness/diarrhea has subsided. These subtypes are by nature virulent.
  • A carrier state with persistent high shedding is not well documented for C. jejuni.
  • People with colonization that might transiently shed at low levels have not been described.
  • People can be a vehicle for transmission of infectious stool to:
  • Other people 
  • Animals
  • The environment including: water, feed, milk
• Animals
  • Poultry
    • Extremely high prevalence of C. jejuni in the intestine without causing illness. The bacteria multiply in the intestine and shed in high numbers within feces.  There is a significant likelihood that the subtypes present would be virulent in humans.
    • Most likely to be the source of contamination in home and commercial food preparation areas from fresh meat and juices contaminated during evisceration and processing.
      • Greatest risk of infection is from direct (physical) contact with living poultry.
  • Cattle/cows
    • Feces/manure
    • Cows can be colonized with limited multiplication of the bacteria and low shedding. These instances are transient, have variable subtypes over time and within a herd. These subtypes are unlikely to be virulent in humans.
    • Super shedding has been documented. Multiplication is still limited but there can be persistent shedding. In these instances there is usually a persistent subtype, still unlikely to be virulent in humans.  
    • Direct physical contact with manure on animals or the ground.
• Environment
  • Feces – only significant if contain high numbers of virulent bacteria
  • Water – (must be contaminated with fecal material with high numbers of virulent bacteria).  Survival is dependent on temperature and time.
  • Biofilm – longer survival of C. jejuni within preformed biofilm from non-pathogen bacteria  (C. jejuni are motile)
    • Persistent within equipment, piping, containers, under normal cleaning operations (experts consider this as the most significant source of contamination of milk).
    • Requires mechanical scrubbing to remove from surfaces
    • Microscopic flakes of biofilm carry embedded bacteria and are not easily diluted, resulting in uneven distribution.
  • Animal Feed (contaminated with feces/manure).
    • Shared feeding; not significant since would need bacteria in the mouth. 
    • Distributed on ground that has feces/manure.
    • Secondarily contaminated with contaminated water.
    • Contaminated by person shedding high numbers
• Milk
  • It maybe theoretically possible with C. jejuni mastitis to shed directly into milk from the udder but may only have been reported once in the literature.
  • Contamination of milk after milking
    • From any of the previously listed sources but must be in high concentration
    • Should be visible in a milk filter if contamination is manure. (Milk filters are designed to trap large particles and make such contamination more conspicuous.)
    • Incidental contamination would usually be diluted in the bulk tank
    • There is poor survival in fresh whole milk at refrigerated temperatures
    • Combination of factors that inhibit multiplication of bacteria in fresh milk (see in Benefits and Values Topic section). An increase in numbers of any bacteria in milk reduces the effectiveness of these inhibitions.
  • Rinse water contaminated with milk (increased survival)
  • Microscopic flakes of biofilm in bulk tank, milk lines, milking equipment (not visible).  Might pass through milk filter
• Other foods
  • Fresh poultry meat.
  • Fresh shellfish (rarely C. jejuni).
  • Leafy vegetables (biofilm) contaminated by bird feces containing virulent forms of C. jejuni.
  • Any food contaminated by person shedding high numbers of virulent forms.
• Contamination of containers by people, contaminated water, fecal/manure
  • Food containers – inside or outside
  • Transportation containers or equipment.

Scenario(s) for transmission of virulent Listeria monocytogenes to people.

• Must be virulent form of L. monocytogenes.
• Virulent form must be in adequate numbers to cause illness
• Assumes person must be susceptible (does not have full immunity)
• Generally assumes transmission by ingestion

Most cases of human listeriosis are not associated with investigated outbreaks.  Since the sporadic cases are rarely investigated there is little information on the modes of transmission or sources of the virulent form of L. monocytogenes.  This is complicated further because of the potential of long incubation times. Conclusions on definitive sources, reservoirs and modes of transmission are also distorted since outbreaks from L. monocytogenes are extremely rare and outbreaks vary considerably.

The systemic form of human “foodborne listeriosis, is a relatively rare but serious disease with high fatality rates (20-30%) compared to other foodborne microbial pathogens.” [1]

Being elderly or a child is not in its self a major risk factor for listeriosis.  However, conditions that are more likely to occur in different age groups (leukemia, cancer, dialysis, use of immunosuppressive drugs) are major risk factors.

Nearly all cases of foodborne listeriosis in people are associated with consumption of very high numbers of virulent organisms, and are associated with foods and food handling that enable multiplication of the bacteria prior to consumption.

It is generally accepted that the general public consumes food contaminated with L. monocytogenes, occasionally and repeatedly throughout their lives.  There is little information on the immunological effect of this exposure.

Source and/or vehicle for transmission

• People
  • People with gastrointestinal illness- during these illnesses the bacteria multiply and are shed very high numbers of the causative subtype of L. monocytogenes in their stool.
  • Adults with systemic infections (listeriosis) have organisms in their blood stream and have very high concentrations of L. monocytogenes within the infected organs.  Other people are unlikely to become infected from contact with the ill person.
  • A carrier state with persistent high shedding is not well documented for L. monocytogenes.
  • People with colonization that might transiently shed at low levels are most common within populations that have greater exposure to environmental L. monocytogenes, such as farmers and meat processors.  Recent studies show a small number of the general adult public may intermittently shed L. monocytogenes in their stool without symptoms, but it is not known if these were virulent forms.
  • People could be a vehicle for transmission of infectious bacteria in their stool to:
    • Other people. People exposed to cases of listeriosis may transiently shed L. monocytogenes in their stool, but rarely have symptoms. 
    • Animals.
    • The environment, including: water and feed.

    Current reviews conclude that the findings listed above are not significant contributors to human illnesses.
    In contrast, pregnant women with L. monocytogenes in their blood stream, even if not significantly ill themselves, are the principle source of transmission to their fetus or newborn.

• Animals
  • Cattle/cows, sheep and goats
    • Feces/manure
      • Cows can be colonized with limited multiplication of the bacteria and low shedding in manure. These instances are transient, have variable subtypes over time and within a herd and the subtypes are unlikely to be virulent in humans.
      • Super shedding is reported. Multiplication is still limited but there can be persistent shedding. These maybe a significant contributor to herd exposure, however, the subtypes are unlikely to be virulent in humans.
    • Infected fetuses, newborns, and products of conception (amniotic fluid, placenta, and blood) contain large numbers of forms virulent in the animals. Workers exposed to these materials may become infected. These materials also contribute to the cycling of L. monocytogenes in the general farm environment.

Wild, land and aquatic animals are not considered a significant source for human listeriosis.

• Environment
  • L. monocytogenes is widely distributed in the environment.
  • Silage – Poorly managed silage is generally accepted as the principle source of listeriosis in cows/cattle. A greater variety of strains are isolated from silage than from animal infections suggesting that far more strains will multiply in poorly managed silage than are able to cause infection in exposed domestic animals.
  • Feces – Generally accepted as a source of L. monocytogenes in the farm environment. However, there are far more strains of L. monocytogenes in the environment than are found in the farm’s animals. Manure spread on fields may contribute to contaminated crops.  This has been shown to be a source of human listeriosis when the crop was subsequently stored in cool damp conditions for months (e.g. cabbage). Fecal contamination of foods entering processing plants may contribute to the introduction of L. monocytogenes into processing plant environments.
  • Water contamination is a significant source, reservoir and transmitter of environmental listeria and is a component of the generalized contamination in the farm environment 
  • Animal Feed other than silage may be contaminated with feces/manure or water. 
  • Can be contaminated by person shedding high numbers.

    Current reviews conclude that the sources listed above are not significant as the source or transmission resulting in human listeriosis.

    More significant sources or methods of transmission of L. monocytogenes to humans.

    • Biofilm - There is longer survival of L. monocytogenes within biofilm. Although the ability to form their own biofilm is variable among different strains, given time, strains with poor production of biofilm are able to establish biofilm.
      • Biofilm is important to the persistence within processing plant environment, equipment, piping, containers, under normal cleaning operations.
      • Requires physical cleansing to remove from surfaces.
    • Microscopic fragments of biofilm carry embedded bacteria. Such fragments do not easily dilute in the product, resulting in uneven distribution.
    • Processing environments:  Commercial, retail and home food processing environments are considered the most significant contributor to human listeriosis. These locations and handling practices harbor and enhance the ability of L. monocytogenes to multiply slowly, persist over extremely long periods, and compete in the environmental ecosystems at refrigerated temperatures and contaminate a variety of foods. Slicing of processed refrigerated meats is one of the most risky procedures.
    • Contaminated water is a significant source, reservoir and transmitter of environmental listeria in processing plants.
• Milk
  • Mastitis is an uncommon location for systemic listeriosis in cows, but might contribute to spread in a herd.  However, the pattern of strains virulent in cows is different than from clinical cases in humans.
  • Contamination of milk after milking:
    • Contamination from manure would require a very large amount to reach infectious doses.
    • Contamination from other dairy environmental sources with conditions that enable multiplication of L. monocytogenes including drains and residual wash water.
    • There is poor survival of inoculated L. monocytogenes in fresh whole milk, even at refrigerated temperatures.
  • Processed milk has been linked to rare outbreaks of listeriosis. However, this contamination was from the processing environment not from inadequate pasteurization or from contamination with pre-pasteurized milk. L. monocytogenes is capable of multiplication in processed milk. Most problems with dairy products have been related to cheese.
  • Although fresh unprocessed whole milk would qualify as a ready-to-eat food; in regard to the conclusion that ready-to-eat foods are a significant source of listeriosis, unprocessed fluid milk does not fit. That is because it is the processing of the foods that confers the most significant risk.

    Fresh unprocessed whole milk has not been linked to human cases of listeriosis in the USA over the last ten years.

• Other foods

All reviews and risk analyses conclude that processed foods (ready-to-eat foods) are the principle source of all of the types of foodborne listeriosis. The patterns in these outbreaks implicate the processing plants themselves and not the specific food.  Environmental contamination in food processing operations with L. monocytogenes is widespread and persistent.  Risk factors include: the plants themselves, the equipment, packaging and storage. Risk significantly increases with the length of storage under refrigeration of the processed product. Recently it has been shown that food delivery services such as deli-type establishments appear to increase the risk for processed meats that are served cold.

Intact fresh unprocessed or undamaged foods have not been linked to human listeriosis.

References:

FDA Bad Bug Book. Listeria, listeriosis, and food safety, Third Edition. 2007  Ryser and Marth.

[1] Risk assessment of Listeria monocytogenes in ready-to-eat foods. WHO, FAO 2004

Scenario(s) for transmission of virulent Salmonella spp. to people

• Must be a salmonella subtype virulent in people.
• Virulent form most be in adequate numbers to cause illness
• Applied to the general population (do not have full immunity or compromised immune condition).
• Generally assumes transmission by ingestion

The vast majority of cases of human salmonellosis are not associated with investigated outbreaks.  Since the sporadic cases are rarely investigated there is little information on the sources or modes of transmission of the virulent subtypes of Salmonella spp.  Conclusions on definitive sources, reservoirs and modes of transmission are also distorted since outbreaks from Salmonella spp. are extremely rare, the subtypes are usually different and outbreak characteristics vary considerably. When outbreaks are recognized they often include large numbers of illnesses and significant rates of hospitalization and some deaths. Systemic infections are uncommon.  However, in very rare large outbreaks the pattern suggests a more virulent form, with more systemic infections (predominately in elderly with associated debilitating conditions), associated with increased rates of hospitalization and more deaths. 

Because typhoid fever (caused by the subtype Salmonella enterica serovar Typhi) is not a significant health problem in the USA at this time, it is not included in this summary.

Nearly all cases of foodborne salmonellosis in people are associated with consumption of high numbers of virulent organisms, and are associated with foods and food handling that enable multiplication of the bacteria prior to consumption.

It is generally accepted that the general public occasionally and repeatedly consumes food contaminated with various subtypes of salmonella throughout their lives.  There is little information on the immunological effect of this exposure.

There have been a number of studies that looked at human cases.  Each tends to have their own pattern of virulent subtypes, and sources.  These change with time, region, and method of collecting isolates. It is common to find studies that span longer periods of time, that show changes in prevalence (both increases and declines) over years. This may be the result of changes in public immunity levels, or alterations in the expression of virulent factors in the subtypes.

Source and/or vehicle for transmission

• People
  • With gastrointestinal illness- During these illnesses the bacteria multiply and are shed with very high numbers of salmonella in their stool.
  • Excluding typhoid fever, a carrier state with persistent high shedding is not well documented for the subtypes of salmonella virulent in humans.
  • People could be a vehicle for transmission of infectious bacteria in their stool to:
    • Other people through handling of food. 
    • The environment, including: water and feed.
• Animals
  • All domestic animals have significant disease caused by Salmonella spp. However, the specific subtypes are frequently animal specific. 
  • Human illness results from consumption of meat or meat products that have been processed, stored or served under conditions that enable multiplication of salmonella.
  • Eggs can be contaminated on the outside from poultry shedding salmonella.
  • Egg content can be infected with the Salmonella enterica Enteritidis from hens with ovarian infections.  
  • Wild land and aquatic animals also have significant disease but the subtypes are also frequently animal specific. Human illness associated with animal disease usually results from direct physical contact with a pet that is sick or is shedding high numbers of a virulent subtype.
  • A carrier state within animal groups is well recognized as a source of transmission to humans through direct contact or through ingestion of meat or from contamination of other food products.
• Environment
  • Water contamination is a significant source, reservoir and transmitter of environmental salmonella and is a component of the generalized contamination in the farm environment.
    It is also a significant source of transmission to humans.
  • Animal Feeds may be contaminated through direct contact with animals or humans, feces/manure or water.
  • Processing environments:  Many of the recent outbreaks have been traced to processed foods. And the processing environments are sometimes contaminated.  However, trace backs have also implicated specific ingredients (that both directly introduce virulent bacteria, or contaminate the processing environment/equipment). Ingredients are often processed, and the processing environment or the source of the ingredient may have contributed to the spread.
• Milk
  • Mastitis is an uncommon location for salmonella infection in cows.  The subtypes virulent in cows are different than from subtypes associated with human illnesses.
  • Contamination of milk after milking:
    • Contamination from manure would require very large amounts of contaminant to reach infectious doses in the farm tank.
    • Contamination from other dairy environmental sources. This would be significant only with conditions that enable multiplication of Salmonella such as in animal feed.
    • There is poor survival of inoculated Salmonella spp. in fresh whole milk at refrigerated temperatures.
• Other foods
  • Although many foods have been associated with human salmonella gastroenteritis, except for eggs, there is no real pattern for specific foods. Almost every cluster of illnesses is associated with a different food. Current outbreaks although rare can be large and each are associated with contamination of a specific food.  Most have in common: handling, storage, or serving conditions that enable multiplication of salmonella. In contrast the outbreaks caused by Salmonella enterica Enteritidis are specifically caused by eggs infected within the laying hens.

Major Reference:

FDA Bad Bug Book (distribute 2010 article from MSU on Michigan farm with salmonella)

Scenario(s) for transmission of virulent E. coli to people

• Must be a virulent form of E. coli.
• The subtype O157:H7 has the most abundant and reliable information; so will focus the scenario on this subtype (serotype).
• Must be in adequate numbers (10 or more bacteria in serving consumed).
• Person must be susceptible (does not have full immunity), but not immunocompromised.
• Must get into the intestinal tract of person (ingestion) to cause illness.

Infection and Illness:  There has been discussion about the distinction between infection (meaning establishment of bacteria with multiplication in or on the cells of the intestine) and illness (meaning persons with symptoms such as diarrhea, abdominal pain, fever, etc.).  This distinction is not always important in understanding epidemiology of foodborne illnesses, however, with the virulent forms of E. coli there is some advantage to understanding this.  Obviously illness does not happen without infection.  But infection does not automatically mean illness.   With certain bacteria, persistent infection in the absence of illness is described as a carrier state.  In the case of the virulent forms of E. coli, a true carrier state has not been reported.  However, a transient colonization with modest multiplication either prior to the onset of symptoms or without symptoms is possible in humans and is the dominate situation in cattle (e.g. E. coli O157:H7).

It’s all about numbers.  Suitable conditions for E. coli multiplication are widespread, primarily within the intestines of most animals, but also many foods (intact, damaged, processed or cooked).  During human illnesses, virulent forms will multiply in the intestine and large numbers of the virulent forms are shed in the diarrheic stool. Becoming ill requires ingestion of adequate numbers of virulent E. coli, however with the O157:H7 subtype the commonly accepted infectious dose is 10 bacteria in a serving. Some human studies cite higher numbers for infectious dose, and with other serotypes the accepted dose is much higher.   Much of the epidemiological information about human illness with the virulent strains of E. coli O157:H7 is more easily understood if you consider that there is an initial stage of infection; with illness following in some of the infected people. 

Although there are abundant conditions favorable for the multiplication of the common E. coli, large numbers of studies using E. coli O157:H7 establish that with this subtype there is a reduction in numbers over time, rather than multiplication. Survival is the consistent measurement, not multiplication. Except for active infectious disease when the virulent forms are present from contamination of feces, the non-virulent forms are present in far greater numbers, and competitively multiply more rapidly than the virulent forms.  There is a study that showed increases in E. coli O157:H7 when inoculated into mismanaged silage, and some reports of increases in the intestinal tract of common flies and birds when allowed to ingest contaminated material. 

Source and/or vehicle for transmission (subtype O157:H7)

• People
  • People ill with diarrhea- the virulent forms including the subtype O157:H7 multiply and shed in very high numbers and are the dominant bacteria in their stool. Shedding persists after illness/diarrhea has subsided. The subtypes that are shed with diarrhea are by nature virulent.
  • A carrier state with persistent high shedding is not well documented for E. coli O157:H7.
  • People with colonization that might transiently shed at low levels have not been described in the literature.
  • People can be a vehicle for transmission of infectious stool  to:
    • Other people.  Data from outbreak investigations consistently document secondary illness in people in physical contact with those with illness.  The percent of the cases that are considered to be secondary infections is not large.  However, the data may be skewed since it is possible that many of the contacts do not become primarily ill because they have some degree of prior immunity.  Given that likelihood the percent of secondary infections maybe underestimated because of that same prior immunity.  In an epidemiological analysis of US outbreaks from 1982-2002 from the CDC published in 2005 by Rangel, et al. 21 percent were associated with ground beef, 21 percent unknown, and the next highest was person-to-person 14 percent.  All dairy products were 2 percent.
    • Animals –see below.
    • The environment including: water, feed, milk, containers, food preparation surfaces and food.
• Animals
  • Cattle/cows – High prevalence of E. coli O157:H7in the intestine without causing illness. The bacteria colonize the intestine (highest rate in the end of the colon) and shedding in low numbers within feces (500 cfu/gram of feces). Colonization is more frequent in calves and heifers.
    There are occasional “super-shedders”, which shed at higher numbers (~1,000 cfu/gram feces) and persist with a single strain of E. coli O157:H7.
  • Other animals
  • Feces/manure from domestic animals
    • Can be colonized with limited multiplication of the bacteria and low shedding. These instances are transient, have variable subtypes over time and within a herd and subtypes are unlikely to be virulent in humans.
    • Super shedding is reported. Multiplication is still limited but there can be persistent shedding.
    • Fecal contamination (other than from human diarrhea) will contain all other fecal bacteria in their normal relative numbers.  Therefore, any virulent forms will be subject to the competitive inhibition and other factors that suppress multiplication.  Furthermore, any food that is contaminated with fecal material will have extremely high levels of background fecal bacteria, intermixed with any rare E. coli O157:H7 that might happen to be present. 
  • Direct physical contact with manure on animals or the ground.
  • E. coli O157:H7 has been isolated from bird feces and flies.
• Environment (All are examples of contamination, not the source and studies document the rate of survival, not increase in numbers)
  • Feces – only significant if contains high enough numbers of virulent bacteria. Numbers decline with time.
  • Water – (must be contaminated with fecal material with high numbers of virulent bacteria).  Survival within contaminants is dependent on temperature and time.
  • Biofilm – survival of E. coli O157:H7 within preformed biofilm
    Preformed from non-pathogen bacteria or produced by E. coli O157:H7 
    Persistent within equipment, piping, containers, under normal cleaning operations.
    Requires physical cleansing to remove from surfaces.
  • Biofilm produced by E. coli O157:H7 is well studied.  It forms within the intestinal contents but also on the lining cell surface of the colon.
  • Microscopic fragments of biofilm carrying embedded bacteria. These free floating fragments do not easily distribute resulting in uneven distribution.
  • Animal Feed. When contaminated with feces/manure or by oral bacteria through shared feeding. 
  • Distributed on ground that has feces/manure
  • Secondarily contaminated with contaminated water
  • Contaminated by person shedding high numbers
  • In cattle herds the intermittent recycling of strains of E. coli O157:H7 are likely to result from the re-ingestion from contaminated feed, water, and other environmental contacts.  However, there is no evidence that the total population of E. coli O157:H7 increases under these conditions.  [see separate diagram of cycle that follows below]
• Milk
  • As the direct/primary source. It maybe theoretically possible with E. coli mastitis shedding directly into milk from the udder
  • Contamination of milk during and after milking
    • From any of above sources but must be in high concentration. Should be visible in the milk filter if contamination is manure. Milk filters are designed to trap large particles and make such contamination more conspicuous.
    • Incidental contamination would usually be diluted in the bulk tank
    • There is poor survival in fresh whole milk at refrigerated temperatures (Massa et al. 1999) [1]
    • Combination of factors that inhibit multiplication of bacteria in fresh milk. (see in benefits topic section)
  • Rinse water contaminated with milk (increased survival compared to whole milk)
  • The microscopic fragments from biofilm in bulk tank, milk lines, and milking equipment.
• Other foods
  • Ground beef.
  • Leafy vegetables contaminated by manure, water, and human contact; increases with damage, cutting, and plant diseases.
  • Fruit juices when fruit is contaminated (humans, on ground, flies).
  • Any food contaminated by person shedding high numbers of a virulent form.
• Contamination of containers by people, contaminated water, fecal/manure
  • Bottles – inside or on outside
  • Transportation containers or equipment.

References for diagram. [2]

References:

[1] Massa, S.E. et al 1999 Fate of Escherichia coli O157:H7 in unpasteurized milk stored at 8°C. Letters in Applied Microbiology 28(1):89-92.

[2] Bach, S.J. et al 2002. Transmission and control of Escherichia coli o157:H7 – A review.  Can. J. Animal Sci. 82:475-490.

DISCUSSION OF INFECTION DOSE

Infectious dose is used to indicate the number of virulent bacteria that if consumed would cause illness.  In the context of the Topic on Risk, the term is used to apply to the general public, exclusive of persons who have acquired immunity, or those who for various reasons are uniquely susceptible to infection. There is no single number of virulent bacteria that when consumed will result in illness. There are even many different ways of expressing infectious dose. 1) Minimal infectious dose: the smallest number of virulent bacteria that must be consumed to cause illness. 2) 50% infectious dose: the number of virulent bacteria that when consumed at one time would result in half of the general public becoming ill.  In principle it would seem that if a bacterium is virulent even one bacterium would cause illness.  In practice, however, that does not hold true for a variety of reasons. 

The way in which the infectious dose has been determined varies. 1) Theoretical:  calculated from real and experimental data.  2). Volunteer studies: determined by having a group of people consume food specifically mixed with known numbers of a virulent strain of bacteria. 3) Epidemiologic: calculated from data on serving size and concentration of bacteria found on food associated with an outbreak. And 4) Laboratory:  based on experiments using animals.

Within the foodborne illnesses it has been found that many factors affect the infectious dose.  1) Virulence of the specific strain of bacteria. 2) Nature of the food with which the bacteria are associated. 3) Other food ingested at the same time.  4) Serving size.  5) Sequence of repetitive consumption of individual servings. 6) Individual differences in personal susceptibility.  7) Differences in the environment of the intestinal tract of the specific individual consuming the food. 8) Health, concurrent medications or concurrent illnesses of the person consuming the food.  9) Health/vitality of the bacteria consumed.

It is unusual to have the specific criteria used to define the infectious dose explained when the term is generally used.  Except in specific instances the number used in the workgroup’s Summary Statements is the “generally or widely accepted” number. 

Other pathogens of historical milk related public health concerns

In the late 1800’s several epidemic diseases dominated the public health scene in the USA.  As advocates for laws requiring pasteurization organized their campaigns, they focused the public on the role of milk in several of these diseases.  Although only one of these, human tuberculosis, continues to be a significant public health concern, each are reviewed here for historical value.  (See also Topic 1. History) 

Diphtheria is caused by the bacteria Corynebacterium diphtheriae, a virulent pathogen host adapted to humans. This is a severe infection of the upper respiratory area. Corynebacterium diphtheriae is essentially an obligate parasite of humans, transmitted between people. It is not a zoonotic disease (it does not grow in cows or other animals).  Historically examples of localized outbreaks of diphtheria were linked to persons with active infections or human carriers who were milking, processing or distributing milk. The organism does not survive long in the environment, and does not grow in milk. Pasteurization does kill these bacteria in milk.  Pasteurization would only be protective in those extremely rare circumstances when large numbers of virulent bacteria contaminated the milk itself from an infected person or carrier coughing directly into the milk, or from sputum containing large numbers of the virulent bacteria getting into the milk from handling prior to pasteurization.  The majority of these clusters were linked to people handling the milk after pasteurization would have occurred and during distribution to homes.  Diphtheria was effectively controlled by public health interventions, specifically mandated immunization of the public.  Examination of the medical records show that the number of cases had a uniform steady decline starting (1880’s), well before pasteurization was commercially used, and had a very low incident at the time mandatory pasteurization was adopted in the United States. 

Scarlet fever is a group of skin disease that can include significant upper respiratory infection caused by forms of streptococci that produce a toxin that destroys red blood cells. Regional epidemics have occurred throughout the world, including significant occurrences at different times in the mid to late 1800’s and 1900’s in the United States.  In the epidemic occurrences the disease is highly contagious through person to person contact.  A few investigations of localized clusters of scarlet fever in the early 1900’s were attributed to milk handlers that had skin rashes.  The real relevance of these cases was that the cases were published because of the distinct finding of a link of cause and effect.  A consistent finding in these cases was that the infection originated from a milk handler (not the animals).  In some of these historical reports, boiling the milk protected the family.  The milkborne spread of the pathogen may have contributed in a minor way to the general public health impact of scarlet fever during this period in history. During the turn of the century (1890-1920) physicians were only beginning to associate skin rashes with scarlet fever. Milking was by hand and contamination of fresh milk from a rash on the hands was possible.   However, the significant route of transmission of the epidemic forms was historically and continues to be by direct physical contact between people.  The significant public health impact of scarlet fever was nearly eliminated with the recognition that:  the disease was caused by bacteria;  the association of the skin rashes to the severe respiratory infections; isolating people with the infection and keeping people who had skin rashes from handling food, including milk. 

Bovine tuberculosis is a chronic debilitating disease of cows caused by Mycobacteria bovis.  The disease was endemic in the United States during the late 1800’s and first half of the 1900’s.  Incidence in domestic herds in Michigan was above 30% in some areas.  Severely infected cows can shed bacteria in their feces and with active mastitis, directly into milk. The cows become ill over long periods of time, and are extremely sick, and milk production drops significantly.  Infection can be transmitted to other animals, and to a limited extent to humans.  Human infection is acquired predominately by direct physical contract with a severely ill animal.  There is rare documentation of transmission to people from consuming heavily contaminated milk.  Pasteurization is effective against this bacterium. Unlike human tuberculosis which is transmitted through airborne droplets the bovine form does not spread through the air. When human infection of the bovine form is from consumption of milk or hand to mouth transfer, very large numbers of virulent organisms must be introduced, and the disease is localized in the lymph nodes of the neck, or along the intestinal tract.  During the late 1800’s and early 1900’s it was difficult to distinguish the bovine disease from the human form and many scientists believed they were the same disease.  However, the diseases in humans can be distinguished now, since we know that the human form is a disease of the lungs, and the bovine form is a disease of the regions of the intestinal tract from the mouth to the abdomen.  The number of “extrapulmonary” forms in people was small compared to the pulmonary forms.  Public health records of the time, which included the small number of bovine forms of disease, show a uniform steady decline starting well before pasteurization was commercially used, and with a very persistent low incident at the time mandatory pasteurization was adopted in the United States.  Because the bovine disease had significant economic impact in cattle and dairy operations, an aggressive federal eradication program of testing and killing has essentially eliminated the disease in the United States. And an active surveillance program continues to watch for and eradicate the disease imported from other countries.  Currently Michigan has a specific problem due to persistent bovine tuberculosis in the deer and other animals in a confined region of the Lower Peninsula and is spending considerable resources to protect the domestic cattle herds from any chance of spread.  Bovine tuberculosis is not a current public health risk in the United States. 

Human tuberculosis is a disease caused by Mycobacterium tuberculosis.  This form of tuberculosis is primarily a chronic disease of the lungs that may last for years without any symptoms, but can become active if the person’s immune system is compromised. When the disease is active, and in rarer circumstances of dissemination throughout the body, these debilitated persons can infect other people. Infection is predominately spread through airborne droplets containing the virulent pathogen, inhaled and causing infection in the lungs.  This organism is an intracellular obligate parasite in humans.  In the vast majority of cases the organism remains growing slowly within cells of the lung, does not cause illness, and is not infectious.  This is not a zoonotic disease, other animals do not become infected from humans, and spread does not occur from animals including cows.  Although bovine and human tuberculosis are fundamentally different diseases, during the late 1800’s the distinction was not widely recognized.  And “tuberculosis” was epidemic in the United States and a major public health concern.  As a result advocates of pasteurization were able to argue that “tuberculosis”, that was known to be a disease of cows, was coming from the cows through milk.  The small proportion of “tuberculosis” that was the bovine form is discussed above.  The major proportion of “tuberculosis” that was human,  does not infect cows, and therefore can not be transmitted through milk.  There were people with tuberculosis that were milking, and processing and distributing milk.  Milk and milk containers could only be a vehicle for transmission of human tuberculosis in the rare circumstance that the milkers or handlers had active tuberculosis and were coughing up infectious sputum.  And although pasteurization was ultimately managed so that it would kill most Mycobacteria tuberculosis, pasteurization would only have intervened in the transmission from humans to humans, if the contamination from infected sputum occurred prior to when pasteurization would have occurred.  If Mycobacteria tuberculosis was present in milk, it would cause disease of the intestinal lymph nodes (not the lungs) and only if present in extremely high numbers. Clinical studies have shown that nearly all intestinal tuberculosis is the results of a person with active human pulmonary disease swallowing sputum containing huge numbers of the pathogen.  If transmission of human tuberculosis occurred in association with milk, it is far more likely that it would have been from contamination of the outside of milk bottles with drying and airborne distribution.   Human tuberculosis was epidemic in the United States and persists as a small but significant public health problem today.  Pasteurization of milk is unlikely to have ever been a significant intervention in the epidemic. Examination of the historical medical records show that the number of cases of “tuberculosis” had a uniform steady decline starting (1880’s), well before pasteurization was commercially used, and with a very low incident at the time mandatory pasteurization was adopted in the United States.

Typhoid fever is a human disease caused by Salmonella enterica subtype Typhi. 
This bacterium is an obligate parasite of humans.  It is not a zoonotic disease and does not infect other animals.   Typhoid fever was epidemic in the United States during the 1800’s and early 1900’s.  It is transmitted from person to person through ingestion of material contaminated from the stools of infected people or rare carriers and drinking contaminated water.  Historically examples of localized outbreaks of typhoid fever were linked to persons with active infections or human carriers who where milking, processing or distributing milk.  The advocates of mandatory pasteurization used these incidents in their campaigns. Pasteurization does kill these bacteria in milk.  Pasteurization would only be protective in those extremely rare circumstances when large numbers of virulent bacteria from an infected person or carrier’s feces was introduced directly into the milk from handling prior to pasteurization.  The majority of those clusters investigated and published were linked to people handling the milk, after pasteurization would have occurred, during handling or distribution of milk to homes. Typhoid fever in the United States has been effectively controlled by public health interventions including: public (both municipal and rural) water and sewage management, isolation and treatment of carriers, and human immunization.  Examination of the historical medical records show that the number of deaths had a uniformly steady decline starting well before pasteurization was commercially used, and with a very low incident at the time mandatory pasteurization was adopted in the United States. 

Brucellosis (undulant fever, Bang’s disease)
Brucellosis is a serious disease in many domestic animals including cows caused by members of the genus brucella. Each species of brucella tends to predominate in a group of animals and have different patterns of disease; however, crossover between animal groups happens.  The species associated with human disease is also variable.  The natural environment for the growth and multiplication of these bacteria is inside the cells of animals. In humans brucellosis can present with acute symptoms, but also may take months before symptoms become evident.  Fever, with a characteristic undulating pattern, and generalized weakness are a manifestation of the systemic spread of the infection. Most human infections are the result of direct physical contact with infected animals or material from infected animal abortions.  In cows, goats and sheep there is a tendency of the disease to include infections of the mammary glands and the uterus.  Milk production is significantly reduced in infected animals.  Even so, infected dairy animals can shed large numbers of the bacteria in the milk they produce.  The milk ring test has been historically available to quickly detect a cow with brucella mastitis.  The current standards for pasteurization are set to inactivate brucella in milk. Historically milkborne brucellosis in humans was a significant public health risk.  Because of the economic impact of reduced milk production and reproductive failures a nationally mandated program to eliminate brucellosis in cattle was initiated in the 1950’s. This aggressive ‘test-and-kill the herd’ policy has effectively eradicated this disease in cattle and cows.  As a result, human brucellosis has become extremely rare in the United States, and is found predominately in immigrants and foreign travelers. 

Categories of risk other than infectious disease for people consuming fresh unprocessed whole milk

Allergies to milk
These are immunologic reactions in individuals to some component of milk. Nearly all are triggered by proteins.  These reactions are classified as hypersensitivity because they can be triggered by very small amounts of milk, or the presence of very small amounts of the specific allergic component in non-dairy products. It is generally accepted that the proteins that trigger these reactions must migrate from inside the intestine into the tissues and intercellular spaces of the body, intact (not digested) to initiate the reaction. Therefore “permeability” of the intestinal lining cells is an important factor in the initial sensitivity and in the triggering of subsequent reactions.  The severity of the reaction is different in different people, ranging from mild symptoms to sudden life-threatening conditions with significant numbers of deaths. Milk allergies are considered the second most common food allergy after allergies to eggs.  Because of the large number of people affected, the widespread use of milk or milk proteins in prepared foods, and the fact that the reactions are triggered by very small amounts, food labeling regulations require statements if there are any milk protein ingredients in the product.

• Early childhood cow’s milk allergy. This allergy adversely affects 2-8 % of infants in the USA. This is a reaction to cow’s milk usually seen when a newborn child is weaned from human breast milk to commercial formulas. Some studies show that the same reaction may occur with goat or sheep milk.  The infant reacts with a variety of symptoms including simple refusal to drink the formula, rashes (the most common reaction), vomiting, diarrhea and rarely, acute pulmonary distress.  One of the characteristics of this immunologic reaction is that as the child grows older the sensitivity to the protein allergen in the milk goes away within a few years. 
• Persistent casein milk allergy.  It adversely affects 1-4 % of the adult public in the USA.  This allergy is well recognized, however the relationship with childhood cow’s milk allergy is still being researched. One view is that some of the children with cow’s milk allergy do not become milk tolerant and their allergy persists into adulthood. Another view is that the persistent form of milk allergy may be first realized in early childhood but are immunologically distinct from the much more common childhood milk allergy. The immune reaction in the adult cases that persist is more intense and more specific.  This is a hypersensitivity immune condition, meaning even very small amounts of the specific, (usually protein) antigen will trigger a significant reaction, and the reactions can be more severe. With a large range of findings, reports say that between 15 to 70% of the children with the generic early childhood allergic reaction to milk, will maintain the hypersensitivity into adulthood.  It is clear that the persistent milk allergy is predominantly hypersensitivity to the casein molecules, but individuals can be triggered by different classes of casein and even the whey proteins (lactoglobulins). Some individuals with this form of milk allergy did not exhibit any reaction to milk in their childhood,  and some “outgrow” the hypersensitivity later in their adult life.

Nearly all research on milk allergies have used commercial cow’s milk.  There does not appear to be any study that used fresh unprocessed whole milk.  And we are unaware of any collection of reports from persons or newborns drinking fresh unprocessed whole milk that would suggest that the allergic reactions do not occur when the milk is fresh and unprocessed. However, because these immunological reactions are very specific to the configuration of the protein allergen, studies could be conducted to see if milk proteins subject to pasteurization and homogenization and those native to the unprocessed milk have the same frequency of allergenic reactions.

Lactose intolerance
Lactose intolerance (also called lactose maldigestion, or lactose malabsorption) adversely affects 10 % of the public in the USA (15% of the households), 29 million Americans. [Opinion Research 2007] Lactose intolerance is not a disease it is a condition that arises in some people as they become older.  The symptoms are variable amounts of abdominal pain, diarrhea, and intestinal gas. People usually learn that the symptoms occur when they drink milk or consume any dairy product.  Lactose is the sugar in milk (of all mammals) and lactose is only present in the milk of mammals.  Lactose is most effectively digested by an enzyme lactase (which is a β-galactosidase) forming glucose and galactose.  These two sugars are readily absorbed from the small intestine and provide a rapid source of energy (glucose) and a more long term source of energy (galactose).   Lactase is produced by the surface lining cells of the small intestine.  As milk is consumed our intestinal lactase splits the lactose into glucose and galactose which are readily absorbed in the small intestine.  In some people the amount of lactase produced by the lining cells declines as they get older.  The amount of reduction is genetically controlled, and varies from person to person, and in people with different ethnic backgrounds.  If the amount of lactase in the small intestine is not adequate to digest all of the lactose passing by, then the residual continues into the large intestine, which does not produce lactase.  Within the large intestine the complex and variable microflora do digest the residual lactose but byproducts of these processes produce gas, irritate the intestine and cause the symptoms of the condition.

To the extent that some of the lactose in the consumed milk is already digested before it reaches the large intestine by mechanisms other than the intestinal lactase activity, the residual entering the large intestine is reduced.  This could happen in the milk prior to consumption as well as within the transit of the milk after it is consumed. There is a large group of naturally occurring bacteria (many present in the dairy environment) that either digest lactose for their own energy needs, or produce exogenous lactases that digest lactose and produce byproducts within the milk. The digestion of lactose by some of these bacteria increases the acidity of the milk by their actions.  The result of the activity of others is to convert lactose into glucose and galactose, resulting in an increase in sweetness of the milk.  Many exogenous lactases are inactivated by the conditions in the stomach.  However, this inactivation is minimized in the presence of milk.  If these bacteria are allowed to be present in the milk, and are not inactivated by heating, they will effectively decrease the lactose load.

Susceptible individuals learn to avoid milk and, depending on the severity of their condition, may need to avoid even small amounts of lactose presence as ingredients in non-dairy products. The list of foods that contain lactose is very long, and even some prescription medications utilize lactose as an ingredient. There is considerable controversy about the naming of the condition, the diagnostic criteria and accuracy of the diagnosis. Consequently the size of the affected population is also controversial.  There are hundreds of published studies on the prevalence of lactose intolerance. But it is impossible to give a definitive answer to the most obvious question, ‘how many people have lactose intolerance?’.  The variability in the reported prevalence is due to differences in population groups, differences in diagnostic criteria, differences in amount of lactose in the challenge dose used, and to some extent the bias of the group performing the study.  North American Caucasian populations have a low percentage, African American have a high percentage.  Examples published include:  50-100% of African Americans, 5-15% of Caucasian Americans.  Almost all current reviews stress that many more people believe that they have lactose intolerant than are diagnosed by laboratory tests. Even with the lowest reported prevalences there are millions of adults in the USA who have this condition. The public health impact from lactose intolerance is not that these people become sick--it is that people who avoid milk because of their lactose intolerance are missing the nutritional benefits of having milk in their diets.

There are testimonials from individuals, who had not been drinking milk (because of lactose intolerance), that they are able to regularly drink fresh unprocessed whole milk. To explore this anecdotal information in more detail, an extensive questionnaire was distributed in May 2007 to families that belong to cowshare dairy groups in Michigan. Included in the questionnaire were questions about lactose intolerance. Of the 2,500 individuals surveyed, 6% reported having received a professional diagnosis of lactose intolerance. More than 80% of those individuals reported that they did not experience symptoms of lactose intolerance after drinking fresh unprocessed whole milk. While not confirmatory, the results suggest that for potentially a large number of people, drinking fresh unprocessed whole milk may represent an  alternative to abstaining from milk altogether. The testimonies and findings from this survey do not provide objective criteria of lactose intolerance nor provide an explanation for the findings."

Adulterants

• From feed.  Feeds are a potential source of ingredients or contaminants that could end up in the milk produced in the cows.  Chemicals applied to forage as part of management, in pasture or once harvested, could also contaminate the milk produced in the cows.
• Residuals from cleaning operations or pharmaceutical treatments of the cows, and drugs used to enhance milk production can end up in the milk.

Both the public’s perception of the consequences of adulterants or residuals, as well as scientific findings of their adverse effects, strongly influence fresh unprocessed whole milk consumer choices.

Adverse consequences unique to fresh unprocessed whole milk consumption

• Initial reaction to higher butterfat content.  There have been instances in which people have had intestinal reactions when consuming generous servings of fresh whole milk for the first time. There may be a temporary laxative effect. One of the unofficial suggestions is that people trying this milk for the first time should start out drinking small amounts.
• Initial reaction to higher concentration of microorganisms.  There have been instances in which people have had transitional changes in intestinal reactions to microorganisms when they first start consuming fresh whole milk. One of the interpretations is that this may be a reaction of their intestinal microflora to the input of additional bacteria in the FUW Milk they drank. 
• Changes in flavors.  There are changes in the taste of FUW Milk from time to time, related to the feed, condition of the lactating animals and other factors. Milk readily absorbs smells from the environment, so some off flavors may come from milk exposed to the farm, milking area, home or refrigerator smells. Consumers need to understand that this is to be expected.  However, there are occasional times when some or many consumers notice a change in the milk that they find objectionable, or change the way the milk behaves. Families are told that when this happens they should contact the farmer.

2. Where do these risks originate?

3.  Is there a difference in the nature of utilization of fresh unprocessed whole milk and pasteurized milk?

See the PDF document for this chapter's references.