|
Human Pathogens on the Farm Director Veterinary Medicine Teaching and Research Center University of California - Davis
The Council for Agricultural Science and Technology (CAST) task force has published a general consensus that foodborne illness in the United States affects 6.5 to 33 million people each year with approximately 9,000 deaths annually. 1 The recommendation for on-farm programs gains emphasis through recommendation 14 in the task force report (Foodborne Pathogens: Risks and Consequences- Interpretive Summary) where it states, "We recommend that control practices be applied from food source to consumption, including the incorporation of Hazard Analysis Critical Control Points (HACCP) principles. New scientific advances should be incorporated into control practices."
Key sources of selected food-poisoning organisms and waterborne human pathogens are presented in Table 1. The risks and consequences of foodborne and waterborne pathogens are coming to the forefront with strong cries for on-farm controls to be implemented immediately. The principle for the establishment of "on-farm pathogen reduction programs" is being pursued as evidenced by the introduction to Congress of the 1994 Pathogen Reduction Act, and the Food and Drug Administration (FDA) announcement for comment in the Federal Register entitled: "Food Safety Assurance Program; Development of Hazard Analysis Critical Control Points; Proposed Rule" is encouraging industries to think in terms of applying HACCP in production procedures. Thus, it will soon be necessary for veterinarians and their dairy clients to adopt a new standard of "Good Dairy Practices" that identify critical control points for both animal disease entities and those organisms that may be of concern to public health.
Target Organisms: CDC Healthy People 2000
The Center for Disease Control and Prevention (CDC) published a report entitled Healthy People 2000 2. In this report, they published health status objectives for the following specific target organisms: Salmonella species, Campylobacter jejuni, Listeria monocytogenes, and Escherichia coli O157:H7. The following is a brief discussion of these organisms, their potential impact on human health and potential sources on the dairy.
·Escherichia coli O157:H7: Escherichia coli is a member of the normal flora of the intestinal tract, but some strains are pathogenic, causing diarrhea and other symptoms by a number of different toxins (Figure 1). Infection with verotoxin producing strains of Escherichia coli (VTEC) in humans can cause symptoms ranging from diarrhea to hemorrhagic colitis and hemolytic uremic syndrome to death from renal failure.3-5 The verotoxin is a heat-labile protein which produces an irreversible cytopathic effect in Vero (African green monkey kidney) cells.6 Two immunologically distinct verotoxins, designated VT1 and VT2, can be produced, either singly or in combination, by VTEC.Because of their close homology to Shiga toxin, VT1 and VT2 are often referred to in the scientific literature as Shiga-like-toxin I (SLT-I), and Shiga-like-toxin II (SLT-II).
Enterobacteriaceae are classified by O:H serotypes, with the O antigen related to the outermost polysaccharide chains of the cell wall, and the H antigen based on the flagella type. Over 50 O:H types of VTEC have been isolated from both human and animal sources. 7 E. coli O157:H7 is the VTEC serotype most commonly isolated from humans, which may be due in part to the widespread use of sorbitol-MacConkey medium designed to detect only this serotype. The organism is similar to most E. coli; however, it does possess distinguishing characteristics. For example, E. coli O157:H7 does not ferment sorbitol within 24 h, does not possess beta-glucuronidase activity, and does not grow well or at all at 44-45.5° C. The organism has no unusual heat resistance capabilities (i.e. heating ground beef sufficiently to kill typical strains of salmonella will also kill E. coli O157:H7).8 The mechanism of pathogenicity has not been fully elucidated, but clinical isolates produce one or more verotoxins which are believed to be important virulence factors for causing disease in humans. Little is known about either the significance of or the presence of pre-formed verotoxins in foods.9
Terminology and Definitions: Escherichia coli
By far, the majority of strains of E. coli isolated from feces is part of the normal intestinal flora and they play an important role in maintaining optimal intestinal physiology. However, within this group of bacteria, there are strains that are pathogenic and cause diarrhea. E. coli that cause diarrhea do so by different mechanisms which have resulted in the following classifications: a) enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroinvasive (EIEC), enterohemorrhagic (EHEC), and verotoxigenic (VTEC). 7
Canadian scientists demonstrated that toxins produced by strains of E. coli serotype O157:H7 were cytotoxic for vero cells; hence, the name "verotoxins" or "verocytotoxins." Additionally, isolation of this pathogen was closely related with hemorrhagic colitis syndrome (HC) in humans. The terms verocytotoxins (VT) and Shiga-like toxins (SLT) are synonymous. E. coli strains that produce these toxins have been referred to as VT-producing E. coli (VTEC) SLT-producing E. coli, and enterohemorrhagic E. coli (EHEC). The term VTEC refers to all E. coli strains that produce VT in culture supernatants (Table 2). The term EHEC refers to strains that have the same clinical, epidemiological, and pathogenic features associated with the prototype EHEC organism E. coli O157:H7. Levine 5 has classified only two VTEC serotypes (O157:H7 and O26:H11) as EHEC. The predominance of serotype E. coli O157 reported is undoubtedly biased because of the wide use of methods adapted only for this serotype. It should be noted once again that more than 50 other serotypes that produce verotoxins have been described.7
E. coli O157:H7 And Farm Animals
Scientists employed DNA-DNA colony hybridization with specific gene probes for VT1 and VT2 to examine 2,100 E. coli strains from the feces of healthy animals. Ten out of 82 milk cows, 20 out of 212 beef cattle, and five out of 75 pigs were reported to carry genes for VT1, VT2 or both toxins. Several of the serotyped isolates have been described to be pathogenic for humans (0157:H7, 082:H8, 0116, 0113, 0126, 091, etc.). 9
In a portion of the National Dairy Heifer Evaluation Project conducted by Veterinary Services (USDA:APHIS), 6,894 heifer calves in 1,068 dairy herds were sampled in 28 states. The study reported a prevalence of isolating E. coli O157:H7 in calves of 3.6/1,000. E. coli O157:H7 was found among calves from two weeks of age to >12 weeks of age; however, no culture positive fecals were found among 633 calves sampled during the first week of life. Culture positive calves were present in all regions of the U.S., and the herd prevalence was estimated to approach 5%. 10 No information concerning the capability of these isolates to produce verotoxins was reported.
A study presented at the 14th Annual Western Food Animal Disease Research Conference (Moscow, ID), estimated the herd prevalence of E. coli O157:H7 in the state of Washington. The organism was isolated from 10 of 3,750 fecal samples (0.28%). This represented 5 of 60 dairy herds examined (8.3%). Postweaning heifers had a higher prevalence than other age groups. It was reported that using current technology, fecal slurry, bulk tank milk, and milk filters were not reliable samples for screening a herd’s status with regard to the presence or absence of E. coli O157:H7. 10 There appears to be no difference in the prevalence of E. coli O157:H7 in animals raised on dairies, in beef feedlots, and cow/calf operations.
Coliform mastitis occurs on every dairy throughout the world and is of major significance because it can become a prevalent form of clinical mastitis. A predominant isolate from many of these clinical cases is Escherichia coli. 11 There have been apprehensions expressed about the possibility that the cows being culled due to coliform mastitis are contaminating the food chain with E. coli O157:H7. At this time, there are no reports in the scientific literature that address this anxiety. We have examined a total of over 500 isolates from field cases of coliform mastitis (California, Arizona, Oregon, and Texas) for the presence of either the VT-1 and/or VT-2 gene. When employing a colony blot hybridization technique, 16 isolates were positive for either or both of the verotoxin probes. It is noteworthy that 10 of these isolates were not E. coli. However, when all 16 of these same isolates were examined after chromosomal DNA extraction and vacuum blot hybridization, they were all VT-1 and VT-2 probe negative.12
· Listeria monocytogenes : Listeria monocytogenes is a Gram-positive, microaerophilic, motile rod that a variety of animals, including domestic and wild mammals, 13-15 fish, avian species, amphibians, and insects can harbor.16 In humans and animals, amnionitis caused by Listeria may result in abortion, stillbirth, or neonatal sepsis. Maternal infection is characteristically symptomatic or mild, but the fetal infection is severe. Despite its in vitro sensitivity to antibiotics, mortality from listeriosis remains of concern to public health officials.
Listeriosis is usually fatal for sheep and pigs, but cattle may recover with permanent torticollis or other signs of injury to the nervous system. 17 The most common clinical manifestations of animal listeriosis are encephalitis, septicemia and abortion. Encephalitis in the ruminant is the typical form of listeriosis that is manifested in clinical settings.18 The clinical signs of listeriosis in ruminants begins with fever which may disappear after several days, dullness, and anorexia, which are followed by the development of nervous symptoms after two to three days.17 Subsequent to the nervous involvement, incoordination appears soon, and the animal has a tendency to turn in circles, in the same direction - "circling disease". Degenerative changes occur in the Central Nervous System (C.N.S.), progressing to focal necrosis and, consequently, to muscle paralysis. Several of the following neurologic signs may develop in a given bovine patient64: dropped jaw, facial hypalgesia, unilateral facial paresis or palsy (resulting in keratitis), depressed ear, ptosis, and salivation around a hypotonic lip, eyelid spasticity, medial strabismus, ataxia, circling, and head tilt toward the affected side, nystagmus, hemiparesis, ataxia of all limbs or recumbency, hypertonia, head tremor, inability to eat and drink, vomiting of ruminal ingesta, depression could vary from mild to severe, dehydration, and fever. Differential diagnosis with special attention to rabies, middle ear infections, polioencephalomalacia, and thromboembolic meningoencephalitis should be considered for evaluation.
L. monocytogenes can cause mastitis in cows, and can be shed in the milk from all four quarters of carrier cows for at least seven months.19-21 This organism has also been reported to be excreted in milk from asymptomatic cows and goats,22 and in feces, respiratory tract mucous, vaginal mucous and milk of clinically normal sheep.23
L. monocytogenes is more likely to contaminate the environment through feces, urine, and secretions such as conjunctival, oral, nasal, and uterine fluids of carriers. 23 Wild birds and silage have been reported to harbor Listeria.,24 roof rats have been shown to harbor L. monocytogenes and can contaminate its environment.15 Although L. monocytogenes can invade the body by ocular, cutaneous, respiratory or urogenital route,23 it is now believed that the oral route is the major port of entrance responsible for human listeriosis.25 Mechanical spread of manure containing Listeria can contaminate vegetables and therefore, may result in the transmission of this pathogen to man.
The occurrence of listeriosis can be either sporadic or epidemic. The sporadic form of the disease is characterized by isolated cases and the epidemic form is characterized by a cluster of cases with a common, usually foodborne, source of infection. Listeriosis in ruminants has often been associated with contaminated silage. 26-30 The pH of the silage seems to be an important factor for the presence of Listeria because it has been demonstrated that organism’s growth is influenced by the pH in media made of grass silage.31 Growth increased in the alkaline pH, and a pH value <5.5 was shown to be the critical point: above this value Listeria was able to multiply, and below that level the organisms viability could not be sustained. However, this pathogen has also been found in a good quality silage with pH = 4.0, although at lower frequencies.29
· Salmonella serovars: Salmonella infections in humans and animals cause a variety of disease manifestations, such as typhoid fever, enteric fevers, food poisoning , septicemia, localized abscesses and inflammatory foci in almost any organ of the body, and a chronic carrier state. These infections are acquired by ingestion of contaminated food or water. Salmonella do not possess enterotoxins but are capable of invading intestinal mucosal cells to cause degenerative changes in the bursh boarder and apical cytoplasm.
The two most frequently isolated Salmonella serotypes from cattle are S. typhimurium and S. dublin. S. dublin infections in humans have been linked to consumption of dairy and beef products that have resulted in a high rate of mortality. 32-33 S. dublin is an invasive pathogen that causes septicemia with high morbidity and mortality in calves, while its most common clinical manifestation in adult cattle is severe enteritis and abortion. Those animals that recover from acute infections shed the organism in their feces from four to six weeks after the clinical event. A small percentage of infected animals recover clinically, but maintain chronic mammary gland and/or enteric infections without overt clinical signs of the disease. Carrier animals may shed billions of S. dublin per day in feces and milk for years; thus, presenting a substantial challenge for susceptible hosts and environmental concerns.34Employing a combination of routine serology plus bacterial culture of milk and feces from suspect animals, persistently infected cattle can be identified and then culled from the herd. Mice and rats may also be infected with S. dublin and must be eradicated as part of an overall control program. 35 Salmonella is widespread in the dairy cow’s environment; thus, it is going to be difficult to eradicate the organism. However, ongoing research is providing insights into effective control measures that can be economically implemented on the farm.36
· Campylobacter jejuni : A comprehensive review of C. jejuni infection due to animal and food sources has been written by Alterkruse et al. 37 This infection is an important cause of sporadic cases of chronic gastritis, enterocolitis, and septicemia in man. However, this disease can result in deaths upon rare occasions. Infection with Campylobactor spp. occurs by ingestion of contaminated milk, poultry, barbecued sausage, or water. Sporadic infections may be derived from zoonotic sources, and domestic dogs can be asymptomatic carriers of this organism. Other reservoirs of this organism include wild birds, cats, ferrets, hamsters, bears, and mule deers. Houseflies may become vectors for C. jejuni.37
C. jejuni is an enteric pathogen that causes enteritis, diarrhea, and abortion in many species of farm animals. This organism can be distinguished in the laboratory from other Campylobacter spp. by growth at 42° C, resistance to cephalothin, inhibition by nalidixic acid , and the presence of heat-labile glycoprotein #1, which does not occur in C. fetus, ssp. venerealis or fetus. Experimental infections with this organism in calves result in clinical manifestations that range from ileitis to colitis, with a mild diarrhea containing blood and mucus. Possible control points in dairy production may include sanitation, water treatment, and elimination of vectors. 37
· Cryotosporidium are capable of infecting most domestic animals and man. 38 It is a protozoal disease that is considered a major pathogen of calves from one to four weeks of age. The parasite invades the enterocytes of the distal small intestine and the large intestine. This organism causes profuse watery diarrhea that may last from days to months. It is the result of villous atrophy leading to maladsorption and secondary milk fermentation. Oocyst secretion coincides with the onset of diarrhea and usually persists for a few days after the end of the diarrheic phase. The diarrhea is often accompanied by abdominal pain, nausea, vomiting, malaise, and fever.
Fecal specimens from 200 stray dogs impounded at the San Bernardino City and County animal shelters and stool specimens from 664 people were submitted to the San Bernardino County Department of Public Health Laboratory for routine parasitologic examination and were screened for Cryptosporidium sp. A total of 4/200 (2%) dogs were reported to be passing cryptosporidial oocysts in their feces. Cryptosporidial oocysts were detected in 20/664 human fecal specimens (3.01%). 39
Recent epidemiologic studies in Tokyo and Glasgow indicate that cats were found to have Cryptosporidium oocysts. Both studies concluded that kittens and young cats were more likely to shed the oocysts, and that there was no difference in prevalence between domestic and feral cats. Arai et al. 40 reported that of a total of 608 cats, 23 (3.8%) were found to have Cryptosporidium oocysts with no apparent clinical symptom such as diarrhea detected. The clinical and post mortem survey of domestic and feral cats in the Glasgow area by Mtambo et al.41 revealed that 19 of 235 (8.1 per cent) were infected with Cryptosporidium species. Two of the seven domestic cats with cryptosporidium infection were also positive for feline immunodeficiency virus.
Outbreaks of gastrointestinal illness due to contaminated municipal water supplies 42,43 have been associated with this organism (Figure 2). A noteworthy occurrence in April 1993 caused prolonged diarrheal illness in over 400,000 Milwaukee, WI residents with approximately 4,400 requiring hospitalization44. Although not documented, the alleged source of the pathogen was considered to be runoff water from local dairies.
Miron et al. 45 performed an epidemiologic study that associated calves with an outbreak of diarrhea due to Cryptospridium in children. The initial case of diarrhea in the index parent occurred during an outbreak of cryptosporidial diarrhea in calves housed in the kibbutz and just 10 days before diarrhea caused by Cryptosporidium in 14/56 children. The outbreak in the children housed in the kibbutz near the dairy was due to an initial animal to human transmission and continued with extensive human to human transmission.
Reducing the availability of this enteropathogen through learning how to manage the environment/ecosystem on the livestock production unit is a practical approach that may be useful in implementing control measures. For instance, mandatory cleaning and disinfection of facilities after each batch of calves plays an important role in reducing contamination of the calf’s environment. Both ammonia and formaldehyde are disinfectants that can be moderately effective against cryptosporidia, although they are inactivated by organic matter. Caution must be exercised because formaldehyde is a highly toxic compound that requires a long contact time to be effective against this pathogen. Medical strategies to detect and eliminate carrier animals must be developed and scientifically evaluated for implementation on the production unit.
Discussion
Food safety is a pressing issue for Government, consumers, food retailers and processors. This sense of urgency must be recognized by dairy producers and veterinarians. Although the burden of microbial foodborne disease is not known with a high degree of certainty, the estimated number of clinical cases and deaths annually 46 is somewhat disturbing even though the United States is among the leaders in providing a safe food supply for our nation (Table 3). As one listens to various presentations around the country, public health officials and regulatory agencies want to reduce or eliminate foodborne and waterborne illness by "stopping the problem at the source." Thus, the proposed concept of pathogen reduction goes back to the farm, ranch or other form of production unit. It is now evident that the movement of animals or products from any "trace back source" of pathogens or residues may be restricted or prohibited until the threat to public health no longer exists, as determined by public health officials. The concept of food safety through on-farm testing will be expensive to implement and has several major deficits in science-based program approaches to assuring that the stated goal(s) are accomplished.
The 1994 FDA announcement for public comment on a Food Safety Assurance Program introduces the rationale for mandating Hazard Analysis Critical Control Points (HACCP). The FDA is considering HACCP as the new foundation for revision of the U.S. food safety assurance program because it is considered a science based, systematic approach to the prevention of food safety problems. In addition, the implementation of HACCP: a) permits more Government oversight, b) places primary responsibility for ensuring food safety on the food manufacturer/distributor, and c) may assist U.S. food companies in competing more effectively in the world market. With a HACCP-based program in place, it is believed that a Government investigator can determine and evaluate both current and past conditions critical to ensuring the safety of the food produced by the facility. Stop and ponder what this may mean for producers and veterinarians when this policy is brought to the production unit.
It is difficult to substantially improve food safety via HACCP on-farm at this point in time. For instance, there is no current scientific evidence supporting any one or more control points available for on-farm implementation to reduce or eliminate the hazard of Escherichia coli O157:H7 (ECO157:H7). The key features necessary to eradicate a pathogen are listed in Figure 4. It is easy to ascertain that this pathogen, as well as many others, does not fit these criteria. There is little or no scientific basis for applying HACCP on-farm (Preharvest) available for the other CDC Healthy People 2000 targeted organisms at the present time. Eradication on the livestock production unit seems very unlikely for major foodborne pathogens, including ECO157:H7.
Until critical control points for zoonotic diseases are known, the dairy industry can adapt and implement Good Dairy Practices (GDP) to aid in managing animal health problems and begin addressing pathogens of concern for foodborne and waterborne illness. It will soon be advisable to establish on-farm monitoring procedures for the presence of emerging and reemerging human pathogens such as those mentioned in this paper. Probable on-farm critical control points for many of these human pathogens will be: a) housing and bedding, b) water and waste management areas, c) hospital pens, calving pens, treatment areas, d) bulk tank milk, and e) young stock and cull animals. By adapting a national standard of GDP for the production of milk and dairy beef, many worries surrounding potential chemical and microbial residues leaving the production unit can be alleviated through documentation and education.
The available pool of highly susceptible people at risk for foodborne and waterborne illness is growing both in the U.S. and around the world. This is occurring because of medical technologies that increase the longevity of patients with chronic and immunosuppressive illness, and an aging population. It appears that consumers are now willing to place more emphasis on addressing both the acute and potential chronic effects of chemical and microbial contaminants in the food supply. Because the world’s population is growing further and further away from understanding production agriculture, it will be difficult for producers and veterinarians to not address these anxieties surrounding public health issues. We must train ourselves and the next generation involved in animal agriculture how to develop working relationships in solving the concerns of Government and consumers surrounding on-farm (Preharvest) food safety issues.
· Acknowledgments: The UC Davis School of Veterinary Medicine is a Charter Member of the Food Animal Production Medicine Consortium. I would like to thank the UC Davis Livestock Disease Research Laboratory and the California Dairy Food Research Center for their generous support of the Dairy Food Safety Laboratory.
References
1. Foegeding, P.M., Roberts, T., et al. . Foodborne Pathogens: Risks and Consequences, Task Force Report No. 122, September 1994; Council for Agricultural Science and Technology, Ames, IA. 2. Public Health Service: Healthy People 2000 (Chapter 12), Department of Human Health Services Pub. 91-50212, 1991. 3. Johnson, W.M., H. Lior, and G.S. Bezanson: Cytotoxic Escherichia coli O157:H7 associated with haemorrhagic colitis in Canada. Lancet i:76, 1987. 4. Riley, L.W., R.S. Remis, S.D. Helgerson, H.B. McGee, J.G. Wells, B.R. Davis, R.J. Herbert, E.S. Olcott, L.M. Johnson, N.T. Hargrett, P.A. Blake, and M.L. Cohen. 1983. Hemorrhagic colitis associated with a rare Escherichia coli serotype. N. Engl. J. Med. 308:681-685. 5. Levine MM. Escherichia coli that cause diarrhea: enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic, and enteroadherent. J Infect Dis 155:377-89, 1987. 6. Konowalchuk, J., J.I. Speirs, and S. Stavric. : Vero response to a cytotoxin of Escherichia coli. Infect. Immun. 18:775-79, 1977. 7. Karmali, M.A. 1989. Infection by verocytotoxin-producing Escherichia coli. Clin. Microbiol. Rev. 2:15-38, 1989. 8. Willshaw GA; Smith HR; Roberts D; Thirlwell J; Cheasty T; Rowe B.: Examination of raw beef products for the presence of Vero cytotoxin producing Escherichia coli, particularly those of serogroup O157. Journal of Applied Bacteriology, 1993 Nov, 75(5):420-6, 1993. 9. Jackson, M.P., R.J. Neill, A.D. O’Brien, R.K. Holmes and J.W. Newland.: Nucleotide sequence analysis and comparison of the structural genes for Shiga-like toxin and Shiga-like toxin II en coded by bacteriophages from Escherichia coli. Fed. Eur. Microbiol. Soc. Microbiol. Lett. 44:109-114, 1987. 10. Hancock, D.D., Wells, S.J., Thomas, L.A., Hurd, H.S., Dargatz, D.A., Hill, G.W., Garber, L.P.: National prevalence study for E. coli O157:H7 in dairy calves. Abstract: 14th Annual Western Food Animal Disease Research Conference (pp. 4), March 28-29, 1993, Moscow, ID. 11. Erskine, R.J., Tyler, J.W., Riddle, M.G., Wilson, R.C.: Theory, use, and realities of efficacy and food safety of antimicrobial treatment of acute coliform mastitis. JAVMA 198(6):980-84, 1991. 12. Cullor, J.S., Carr, M., Smith, W.L.: False positive outcomes with colony blot hybridization for E. coli O157:H7 on clinical coliform mastitis field isolates. (Submitted: 1994). 13. Cranfield M, Eckhaus MA, Valentine BA, Strandberg JD: Listeriosis in Angolian giraffes. J Am Vet Med Ass 187(11):1238-1240, 1985. 14. Gray ML, Killinger AH: Listeria monocytogenes and listeric infections. Bacteriol Rev 30(2):309-382, 1966. 15. Inove S, Iida T, Tanikawa T: Isolation of Listeria monocytogenes from roof rats (rattus rattus) in builds in Tokyo. J Vet Med Sci 53(3):521-522, 1991. 16. Brackett RE: Presence and persistence of Listeria monocytogenes in food and water. Food Technol 42(4):162-164, 1988 17.Hyslop NStG, Osborne AD: Listeriosis: a potential danger to public health. Vet Rec 71(45):1082-1091, 1959
119(19):467-470, 1986. 19. Donker-Voet J: My view on the epidemiology of Listeria infections. In: Second symposium on listeric infections, ed. Gray ML. pp. 133-139. Montana State College, Bozeman, Montana, 1962. 20. Fenlon DR, Wilson J: The incidence of Listeria monocytogenes in raw milk from farm bulk tanks in North-East Scotland. J Appl Bacteriol 66(3):191-196, 1989. 21. Van Daelen AM, Jaartsveld FH: [Listeria mastites in cattle]. Tijdschrift voor Diergeneeskunde 1139(7):380-383, 1988. 22. Loken T, Aspoey E, Gronstoel H: Listeria monocytogenes excretion and humoral immunity in goats in a herd with outbreaks of listeriosis and in a healthy herd. Act Vet Scand 23(3):392-399, 1982. 23. Ralovich B: Listeriosis Research. Present Situation and Perspective. pp. 1-222. Akadeniai Kiado, Budapest, 1984. 24. Fenlon DR: Wild birds and silage as reservoir of Listeria in the agricultural environment. J Appl Bacteriol 59(6):537-543, 1985. 25. Lovett J: Listeria monocytogenes. In: Foodborne Bacterial Pathogens, ed. Doyle MP, pp. 283-310. Marcel Dekker, Inc., New York, 1989. 26. Blenden DC, Gates GA, Silberg SL: Epidemiological studies on an outbreak of listeriosis in a sheep flock. Proceedings 3rd Int Symp Listeriosis pp. 223-241, 1966. 27. Fenlon DR: Rapid quantitative assessment of the distribution of Listeria in silage implicated in a suspected outbreak of listeriosis in calves. Vet Rec 118(9):240-242, 1986. 28. Gray ML: Isolation of Listeria monocytogenes from oat silage. Science 132(3441):1767-1768, 1960. 29. Gronstol H: Listeriosis in sheep. Isolation of Listeria monocytogenes from grass silage. Acta Vet Scand 20(4):492-497, 1979 30. Low JC, Renton CP: Septicaemia, encephalitis and abortions in a housed flock of sheep caused by Listeria monocytogenes type 1/2. Vet Rec 116(6):147-150, 1985 31. Irvin AD: The effect of pH on the multiplication of Listeria monocytogenes in grass silage media. Vet Rec 82(4):115-116, 1968 32. Ferris KE, Miller DA. Salmonella serotypes from animals and related sources reported during July 1990-91. Proc US Ani Health Assn pp.440-454, San Diego, CA, 1991. 33. Lammerding AM, Garcia MM, Mann ED, Robinson Y, Dorword WJ, Truscott RB, Tittiger F. Prevalence of Salmonella and thermophilic Campylobacter in fresh pork, beef, veal, and poultry in Canada. J Food Prot 51:47-52, 1988. 34. Smith BP, Oliver DG, Singh P, et al. Detection of Salmonella dublin mammary gland infection in carrier cows using an enzyme linked immunosorbent assay for antibody in milk and serum. Am J Vet Res 50:1352-60, 1989. 35. Tablante NL, DuBose DA. Field investigations of sporadic S. dublin outbreaks in a closed dairy herd. Proc 8th Annual Western Conference for Food Animal Disease, Boise, ID, 1987. 36. House JK, Smith BP, Dilling GW, et al. Enzyme-linked immunosorbent assay for serologic detection of Salmonella dublin carriers on a large dairy. Am J Vet Res 54(a):1391-99, 1993. 37. Altekruse SF; Hunt JM; Tollefson LK; Madden JM. Food and animal sources of human Campylobacter jejuni infection. Journal of the American Veterinary Medical Association, 204(1):57-61, 1994. 38. Berkelman RL. Emerging infectious diseases in the United States, 1993. J Infect Dis 170:272-22, 1994. 39. el-Ahraf A; Tacal JV Jr; Sobih M; Amin M; Lawrence W; Wilcke BW. Prevalence of cryptosporidiosis in dogs and human beings in San Bernardino County, California. Journal of the American Veterinary Medical Association, Feb 15, 198(4):631-4, 1991. 40. Arai H; Fukuda Y; Hara T; Funakoshi Y; Kaneko S; Yoshida T; Asahi H; Kumada M; Kato K; Koyama T. Prevalence of Cryptosporidium infection among domestic cats in the Tokyo Metropolitan District, Japan. Japanese Journal of Medical Science and Biology, Feb, 43(1):7-14, 1990.
42. Moore AC; Herwaldt BL; Craun GF; Calderon RL; Highsmith AK; Juranek DD. Surveillance for waterborne disease outbreaks--United States, 1991-1992. Mmwr Cdc Surveillance Summa ries, Nov 19, 42(5):1-22, 1993. 43. From the Centers for Disease Control and Prevention. Cryptosporidium infections associated with swimming pools--Dane County, Wisconsin, 1993. Jama, Sep 28, 272(12):914-5, 1994. 44. Mac Kenzie WR; Hoxie NJ; Proctor ME; Gradus MS; Blair KA; Peterson DE; Kazmierczak JJ; Addiss DG; Fox KR; Rose JB; et al. A massive outbreak in Milwaukee of cryptosporidium infection transmitted through the public water supply. New England Journal of Medicine, Jul 21, 331(3):161-7, 1994. 45. Miron D, Kenes J, Dagan R. Calves as a source of an outbreak of cryptosporidiosis among young children in an agricultural closed community. Pediatric Inf Dis J 10(6):438-441, 1991. 46. Roberts T, Unnevehr L. Charting the costs of food safety; Food Review 17(2): 7, 1994.
TABLE 1. Major sources of selected food-poisoning organsims and waterborne pathogens that may be on the dairy
Salmonella Raw or undercooked meat, poultry, milk, eggs, fish, shellfish, pork, ice cream
Escherichia coli Raw or undercooked meat, poultry, pork, lamb, cheese, raw milk, apple cider, green salads
Cryptosporidiosis water
Figure 1. Escherichia coli of the Human Gastrointestinal Tract
· Enterpathogenic (EPEC): appear to destroy microvilli without further invasion; only a minority of these organisms produce verotoxins.
· Enteroinvasive (EIEC): invades and proliferates within epithelial cells and cause cell death.
· Enterotoxigenic (ETEC): penetrate the mucous layer of proximal small intestine where they adhere to mucosal cells and elaborate heat stable or heat labile enterotoxins. This type is frequently responsible for causing traveler’s diarrhea.
· Enterohemorrhagic (EHEC: ECO157:H7 and ECO26:H11): mechanism of causing illness has not been fully defined; potent verotoxins are associated with this disease process. Verotoxigenic (VTEC): strains of E. coli that produce heat-labile toxins that are cytotoxic for vero cells in an in vitro assay.
Figure 2: Appearance of the foodborne pathogen Escherichia coli O157:H7 a
‘82: The organism was first recognized as a human pathogen due to an outbreak from ground beef. ‘84: Outbreak of gastrointestinal disease in a child care center ‘85: The organism is associated with Hemolytic Uremic Syndrome (HUS: currently the leading cause of kidney failure in children) ‘87: The disease is now considered more common than Shigella in the United States ‘90: Outbreak from contaminated drinking water ‘91: Outbreaks from contaminated apple cider and from swimming in a lake ‘92: Now recognized as the most common bacterial cause of bloody diarrhea in the United States ‘93: Multi-state outbreak from fast-food hamburgers ‘94: >25 outbreaks due to home-cooked hamburgers
a Adapted from Berkelman RL. Emerging infectious diseases in the United States, 1993. J Infect Dis 170:272-22, 1994.
Figure 3: Time sequence of outbreaks of disease due to Cryptosporidium a
‘07: First described ‘76: First human case diagnosed ‘81: First AIDS patient diagnosed with clinical illness due to this organism ‘83: Initial child care center outbreak ‘87: Carrolton, GA- outbreak associated with surface water ‘88: Los Angeles, CA- outbreak due to a contaminated swimming pool ‘92: Medford and Talent, OR- waterborne outbreaks ‘93: Milwaukee, WI- most substantial waterborne outbreak recorded in the United States
a Adapted from Berkelman RL. Emerging infectious diseases in the United States, 1993. J Infect Dis 170:272-22, 1994.
Figure 4. Criteria necessary to eradication of a pathogen
1. A single host species with no external reservoir 2. Present on only a small percent of production units
3. Pathogen serves as a disease marker for endemic herds
4. Appropriate assays exist that can correctly identify carrier animals, plus a means of interven- ing in the chain of infection after carrier animals have been removed from the herd
5. Billions of dollars
6. Resolve by all involved to fully implement all measures necessary for eradication
|